User login
In weighing PCI vs. CABG for left main disease, diabetes matters
WASHINGTON – For patients with diabetes, there are trade-offs for selecting a percutaneous intervention (PCI) over coronary artery bypass grafting (CABG) for left main artery disease when either can be considered, according to a hypothesis-generating pooled analysis.
The pooled data from four trials indicate that either method of revascularization is “reasonable,” but risk of myocardial infarction and revascularization is higher and risk of stroke is lower in patients with diabetes following PCI relative to CABG, Prakriti Gaba, MD, said in presenting the analysis at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
Despite decades of advances in both PCI and CABG, the findings are remarkably similar to those of Emory Angioplasty Versus Surgery Trial (EAST), the first major study to compare PCI to CABG, which were published almost 30 years ago. In the new analysis, like in EAST, PCI and CABG were comparable for a primary composite endpoint overall, but patients with diabetes were the exception. In those, outcomes were modestly better after CABG, said Dr. Gaba, a cardiology fellow at Brigham and Women’s Hospital, Harvard Medical School, both in Boston.
“More and more I am hearing from practitioners that diabetes does not matter, but what I get from your data is that diabetes still matters,” said Spencer B. King, MD, a pioneer of PCI affiliated with Emory University, Atlanta.
Dr. King, the first author of the 1994 paper and a panelist in the late-breaking trial session where the new data were presented, pointed out that a relatively limited proportion of patients with diabetes are equally suitable for PCI and CABG because of other considerations. However, he said an updated look once again suggesting that PCI and CABG are not equivalent for left main lesions in patients with diabetes “is helpful to see.”
CABG traditionally preferred for left main revascularization
The issue was revisited because CABG has been preferred traditionally for left main disease, but there was increasing evidence that PCI is associated with similar survival, according to Dr. Gaba. These new data support that contention, even if it shows that outcomes are not the same in those with diabetes relative to those without.
In this pooled analysis, data were drawn from four trials. Each compared PCI with drug-eluting stents with CABG in patients that were considered suitable for either. From the four trials, the numbers in this analysis included 705 patients from SYNTAX, 600 patients from PRECOMBAT, 1,184 patients from NOBLE, and 1,905 patients from EXCEL.
The focus was on the 1,104 patients with diabetes relative to the 3,289 without. The primary endpoint was all-cause death at 5 years. The multiple secondary endpoints included cardiovascular (CV) death, MI, stroke, and revascularization.
Overall, the 5-year mortality, independent of revascularization procedure, was 14.8% for those with diabetes and 9.3% for those without (P < .001). For this endpoint, the rates were numerically lower but not statistically different for CABG whether patients had diabetes (14.1% vs. 15.3%) or no diabetes (8.9% vs. 9.7%).
However, the rate of spontaneous MI was twice as great with PCI than with CABG for those with diabetes (8.9% vs. 4.4%), which doubled the hazard ratio within significant confidence intervals (HR, 2.01; 95% CI, 1.21-3.35). The rates of revascularization were also about twice as great with PCI than with CABG (24.5% vs. 12.4%), again producing a twofold increase in risk (HR, 2.12; 95% CI, 1.56-2.87).
For stroke in patients with diabetes, there was no difference in events at 5 years for PCI relative to CABG (2.1% in both groups). However, in those without diabetes, a trend approaching significance favored CABG over PCI (1.2% vs. 2.1%; HR, 0.177; 95% CI, 0.99-1.77). This difference was concentrated in the first year, when stroke rates among those treated with CABG were more than double the rates among those treated with PCI. Over time, this difference dissipated so that the difference was reduced to a trend at the end of follow-up.
Data considered hypothesis generating
Although patients with diabetes were prespecified as a subgroup of interest in these studies, Dr. Gaba said that the data can only be considered hypothesis generating and pointed out several limitations, including the fact that these studies preceded some therapies, such as sodium-glucose cotransporter 2 inhibitors, that are known to affect CV outcomes.
However, Dr. King was not alone in suggesting that these data once again show that diabetes matters. Several panelists agreed, including the moderator of the session, Robert A Byrne, MBBcH, PhD, director of cardiology, Mater Private Hospital, Dublin.
“Of course, there has been a lot of discussion over the last 4 or 5 years about this issue since the long-term EXCEL data were presented,” Dr. Byrne said. He added that the team of investigators who put this together “have done a great service to the community” by providing a detailed combined analysis to explore the interaction between diabetes and outcomes relative to method of revascularization. Although PCI and CABG are not always equivalent choices for reasons other than diabetes, he echoed the sentiment that diabetes likely remains a variable to consider when considering revascularization of left main artery disease.
Dr. Gabi, Dr. Spencer, and Dr. Byrne report no potential conflicts of interest.
WASHINGTON – For patients with diabetes, there are trade-offs for selecting a percutaneous intervention (PCI) over coronary artery bypass grafting (CABG) for left main artery disease when either can be considered, according to a hypothesis-generating pooled analysis.
The pooled data from four trials indicate that either method of revascularization is “reasonable,” but risk of myocardial infarction and revascularization is higher and risk of stroke is lower in patients with diabetes following PCI relative to CABG, Prakriti Gaba, MD, said in presenting the analysis at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
Despite decades of advances in both PCI and CABG, the findings are remarkably similar to those of Emory Angioplasty Versus Surgery Trial (EAST), the first major study to compare PCI to CABG, which were published almost 30 years ago. In the new analysis, like in EAST, PCI and CABG were comparable for a primary composite endpoint overall, but patients with diabetes were the exception. In those, outcomes were modestly better after CABG, said Dr. Gaba, a cardiology fellow at Brigham and Women’s Hospital, Harvard Medical School, both in Boston.
“More and more I am hearing from practitioners that diabetes does not matter, but what I get from your data is that diabetes still matters,” said Spencer B. King, MD, a pioneer of PCI affiliated with Emory University, Atlanta.
Dr. King, the first author of the 1994 paper and a panelist in the late-breaking trial session where the new data were presented, pointed out that a relatively limited proportion of patients with diabetes are equally suitable for PCI and CABG because of other considerations. However, he said an updated look once again suggesting that PCI and CABG are not equivalent for left main lesions in patients with diabetes “is helpful to see.”
CABG traditionally preferred for left main revascularization
The issue was revisited because CABG has been preferred traditionally for left main disease, but there was increasing evidence that PCI is associated with similar survival, according to Dr. Gaba. These new data support that contention, even if it shows that outcomes are not the same in those with diabetes relative to those without.
In this pooled analysis, data were drawn from four trials. Each compared PCI with drug-eluting stents with CABG in patients that were considered suitable for either. From the four trials, the numbers in this analysis included 705 patients from SYNTAX, 600 patients from PRECOMBAT, 1,184 patients from NOBLE, and 1,905 patients from EXCEL.
The focus was on the 1,104 patients with diabetes relative to the 3,289 without. The primary endpoint was all-cause death at 5 years. The multiple secondary endpoints included cardiovascular (CV) death, MI, stroke, and revascularization.
Overall, the 5-year mortality, independent of revascularization procedure, was 14.8% for those with diabetes and 9.3% for those without (P < .001). For this endpoint, the rates were numerically lower but not statistically different for CABG whether patients had diabetes (14.1% vs. 15.3%) or no diabetes (8.9% vs. 9.7%).
However, the rate of spontaneous MI was twice as great with PCI than with CABG for those with diabetes (8.9% vs. 4.4%), which doubled the hazard ratio within significant confidence intervals (HR, 2.01; 95% CI, 1.21-3.35). The rates of revascularization were also about twice as great with PCI than with CABG (24.5% vs. 12.4%), again producing a twofold increase in risk (HR, 2.12; 95% CI, 1.56-2.87).
For stroke in patients with diabetes, there was no difference in events at 5 years for PCI relative to CABG (2.1% in both groups). However, in those without diabetes, a trend approaching significance favored CABG over PCI (1.2% vs. 2.1%; HR, 0.177; 95% CI, 0.99-1.77). This difference was concentrated in the first year, when stroke rates among those treated with CABG were more than double the rates among those treated with PCI. Over time, this difference dissipated so that the difference was reduced to a trend at the end of follow-up.
Data considered hypothesis generating
Although patients with diabetes were prespecified as a subgroup of interest in these studies, Dr. Gaba said that the data can only be considered hypothesis generating and pointed out several limitations, including the fact that these studies preceded some therapies, such as sodium-glucose cotransporter 2 inhibitors, that are known to affect CV outcomes.
However, Dr. King was not alone in suggesting that these data once again show that diabetes matters. Several panelists agreed, including the moderator of the session, Robert A Byrne, MBBcH, PhD, director of cardiology, Mater Private Hospital, Dublin.
“Of course, there has been a lot of discussion over the last 4 or 5 years about this issue since the long-term EXCEL data were presented,” Dr. Byrne said. He added that the team of investigators who put this together “have done a great service to the community” by providing a detailed combined analysis to explore the interaction between diabetes and outcomes relative to method of revascularization. Although PCI and CABG are not always equivalent choices for reasons other than diabetes, he echoed the sentiment that diabetes likely remains a variable to consider when considering revascularization of left main artery disease.
Dr. Gabi, Dr. Spencer, and Dr. Byrne report no potential conflicts of interest.
WASHINGTON – For patients with diabetes, there are trade-offs for selecting a percutaneous intervention (PCI) over coronary artery bypass grafting (CABG) for left main artery disease when either can be considered, according to a hypothesis-generating pooled analysis.
The pooled data from four trials indicate that either method of revascularization is “reasonable,” but risk of myocardial infarction and revascularization is higher and risk of stroke is lower in patients with diabetes following PCI relative to CABG, Prakriti Gaba, MD, said in presenting the analysis at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
Despite decades of advances in both PCI and CABG, the findings are remarkably similar to those of Emory Angioplasty Versus Surgery Trial (EAST), the first major study to compare PCI to CABG, which were published almost 30 years ago. In the new analysis, like in EAST, PCI and CABG were comparable for a primary composite endpoint overall, but patients with diabetes were the exception. In those, outcomes were modestly better after CABG, said Dr. Gaba, a cardiology fellow at Brigham and Women’s Hospital, Harvard Medical School, both in Boston.
“More and more I am hearing from practitioners that diabetes does not matter, but what I get from your data is that diabetes still matters,” said Spencer B. King, MD, a pioneer of PCI affiliated with Emory University, Atlanta.
Dr. King, the first author of the 1994 paper and a panelist in the late-breaking trial session where the new data were presented, pointed out that a relatively limited proportion of patients with diabetes are equally suitable for PCI and CABG because of other considerations. However, he said an updated look once again suggesting that PCI and CABG are not equivalent for left main lesions in patients with diabetes “is helpful to see.”
CABG traditionally preferred for left main revascularization
The issue was revisited because CABG has been preferred traditionally for left main disease, but there was increasing evidence that PCI is associated with similar survival, according to Dr. Gaba. These new data support that contention, even if it shows that outcomes are not the same in those with diabetes relative to those without.
In this pooled analysis, data were drawn from four trials. Each compared PCI with drug-eluting stents with CABG in patients that were considered suitable for either. From the four trials, the numbers in this analysis included 705 patients from SYNTAX, 600 patients from PRECOMBAT, 1,184 patients from NOBLE, and 1,905 patients from EXCEL.
The focus was on the 1,104 patients with diabetes relative to the 3,289 without. The primary endpoint was all-cause death at 5 years. The multiple secondary endpoints included cardiovascular (CV) death, MI, stroke, and revascularization.
Overall, the 5-year mortality, independent of revascularization procedure, was 14.8% for those with diabetes and 9.3% for those without (P < .001). For this endpoint, the rates were numerically lower but not statistically different for CABG whether patients had diabetes (14.1% vs. 15.3%) or no diabetes (8.9% vs. 9.7%).
However, the rate of spontaneous MI was twice as great with PCI than with CABG for those with diabetes (8.9% vs. 4.4%), which doubled the hazard ratio within significant confidence intervals (HR, 2.01; 95% CI, 1.21-3.35). The rates of revascularization were also about twice as great with PCI than with CABG (24.5% vs. 12.4%), again producing a twofold increase in risk (HR, 2.12; 95% CI, 1.56-2.87).
For stroke in patients with diabetes, there was no difference in events at 5 years for PCI relative to CABG (2.1% in both groups). However, in those without diabetes, a trend approaching significance favored CABG over PCI (1.2% vs. 2.1%; HR, 0.177; 95% CI, 0.99-1.77). This difference was concentrated in the first year, when stroke rates among those treated with CABG were more than double the rates among those treated with PCI. Over time, this difference dissipated so that the difference was reduced to a trend at the end of follow-up.
Data considered hypothesis generating
Although patients with diabetes were prespecified as a subgroup of interest in these studies, Dr. Gaba said that the data can only be considered hypothesis generating and pointed out several limitations, including the fact that these studies preceded some therapies, such as sodium-glucose cotransporter 2 inhibitors, that are known to affect CV outcomes.
However, Dr. King was not alone in suggesting that these data once again show that diabetes matters. Several panelists agreed, including the moderator of the session, Robert A Byrne, MBBcH, PhD, director of cardiology, Mater Private Hospital, Dublin.
“Of course, there has been a lot of discussion over the last 4 or 5 years about this issue since the long-term EXCEL data were presented,” Dr. Byrne said. He added that the team of investigators who put this together “have done a great service to the community” by providing a detailed combined analysis to explore the interaction between diabetes and outcomes relative to method of revascularization. Although PCI and CABG are not always equivalent choices for reasons other than diabetes, he echoed the sentiment that diabetes likely remains a variable to consider when considering revascularization of left main artery disease.
Dr. Gabi, Dr. Spencer, and Dr. Byrne report no potential conflicts of interest.
AT CRT 2023
Drinking beet juice tied to reduced post-PCI restenosis
WASHINGTON – Late lumen loss (LLL) after percutaneous interventions (PCI) can be reduced significantly by a daily glass of beet juice, according to a phase 2 randomized trial.
The protection against LLL, attributed to the nitrate contained in beet juice, was accompanied by a trend for a reduced risk of major adverse cardiovascular events (MACE), according to Krishnaraj Rathod, MBBS, BMedSci, PhD, who presented results at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
The study grew out of relatively recent evidence that ingestion of nitrate-rich foods, such as beets, can trigger noncanonical pathways for nitric oxide generation, sometimes referred to as the nitrate-nitrite-nitric oxide sequence. Dr. Rathod cited experimental evidence associating this pathway with the traditional benefits of NO generation, such as anti-inflammatory and antithrombotic effects.
In this study, 300 patients scheduled for PCI to treat stable angina were randomized to the experimental arm of nitrate-rich beetroot juice or the control arm of nitrate-depleted beetroot juice. Each had a 70-mL glass of juice once daily. Dr. Rathod, a senior interventional cardiology registrar, Barts Heart Centre, London, described this as the equivalent of about four beets.
The primary endpoint of the study was in-stent LLL assessed by quantitative coronary angiography (QCA) at 6 months.
MACE, defined as death, MI, need for revascularization, and in-stent thrombosis, was assessed at 3, 9, 12, and 24 months. In addition, markers of NO activation, platelet reactivity, and inflammation were monitored.
Lumen loss reduced less than 50%
On OCA, the median stent LLL at 6 months was 0.244 mm in the nitrate-depleted beet juice group and 0.117 mm (P = .0165) in the group that received natural beet juice. The mean segment LLL similarly favored the natural beet juice (0.269 vs. 0.050 mm; P = .0011).
The same effect was reflected in the measurement of mean change in minimum lumen diameter at 6 months. From baseline, this in-stent measure was reduced at 6 months by 0.244 mm in the control group, but by only 0.117 mm in the group receiving the dietary nitrate (P = .0154 for two-way analysis of variance).
Over 24 months of follow-up, there were 18 MACE events in the control arm versus 9 in the arm randomized to dietary nitrate (P = .0718). There were no in-stent thromboses observed in either group, but death (two vs. five), MI (one vs. six), and target-vessel revascularization (six vs. seven) were all numerically lower in the group receiving dietary nitrate.
“Once-a-day oral dietary nitrate for 6 months was well tolerated and safe,” Dr. Rathod reported at the meeting.
Asked specifically about the taste of the daily glass of beet juice, Dr. Rathod acknowledged that some patients were not enamored, but many had no objections or even liked the taste.
The patients were reasonably representative of a PCI population. The mean age in both groups was 61 years. There were no significant differences in body mass index (approximately 29 kg/m2) or proportion with diabetes (22%), hypertension, or hypercholesterolemia (about 70% in both groups) and other comorbidities.
More PCI was performed in the left anterior descending artery (36.7% vs. 44.0%) in the control group, while less PCI was performed in the right coronary (27.3% vs. 30.7%). Neither difference was significant. The vast majority (~90%) of patients received drug-eluting stents with a mean of 1.4 implanted. Procedural success was 100% in both groups.
Discharge medications, including antiplatelet and antithrombotic therapies, were similar in the two groups.
Results characterized as highly positive
Based on the 53% reduction in LLL at 6 months and the trend for a MACE reduction, Dr. Rathod concluded that the results were highly positive.
“These results suggest that dietary nitrate may have a therapeutic role in reducing restenosis following PCI for stable angina,” he said.
In the discussion, several panelists pointed out that nearly one-third of patients were not available for evaluation at 6 months (41 of 150 in the experimental group and 51 of 150 in the control group) with further attrition at 1 and 2 years of follow-up. Of these about half were lost to follow-up and the other half withdrew.
The lack of follow-up on such a high proportion of participants is one weakness of this study,” acknowledged Hector M. Garcia-Garcia, MD, PhD, a cardiovascular researcher at MedStar Washington Hospital Center. However, he remains enthusiastic about the premise.
“It was encouraging to see every signal moving in the right direction,” said Dr. Garcia, who consulted with Dr. Rathod’s group on the design of the study. He called these data “promising,” and said they provide support for larger trial for a treatment with potential benefits at low cost.
George Dangas, MD, PhD, professor of medicine at the Icahn School of Medicine at Mount Sinai, New York, was among panelists who seemed surprised by such positive findings from a simple but novel concept. However, he remains open to further evaluations.
“As with any surprising result, further confirmation in a large and multicenter trial should be anticipated,” he said in an interview. If, as this study suggests, dietary changes are capable of providing therapeutic NO at the vascular level, he suggested studies to demonstrate anti-inflammatory effects or other mechanistic benefits would be helpful.
“Other sources of oral nitrate would also be a worthwhile investigation,” he said.
Dr. Rathod reports no potential conflicts of interest. Dr. Garcia-Garcia reports ties to Abbott, Biotronik, Boston Scientific, CorFlow, Medtronic, Neovasc, Phillips, and Shockwave. Dr. Dangas reports financial relationships with Abbott Vascular, AstraZeneca, Boston Scientific, Daiichi-Sankyo, and Medtronic.
WASHINGTON – Late lumen loss (LLL) after percutaneous interventions (PCI) can be reduced significantly by a daily glass of beet juice, according to a phase 2 randomized trial.
The protection against LLL, attributed to the nitrate contained in beet juice, was accompanied by a trend for a reduced risk of major adverse cardiovascular events (MACE), according to Krishnaraj Rathod, MBBS, BMedSci, PhD, who presented results at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
The study grew out of relatively recent evidence that ingestion of nitrate-rich foods, such as beets, can trigger noncanonical pathways for nitric oxide generation, sometimes referred to as the nitrate-nitrite-nitric oxide sequence. Dr. Rathod cited experimental evidence associating this pathway with the traditional benefits of NO generation, such as anti-inflammatory and antithrombotic effects.
In this study, 300 patients scheduled for PCI to treat stable angina were randomized to the experimental arm of nitrate-rich beetroot juice or the control arm of nitrate-depleted beetroot juice. Each had a 70-mL glass of juice once daily. Dr. Rathod, a senior interventional cardiology registrar, Barts Heart Centre, London, described this as the equivalent of about four beets.
The primary endpoint of the study was in-stent LLL assessed by quantitative coronary angiography (QCA) at 6 months.
MACE, defined as death, MI, need for revascularization, and in-stent thrombosis, was assessed at 3, 9, 12, and 24 months. In addition, markers of NO activation, platelet reactivity, and inflammation were monitored.
Lumen loss reduced less than 50%
On OCA, the median stent LLL at 6 months was 0.244 mm in the nitrate-depleted beet juice group and 0.117 mm (P = .0165) in the group that received natural beet juice. The mean segment LLL similarly favored the natural beet juice (0.269 vs. 0.050 mm; P = .0011).
The same effect was reflected in the measurement of mean change in minimum lumen diameter at 6 months. From baseline, this in-stent measure was reduced at 6 months by 0.244 mm in the control group, but by only 0.117 mm in the group receiving the dietary nitrate (P = .0154 for two-way analysis of variance).
Over 24 months of follow-up, there were 18 MACE events in the control arm versus 9 in the arm randomized to dietary nitrate (P = .0718). There were no in-stent thromboses observed in either group, but death (two vs. five), MI (one vs. six), and target-vessel revascularization (six vs. seven) were all numerically lower in the group receiving dietary nitrate.
“Once-a-day oral dietary nitrate for 6 months was well tolerated and safe,” Dr. Rathod reported at the meeting.
Asked specifically about the taste of the daily glass of beet juice, Dr. Rathod acknowledged that some patients were not enamored, but many had no objections or even liked the taste.
The patients were reasonably representative of a PCI population. The mean age in both groups was 61 years. There were no significant differences in body mass index (approximately 29 kg/m2) or proportion with diabetes (22%), hypertension, or hypercholesterolemia (about 70% in both groups) and other comorbidities.
More PCI was performed in the left anterior descending artery (36.7% vs. 44.0%) in the control group, while less PCI was performed in the right coronary (27.3% vs. 30.7%). Neither difference was significant. The vast majority (~90%) of patients received drug-eluting stents with a mean of 1.4 implanted. Procedural success was 100% in both groups.
Discharge medications, including antiplatelet and antithrombotic therapies, were similar in the two groups.
Results characterized as highly positive
Based on the 53% reduction in LLL at 6 months and the trend for a MACE reduction, Dr. Rathod concluded that the results were highly positive.
“These results suggest that dietary nitrate may have a therapeutic role in reducing restenosis following PCI for stable angina,” he said.
In the discussion, several panelists pointed out that nearly one-third of patients were not available for evaluation at 6 months (41 of 150 in the experimental group and 51 of 150 in the control group) with further attrition at 1 and 2 years of follow-up. Of these about half were lost to follow-up and the other half withdrew.
The lack of follow-up on such a high proportion of participants is one weakness of this study,” acknowledged Hector M. Garcia-Garcia, MD, PhD, a cardiovascular researcher at MedStar Washington Hospital Center. However, he remains enthusiastic about the premise.
“It was encouraging to see every signal moving in the right direction,” said Dr. Garcia, who consulted with Dr. Rathod’s group on the design of the study. He called these data “promising,” and said they provide support for larger trial for a treatment with potential benefits at low cost.
George Dangas, MD, PhD, professor of medicine at the Icahn School of Medicine at Mount Sinai, New York, was among panelists who seemed surprised by such positive findings from a simple but novel concept. However, he remains open to further evaluations.
“As with any surprising result, further confirmation in a large and multicenter trial should be anticipated,” he said in an interview. If, as this study suggests, dietary changes are capable of providing therapeutic NO at the vascular level, he suggested studies to demonstrate anti-inflammatory effects or other mechanistic benefits would be helpful.
“Other sources of oral nitrate would also be a worthwhile investigation,” he said.
Dr. Rathod reports no potential conflicts of interest. Dr. Garcia-Garcia reports ties to Abbott, Biotronik, Boston Scientific, CorFlow, Medtronic, Neovasc, Phillips, and Shockwave. Dr. Dangas reports financial relationships with Abbott Vascular, AstraZeneca, Boston Scientific, Daiichi-Sankyo, and Medtronic.
WASHINGTON – Late lumen loss (LLL) after percutaneous interventions (PCI) can be reduced significantly by a daily glass of beet juice, according to a phase 2 randomized trial.
The protection against LLL, attributed to the nitrate contained in beet juice, was accompanied by a trend for a reduced risk of major adverse cardiovascular events (MACE), according to Krishnaraj Rathod, MBBS, BMedSci, PhD, who presented results at the Cardiovascular Research Technologies conference, sponsored by MedStar Heart & Vascular Institute.
The study grew out of relatively recent evidence that ingestion of nitrate-rich foods, such as beets, can trigger noncanonical pathways for nitric oxide generation, sometimes referred to as the nitrate-nitrite-nitric oxide sequence. Dr. Rathod cited experimental evidence associating this pathway with the traditional benefits of NO generation, such as anti-inflammatory and antithrombotic effects.
In this study, 300 patients scheduled for PCI to treat stable angina were randomized to the experimental arm of nitrate-rich beetroot juice or the control arm of nitrate-depleted beetroot juice. Each had a 70-mL glass of juice once daily. Dr. Rathod, a senior interventional cardiology registrar, Barts Heart Centre, London, described this as the equivalent of about four beets.
The primary endpoint of the study was in-stent LLL assessed by quantitative coronary angiography (QCA) at 6 months.
MACE, defined as death, MI, need for revascularization, and in-stent thrombosis, was assessed at 3, 9, 12, and 24 months. In addition, markers of NO activation, platelet reactivity, and inflammation were monitored.
Lumen loss reduced less than 50%
On OCA, the median stent LLL at 6 months was 0.244 mm in the nitrate-depleted beet juice group and 0.117 mm (P = .0165) in the group that received natural beet juice. The mean segment LLL similarly favored the natural beet juice (0.269 vs. 0.050 mm; P = .0011).
The same effect was reflected in the measurement of mean change in minimum lumen diameter at 6 months. From baseline, this in-stent measure was reduced at 6 months by 0.244 mm in the control group, but by only 0.117 mm in the group receiving the dietary nitrate (P = .0154 for two-way analysis of variance).
Over 24 months of follow-up, there were 18 MACE events in the control arm versus 9 in the arm randomized to dietary nitrate (P = .0718). There were no in-stent thromboses observed in either group, but death (two vs. five), MI (one vs. six), and target-vessel revascularization (six vs. seven) were all numerically lower in the group receiving dietary nitrate.
“Once-a-day oral dietary nitrate for 6 months was well tolerated and safe,” Dr. Rathod reported at the meeting.
Asked specifically about the taste of the daily glass of beet juice, Dr. Rathod acknowledged that some patients were not enamored, but many had no objections or even liked the taste.
The patients were reasonably representative of a PCI population. The mean age in both groups was 61 years. There were no significant differences in body mass index (approximately 29 kg/m2) or proportion with diabetes (22%), hypertension, or hypercholesterolemia (about 70% in both groups) and other comorbidities.
More PCI was performed in the left anterior descending artery (36.7% vs. 44.0%) in the control group, while less PCI was performed in the right coronary (27.3% vs. 30.7%). Neither difference was significant. The vast majority (~90%) of patients received drug-eluting stents with a mean of 1.4 implanted. Procedural success was 100% in both groups.
Discharge medications, including antiplatelet and antithrombotic therapies, were similar in the two groups.
Results characterized as highly positive
Based on the 53% reduction in LLL at 6 months and the trend for a MACE reduction, Dr. Rathod concluded that the results were highly positive.
“These results suggest that dietary nitrate may have a therapeutic role in reducing restenosis following PCI for stable angina,” he said.
In the discussion, several panelists pointed out that nearly one-third of patients were not available for evaluation at 6 months (41 of 150 in the experimental group and 51 of 150 in the control group) with further attrition at 1 and 2 years of follow-up. Of these about half were lost to follow-up and the other half withdrew.
The lack of follow-up on such a high proportion of participants is one weakness of this study,” acknowledged Hector M. Garcia-Garcia, MD, PhD, a cardiovascular researcher at MedStar Washington Hospital Center. However, he remains enthusiastic about the premise.
“It was encouraging to see every signal moving in the right direction,” said Dr. Garcia, who consulted with Dr. Rathod’s group on the design of the study. He called these data “promising,” and said they provide support for larger trial for a treatment with potential benefits at low cost.
George Dangas, MD, PhD, professor of medicine at the Icahn School of Medicine at Mount Sinai, New York, was among panelists who seemed surprised by such positive findings from a simple but novel concept. However, he remains open to further evaluations.
“As with any surprising result, further confirmation in a large and multicenter trial should be anticipated,” he said in an interview. If, as this study suggests, dietary changes are capable of providing therapeutic NO at the vascular level, he suggested studies to demonstrate anti-inflammatory effects or other mechanistic benefits would be helpful.
“Other sources of oral nitrate would also be a worthwhile investigation,” he said.
Dr. Rathod reports no potential conflicts of interest. Dr. Garcia-Garcia reports ties to Abbott, Biotronik, Boston Scientific, CorFlow, Medtronic, Neovasc, Phillips, and Shockwave. Dr. Dangas reports financial relationships with Abbott Vascular, AstraZeneca, Boston Scientific, Daiichi-Sankyo, and Medtronic.
AT CRT 2023
A doctor must go to extremes to save a choking victim
Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.
The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.
Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.
Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.
Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.
At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.
Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.
So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.
I said, “We have to put her down on the floor.” And then I said, “Knife!”
I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.
I had never done this in my life.
While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.
I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.
I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.
It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”
Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.
She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.
She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.
They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.
I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”
That surprised me. I didn’t think we were going to go there.
I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.
Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.
A version of this article first appeared on Medscape.com.
Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.
The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.
Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.
Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.
Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.
At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.
Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.
So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.
I said, “We have to put her down on the floor.” And then I said, “Knife!”
I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.
I had never done this in my life.
While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.
I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.
I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.
It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”
Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.
She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.
She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.
They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.
I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”
That surprised me. I didn’t think we were going to go there.
I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.
Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.
A version of this article first appeared on Medscape.com.
Some time ago I was invited to join a bipartisan congressional task force on valley fever, also known as coccidioidomycosis. A large and diverse crowd attended the task force’s first meeting in Bakersfield, Calif. – a meeting for everyone: the medical profession, the public, it even included veterinarians.
The whole thing was a resounding success. Francis Collins was there, the just-retired director of the NIH. Tom Frieden, then-director of the Centers for Disease Control and Prevention was there, as were several congresspeople and also my college roommate, a retired Navy medical corps captain. I was enjoying it.
Afterward, we had a banquet dinner at a restaurant in downtown Bakersfield. One of the people there was a woman I knew well – her husband was a physician friend. The restaurant served steak and salmon, and this woman made the mistake of ordering the steak.
Not long after the entrees were served, I heard a commotion at the table just behind me. I turned around and saw that woman in distress. A piece of steak had wedged in her trachea and she couldn’t breathe.
Almost immediately, the chef showed up. I don’t know how he got there. The chef at this restaurant was a big guy. I mean, probably 6 feet, 5 inches tall and 275 pounds. He tried the Heimlich maneuver. It didn’t work.
At that point, I jumped up. I thought, “Well, maybe I know how to do this better than him.” Probably not, actually. I tried and couldn’t make it work either. So I knew we were going to have to do something.
Paul Krogstad, my friend and research partner who is a pediatric infectious disease physician, stepped up and tried to put his finger in her throat and dig it out. He couldn’t get it. The patient had lost consciousness.
So, I’m thinking, okay, there’s really only one choice. You have to get an airway surgically.
I said, “We have to put her down on the floor.” And then I said, “Knife!”
I was looking at the steak knives on the table and they weren’t to my liking for doing a procedure. My college roommate – the retired Navy man – whipped out this very good pocketknife.
I had never done this in my life.
While I was making the incision, somebody gave Paul a ballpoint pen and he broke it into pieces to make a tracheostomy tube. Once I’d made the little incision, I put the tube in. She wasn’t breathing, but she still had a pulse.
I leaned forward and blew into the tube and inflated her lungs. I could see her lungs balloon up. It was a nice feeling, because I knew I was clearly in the right place.
I can’t quite explain it, but while I was doing this, I was enormously calm and totally focused. I knew there was a crowd of people around me, all looking at me, but I wasn’t conscious of that.
It was really just the four of us: Paul and Tom and me and our patient. Those were the only people that I was really cognizant of. Paul and Tom were not panic stricken at all. I remember somebody shouting, “We have to start CPR!” and Frieden said, “No. We don’t.”
Moments later, she woke up, sat up, coughed, and shot the piece of steak across the room.
She was breathing on her own, but we still taped that tube into place. Somebody had already summoned an ambulance; they were there not very long after we completed this procedure. I got in the ambulance with her and we rode over to the emergency room at Mercy Truxtun.
She was stable and doing okay. I sat with her until a thoracic surgeon showed up. He checked out the situation and decided we didn’t need that tube and took it out. I didn’t want to take that out until I had a surgeon there who could do a formal tracheostomy.
They kept her in the hospital for 3 or 4 days. Now, this woman had always had difficulties swallowing, so steak may not have been the best choice. She still had trouble swallowing afterward but recovered.
I’ve known her and her husband a long time, so it was certainly rewarding to be able to provide this service. Years later, though, when her husband died, I spoke at his funeral. When she was speaking to the gathering, she said, “And oh, by the way, Royce, thanks for saving my life.”
That surprised me. I didn’t think we were going to go there.
I’d never tried to practice medicine “at the roadside” before. But that’s part of the career.
Royce Johnson, MD, is the chief of the division of infectious disease among other leadership positions at Kern Medical in Bakersfield, Calif., and the medical director of the Valley Fever Institute.
A version of this article first appeared on Medscape.com.
Cardiac issues twice as likely with COVID plus high troponin
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Hospitalized COVID-19 patients with high troponin levels are twice as likely to have cardiac abnormalities than those with normal troponin, with or without COVID-19, a multicenter U.K. study suggests.
The causes were diverse, myocarditis prevalence was lower than previously reported, and myocardial scar emerged as an independent risk factor for adverse cardiovascular outcomes at 12 months.
“We know that multiorgan involvement in hospitalized patients with COVID-19 is common ... and may result in acute myocardial injury, detected by an increase in cardiac troponin concentrations,” John P. Greenwood, PhD, of the University of Leeds (England), told this news organization. “Elevated cardiac troponin is associated with a worse prognosis.”
“Multiple mechanisms of myocardial injury have been proposed and ... mitigation or prevention strategies likely depend on the underpinning mechanisms,” he said. “The sequelae of scar may predispose to late events.”
The study, published online in Circulation, also identified a new pattern of microinfarction on cardiac magnetic resonance (CMR) imaging, highlighting the pro-thrombotic nature of SARS-CoV-2, Dr. Greenwood said.
Injury patterns different
Three hundred and forty-two patients with COVID-19 and elevated troponin levels (COVID+/troponin+) across 25 centers were enrolled between June 2020 and March 2021 in COVID-HEART, deemed an “urgent public health study” in the United Kingdom. The aim was to characterize myocardial injury and its associations and sequelae in convalescent patients after hospitalization with COVID-19.
Enrollment took place during the Wuhan and Alpha waves of COVID-19: before vaccination and when dexamethasone and anticoagulant protocols were emerging. All participants underwent CMR at a median of 21 days after discharge.
Two prospective control groups also were recruited: 64 patients with COVID-19 and normal troponin levels (COVID+/troponin−) and 113 without COVID-19 or elevated troponin matched by age and cardiovascular comorbidities (COVID−/comorbidity+).
Overall, participants’ median age was 61 years and 69% were men. Common comorbidities included hypertension (47%), obesity (43%), and diabetes (25%).
The frequency of any heart abnormality – for example, left or right ventricular impairment, scar, or pericardial disease – was twice as great (61%) in COVID+/troponin+ cases, compared with controls (36% for COVID+/troponin− patients versus 31% for COVID−/comorbidity+ patients).
Specifically, more cases than controls had ventricular impairment (17.2% vs. 3.1% and 7.1%) or scar (42% vs. 7% and 23%).
The myocardial injury pattern differed between cases and controls, with cases more likely to have infarction (13% vs. 2% and 7%) or microinfarction (9% vs. 0% and 1%).
However, there was no between-group difference in nonischemic scar (13% vs. 5% and 14%).
The prevalence of probable recent myocarditis was 6.7% in cases, compared with 1.7% in controls without COVID-19 – “much lower” than in previous studies, Dr. Greenwood noted.
During follow-up, four COVID+/troponin+ patients (1.2%) died, and 34 (10%) experienced a subsequent major adverse cardiovascular event (MACE; 10.2%), which was similar to controls (6.1%).
Myocardial scar, but not previous COVID-19 infection or troponin level, was an independent predictor of MACE (odds ratio, 2.25).
“These findings suggest that macroangiopathic and microangiopathic thrombosis may be the key pathologic process for myocardial injury in COVID-19 survivors,” the authors conclude.
Dr. Greenwood added, “We are currently analyzing the 6-month follow-up CMR scans, the quality-of-life questionnaires, and the 6-minute walk tests. These will give us great understanding of how the heart repairs after acute myocardial injury associated with COVID-19. It will also allow us to assess the impact on patient quality of life and functional capacity.”
‘Tour de force’
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and a professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said, “This is a tour de force collaboration – obtaining this many MRIs across multiple centers in the pandemic is quite remarkable. The study highlights the multiple different processes that lead to cardiac injury in COVID patients, complements autopsy studies and prior smaller MRI studies, [and] also provides the best data on the rate of myocarditis to date among the subset of COVID patients with cardiac injury.”
Overall, he said, the findings “do support closer follow-up for patients who had COVID and elevated troponins. We need to see follow-up MRI results in this cohort, as well as longer term outcomes. We also need studies on newer, more benign variants that are likely to have lower rates of cardiac injury and even fewer MRI abnormalities.”
Matthias Stuber, PhD, and Aaron L. Baggish, MD, both of Lausanne University Hospital and University of Lausanne, Switzerland, noted in a related editorial, “We are also reminded that the clinical severity of COVID-19 is most often dictated by the presence of pre-existing comorbidity, with antecedent ischemic scar now added to the long list of bad actors. Although not the primary focus of the COVID-HEART study, the question of whether cardiac troponin levels should be checked routinely and universally during the index admission for COVID-19 remains unresolved,” they noted.
“In general, we are most effective as clinicians when we use tests to confirm or rule out the specific disease processes suspected by careful basic clinical assessment rather than in a shotgun manner among undifferentiated all-comers,” they conclude.
No commercial funding or relevant financial relationships were reported.
A version of this article originally appeared on Medscape.com.
Must-read acute care medicine articles from 2022
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
When 2022 began, we started seeing some light at the end of the COVID-19 tunnel. Vaccines were widely available, and even with new variants of the virus still occasionally emerging, the rates of severe morbidity and mortality appeared to be decreasing.
Expectedly, journals appeared to start moving more toward mainstream topics and publications rather than what seemed like a major focus on COVID-19 publications. The resulting literature was fantastic.
Several of those topics were discussed in a prior Emergency Medicine Viewpoint from this news organization, and many more of the research advances of 2022 will be discussed in the near future. However, in this Viewpoint, I would like to present my annual review of my three “must-read” articles of the past year.
As in past years, I am choosing reviews of the literature rather than original research articles (which, all too often, become outdated or debunked within a few years). I choose these articles in the hopes that readers will not simply settle for my brief reviews of the key points but instead will feel compelled to download and read the entire articles. These publications address common conditions and quandaries we face in the daily practice of emergency medicine and are practice-changing.
Myocardial dysfunction after cardiac arrest: Tips and pitfalls
The management of post–cardiac arrest patients remains a hot topic in the resuscitation literature as we continue to understand that the immediate post-arrest period is critical to patient outcome.
Ortuno and colleagues reviewed the current literature on post-arrest care and wrote an outstanding summary of how to optimally care for these patients. More specifically, they focused on post-arrest patients who demonstrate continued shock, or “post–cardiac arrest myocardial dysfunction” (PCAMD).
They propose three mechanisms for the pathogenesis of PCAMD: ischemia reperfusion phenomenon, systemic inflammatory response, and increased catecholamine release
I will skip through the details of the pathophysiology that they describe in the article, but I certainly do recommend that everyone review their descriptions.
Management of these patients begins with a good hemodynamic assessment, which includes clinical markers of perfusion (blood pressure, capillary refill), ECG, and point-of-care ultrasound (POCUS). If the initial assessment reveals an obvious cause of the cardiac arrest (e.g., massive pulmonary embolism, myocardial infarction, pericardial tamponade), then the underlying cause should be treated expeditiously.
In the absence of an obvious treatable cause of the shock, the fluid status and cardiac function should be addressed with POCUS. If the patient is hypovolemic, intravenous fluids should be administered. If the fluid status is adequate, POCUS should be used to estimate the patient’s ventricular function. If the ventricle appears to be hyperdynamic with good contractility, shock should be treated with norepinephrine. On the other hand, if the ventricle is hypodynamic, dobutamine should be substituted for norepinephrine or, more often, added to norepinephrine.
The above represents a simplified summary of the critical points, but the authors do delve into further detail and also discuss some other options for therapies, including steroids, coronary revascularization, extracorporeal membrane oxygenation, and so on. The review is very thoughtful, thorough, and definitely worth a full read.
Top myths of diagnosis and management of infectious diseases in hospital medicine
Most, if not all of us in medicine, have heard the saying that 50% of what we learn in medical school (or residency) will turn out to be wrong. I certainly believe in this concept and consequently, like many of you, I enjoy reading about myths and misconceptions that we have been taught. With that in mind, I have to say that I love this article because it seems to have been written specifically to address what I was taught!
This author group, consisting mostly of clinical PharmDs who are experts in antibiotic use, provide us with an evidence-based discussion of myths and pitfalls in how antibiotics are often used in current clinical practice. The authors review their top 10 myths involving the use of antibiotics in treating infections in the hospital setting. A few of these relate more to the inpatient setting, but here are my favorite emergency department (ED)–related myths that they address:
- “Antibiotics do no harm.” The authors address the risk-benefit of antibiotics based on assumed vs. confirmed infections, including a brief discussion of adverse drug effects.
- “Antibiotic durations of 7, 14, or 21 days are typically necessary.” The authors address appropriate duration of antibiotic use and the fact that unnecessarily long durations of use can lead to resistance. They also provide reassurance that some infections can be treated with quite short durations of antibiotics.
- “If one drug is good, two (or more!) is better.” The use of multiple antibiotics, often with overlapping bacterial coverage, is rampant in medicine and further increases the risk for adverse drug effects and resistance.
- “Oral antibiotics are not as good as intravenous antibiotics for hospitalized patients.” This is definitely a myth that I learned. I recall being taught by many senior physicians that anyone sick enough for admission should be treated with intravenous antibiotics. As it turns out, absorption and effectiveness of most oral antibiotics is just as good as intravenous antibiotics, and the oral formulations are often safer.
- “A history of a penicillin allergy means the patient can never receive a beta-lactam antibiotic.” This is a myth that was debunked quite a few years ago, but it seems that many clinicians still need a reminder.
The authors included five more myths that are worth the read. This is an article that needs to be disseminated among all hospital clinicians.
Guidelines for low-risk, recurrent abdominal pain in the emergency department
The Society for Academic Emergency Medicine (SAEM) recently initiated a program focused on creating evidence-based approaches to challenging chief complaints and presentations in the emergency department (ED). In 2021, they published an approach to managing patients with recurrent, low-risk chest pain in the ED. This past year, they published their second guideline, focused on the management of patients with low-risk, recurrent abdominal pain in the ED.
Recurrent low-risk abdominal pain is a common and vexing presentation to EDs around the world, and there is little prior published guidance. Do all of these patients need repeat imaging? How do we manage their pain? Are there nonabdominal conditions that should be considered?
Broder and colleagues did a fantastic review of the current literature and, on behalf of SAEM, have provided a rational approach to optimal management of these patients. The four major questions they addressed, with brief summaries of their recommendations, are:
- Should adult ED patients with low-risk, recurrent and previously undifferentiated abdominal pain receive a repeat CT abdomen-pelvis (CTAP) after a negative CTAP within the past 12 months? This is a typical question that we all ponder when managing these patients. Unfortunately, the writing group found insufficient evidence to definitively identify populations in whom CTAP was recommended vs could be safely withheld. It is a bit disappointing that there is no definite answer to the question. On the other hand, it is reassuring to know that the world’s best evidence essentially says that it is perfectly appropriate to use your own good clinical judgment.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain with a negative CTAP receive additional imaging with abdominal ultrasound? In this case, the writing group found enough evidence, though low-level, to suggest against routine ultrasound in the absence of concern specifically for pelvic or hepatobiliary pathology. Like most tests, ultrasound is best used when there are specific concerns rather than being used in an undifferentiated fashion.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive screening for depression/anxiety? The writing group found enough evidence, though low-level again, to suggest that screening for depression and/or anxiety be performed during the ED evaluation. This could lead to successful therapy for the abdominal pain.
- Should adult ED patients with low-risk, recurrent, and previously undifferentiated abdominal pain receive nonopioid and/or nonpharmacologic analgesics? The writing group found little evidence to suggest for or against these analgesics, but they made a consensus recommendation suggesting an opioid-minimizing strategy for pain control.
Although the final recommendations of the writing group were not definitive or based on the strongest level of evidence, I find it helpful to have this guidance, nevertheless, on behalf of a major national organization. I also find it helpful to know that even with the best evidence available, optimal patient care will often boil down to physician experience and gestalt. I should also add that the overall article is chock-full of pearls and helpful information that will further inform the readers’ decisions, and so the full version is definitely worth the read.
In summary
There you have it – my three favorite practice-changing articles of 2022. Although I have tried to provide key points here, the full discussions of those key points in the published articles will provide a great deal more education than I can offer in this brief write-up, and so I strongly encourage everyone to read the full versions. Please be sure to include in the comments section your own pick for favorite or must-read articles from the past year.
Amal Mattu, MD, is a professor, vice chair of education, and codirector of the emergency cardiology fellowship in the department of emergency medicine at the University of Maryland, Baltimore. She reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Guidance for PCI without on-site surgical backup updated
such as ambulatory surgery centers (ASCs) and office-based laboratories and which are best left to more traditional settings, such as hospitals with full cardiac support.
PCI has evolved quickly since SCAI issued its last update almost 9 years ago. The updated statement, published online in the Journal of the Society for Cardiovascular Angiography and Interventions, notes that the proportion of same-day PCI discharges has increased from 4.5% in 2009 to 28.6% in 2017.
The statement also notes that the Medicare facility fee for outpatient PCI in an ASC is about 40% less than the hospital fee: $6,111 versus $10,258 for the facility fee for 2022. The Centers for Medicare & Medicaid Services in 2020 extended coverage for PCIs in ASCs.
Rationale for update
Writing group chair Cindy Grines, MD, explained the rationale for updating the statement now. “The 2014 SCAI statement was very conservative, recommending only the simplest of cases be done without surgical backup,” Dr. Grines, chief scientific officer at Northside Hospital Cardiovascular Institute in Atlanta, said in an interview.
The statement drew on 12 global studies from 2015 to 2022 that evaluated more than 8 million PCIs at facilities with and without surgery on site. Dr. Grines noted those studies reported complication rates as low as 0.1% in PCI procedures in centers without surgical backup.
She also noted that the writing committee also received input that “by restricting the use of certain devices such as atherectomy, some patients who needed it as a bailout could be harmed.”
Another factor in prompting the statement update, Dr. Grines said: “Many hospitals have consolidated into heath systems, and these systems consolidated bypass surgery into one center. Therefore, centers with high volume, experienced operators, and excellent outcomes were now left with no surgery on site. It didn’t make sense to withdraw complex PCI from these centers who haven’t sent a patient for emergency bypass in several years.”
Statement guidance
The centerpiece of the update is an algorithm that covers the range of settings for PCI, from having a surgeon on site to ACS or office-based lab.
For example, indications for on-site surgical capability are PCI of the last remaining patent vessel or retrograde approach to epicardial chronic total occlusion (CTO), and when the patient is a candidate for surgery.
Indications for PCI in a hospital without on-site surgery but with percutaneous ventricular assist device or extracorporeal membrane oxygenation, calcium modification devices and high PCI volume are patients with decreased left ventricular ejection fraction, unprotected left main artery, CTO, or degenerated vein grafts.
For patients at high risk for transfusion, acute kidney injury or vascular complications, or who have high baseline respiratory risk, a hospital without on-site surgery but with respiratory care, blood bank, and vascular surgery services is indicated.
And for patients with none of the aforementioned characteristics or risks, ASC, office-based lab, or any hospital facility is acceptable.
The statement also provides guidance for operator experience. Those with less than 3 years’ experience, considered to have limited exposure to atherectomy devices and limited ST-segmented elevation MI (STEMI)/shock experience, should avoid doing PCIs in an ASC and performing atherectomy cases on their own, and have a colleague review case selection and assist in higher-risk cases. Experienced (3-10 years’ experience) and very experienced (more than 10 years’) should be able to perform in any setting and be competent with, if not highly experienced with, atherectomy and STEMI/shock.
Dr. Grines acknowledged the writing group didn’t want to set a specific operator volume requirement. “However, we recognize that lifetime operator experience is particularly important in more complex cases such as CTO, atherectomy, bifurcation stenoses, etc.,” she said. “In addition, performing these cases at a larger institution that has other operators that may assist in the event of a complication is very important. Specifically, we did not believe that recent fellow graduates with less than 3 years in practice or low-volume operators should attempt higher-risk cases in a no-SOS [surgeon-on-site] setting or perform cases in ASC or office-based labs where no colleagues are there to assist in case of a complication.”
In an interview, Gregory J. Dehmer, MD, professor of medicine at Virginia Tech University, Roanoke, reprised the theme of his accompanying editorial. “Things are evolving again, as Bob Dylan would say, ‘The Times They Are A-Changin’, so it’s very timely that the society in collaboration with other professional societies updated what are guidelines and rules of road if you’re going to do PCI in ASCs or office based laboratories,” said Dr. Dehmer, who chaired the writing committees of the 2007 and 2014 SCAI expert statements on PCI.
Having this statement is important for centers that don’t have on-site surgical backup, he said. “You couldn’t sustain a PCI operation at a rural hospital on just acute MIs alone. The key thing is that all of this built upon numerous studies both in the U.S. and abroad that showed the safety of doing elective cases – not only STEMIs, but elective PCI – at facilities without on-site surgery.”
CMS pushed the envelope when it decided to reimburse PCIs done in ASCs, Dr. Dehmer said. “That was not based on a lot of data. It was kind of a leap of faith. It’s logical that this should work, but in order for it to work and be safe for pats you have to follow the rules. That’s where SCAI stepped in at this point and said this is a whole new environment and we need to set some ground rules for physicians of who and who should not be having these procures in an office-based lab or an ambulatory surgery center.”
Dr. Grines and Dr. Dehmer have no relevant disclosures.
such as ambulatory surgery centers (ASCs) and office-based laboratories and which are best left to more traditional settings, such as hospitals with full cardiac support.
PCI has evolved quickly since SCAI issued its last update almost 9 years ago. The updated statement, published online in the Journal of the Society for Cardiovascular Angiography and Interventions, notes that the proportion of same-day PCI discharges has increased from 4.5% in 2009 to 28.6% in 2017.
The statement also notes that the Medicare facility fee for outpatient PCI in an ASC is about 40% less than the hospital fee: $6,111 versus $10,258 for the facility fee for 2022. The Centers for Medicare & Medicaid Services in 2020 extended coverage for PCIs in ASCs.
Rationale for update
Writing group chair Cindy Grines, MD, explained the rationale for updating the statement now. “The 2014 SCAI statement was very conservative, recommending only the simplest of cases be done without surgical backup,” Dr. Grines, chief scientific officer at Northside Hospital Cardiovascular Institute in Atlanta, said in an interview.
The statement drew on 12 global studies from 2015 to 2022 that evaluated more than 8 million PCIs at facilities with and without surgery on site. Dr. Grines noted those studies reported complication rates as low as 0.1% in PCI procedures in centers without surgical backup.
She also noted that the writing committee also received input that “by restricting the use of certain devices such as atherectomy, some patients who needed it as a bailout could be harmed.”
Another factor in prompting the statement update, Dr. Grines said: “Many hospitals have consolidated into heath systems, and these systems consolidated bypass surgery into one center. Therefore, centers with high volume, experienced operators, and excellent outcomes were now left with no surgery on site. It didn’t make sense to withdraw complex PCI from these centers who haven’t sent a patient for emergency bypass in several years.”
Statement guidance
The centerpiece of the update is an algorithm that covers the range of settings for PCI, from having a surgeon on site to ACS or office-based lab.
For example, indications for on-site surgical capability are PCI of the last remaining patent vessel or retrograde approach to epicardial chronic total occlusion (CTO), and when the patient is a candidate for surgery.
Indications for PCI in a hospital without on-site surgery but with percutaneous ventricular assist device or extracorporeal membrane oxygenation, calcium modification devices and high PCI volume are patients with decreased left ventricular ejection fraction, unprotected left main artery, CTO, or degenerated vein grafts.
For patients at high risk for transfusion, acute kidney injury or vascular complications, or who have high baseline respiratory risk, a hospital without on-site surgery but with respiratory care, blood bank, and vascular surgery services is indicated.
And for patients with none of the aforementioned characteristics or risks, ASC, office-based lab, or any hospital facility is acceptable.
The statement also provides guidance for operator experience. Those with less than 3 years’ experience, considered to have limited exposure to atherectomy devices and limited ST-segmented elevation MI (STEMI)/shock experience, should avoid doing PCIs in an ASC and performing atherectomy cases on their own, and have a colleague review case selection and assist in higher-risk cases. Experienced (3-10 years’ experience) and very experienced (more than 10 years’) should be able to perform in any setting and be competent with, if not highly experienced with, atherectomy and STEMI/shock.
Dr. Grines acknowledged the writing group didn’t want to set a specific operator volume requirement. “However, we recognize that lifetime operator experience is particularly important in more complex cases such as CTO, atherectomy, bifurcation stenoses, etc.,” she said. “In addition, performing these cases at a larger institution that has other operators that may assist in the event of a complication is very important. Specifically, we did not believe that recent fellow graduates with less than 3 years in practice or low-volume operators should attempt higher-risk cases in a no-SOS [surgeon-on-site] setting or perform cases in ASC or office-based labs where no colleagues are there to assist in case of a complication.”
In an interview, Gregory J. Dehmer, MD, professor of medicine at Virginia Tech University, Roanoke, reprised the theme of his accompanying editorial. “Things are evolving again, as Bob Dylan would say, ‘The Times They Are A-Changin’, so it’s very timely that the society in collaboration with other professional societies updated what are guidelines and rules of road if you’re going to do PCI in ASCs or office based laboratories,” said Dr. Dehmer, who chaired the writing committees of the 2007 and 2014 SCAI expert statements on PCI.
Having this statement is important for centers that don’t have on-site surgical backup, he said. “You couldn’t sustain a PCI operation at a rural hospital on just acute MIs alone. The key thing is that all of this built upon numerous studies both in the U.S. and abroad that showed the safety of doing elective cases – not only STEMIs, but elective PCI – at facilities without on-site surgery.”
CMS pushed the envelope when it decided to reimburse PCIs done in ASCs, Dr. Dehmer said. “That was not based on a lot of data. It was kind of a leap of faith. It’s logical that this should work, but in order for it to work and be safe for pats you have to follow the rules. That’s where SCAI stepped in at this point and said this is a whole new environment and we need to set some ground rules for physicians of who and who should not be having these procures in an office-based lab or an ambulatory surgery center.”
Dr. Grines and Dr. Dehmer have no relevant disclosures.
such as ambulatory surgery centers (ASCs) and office-based laboratories and which are best left to more traditional settings, such as hospitals with full cardiac support.
PCI has evolved quickly since SCAI issued its last update almost 9 years ago. The updated statement, published online in the Journal of the Society for Cardiovascular Angiography and Interventions, notes that the proportion of same-day PCI discharges has increased from 4.5% in 2009 to 28.6% in 2017.
The statement also notes that the Medicare facility fee for outpatient PCI in an ASC is about 40% less than the hospital fee: $6,111 versus $10,258 for the facility fee for 2022. The Centers for Medicare & Medicaid Services in 2020 extended coverage for PCIs in ASCs.
Rationale for update
Writing group chair Cindy Grines, MD, explained the rationale for updating the statement now. “The 2014 SCAI statement was very conservative, recommending only the simplest of cases be done without surgical backup,” Dr. Grines, chief scientific officer at Northside Hospital Cardiovascular Institute in Atlanta, said in an interview.
The statement drew on 12 global studies from 2015 to 2022 that evaluated more than 8 million PCIs at facilities with and without surgery on site. Dr. Grines noted those studies reported complication rates as low as 0.1% in PCI procedures in centers without surgical backup.
She also noted that the writing committee also received input that “by restricting the use of certain devices such as atherectomy, some patients who needed it as a bailout could be harmed.”
Another factor in prompting the statement update, Dr. Grines said: “Many hospitals have consolidated into heath systems, and these systems consolidated bypass surgery into one center. Therefore, centers with high volume, experienced operators, and excellent outcomes were now left with no surgery on site. It didn’t make sense to withdraw complex PCI from these centers who haven’t sent a patient for emergency bypass in several years.”
Statement guidance
The centerpiece of the update is an algorithm that covers the range of settings for PCI, from having a surgeon on site to ACS or office-based lab.
For example, indications for on-site surgical capability are PCI of the last remaining patent vessel or retrograde approach to epicardial chronic total occlusion (CTO), and when the patient is a candidate for surgery.
Indications for PCI in a hospital without on-site surgery but with percutaneous ventricular assist device or extracorporeal membrane oxygenation, calcium modification devices and high PCI volume are patients with decreased left ventricular ejection fraction, unprotected left main artery, CTO, or degenerated vein grafts.
For patients at high risk for transfusion, acute kidney injury or vascular complications, or who have high baseline respiratory risk, a hospital without on-site surgery but with respiratory care, blood bank, and vascular surgery services is indicated.
And for patients with none of the aforementioned characteristics or risks, ASC, office-based lab, or any hospital facility is acceptable.
The statement also provides guidance for operator experience. Those with less than 3 years’ experience, considered to have limited exposure to atherectomy devices and limited ST-segmented elevation MI (STEMI)/shock experience, should avoid doing PCIs in an ASC and performing atherectomy cases on their own, and have a colleague review case selection and assist in higher-risk cases. Experienced (3-10 years’ experience) and very experienced (more than 10 years’) should be able to perform in any setting and be competent with, if not highly experienced with, atherectomy and STEMI/shock.
Dr. Grines acknowledged the writing group didn’t want to set a specific operator volume requirement. “However, we recognize that lifetime operator experience is particularly important in more complex cases such as CTO, atherectomy, bifurcation stenoses, etc.,” she said. “In addition, performing these cases at a larger institution that has other operators that may assist in the event of a complication is very important. Specifically, we did not believe that recent fellow graduates with less than 3 years in practice or low-volume operators should attempt higher-risk cases in a no-SOS [surgeon-on-site] setting or perform cases in ASC or office-based labs where no colleagues are there to assist in case of a complication.”
In an interview, Gregory J. Dehmer, MD, professor of medicine at Virginia Tech University, Roanoke, reprised the theme of his accompanying editorial. “Things are evolving again, as Bob Dylan would say, ‘The Times They Are A-Changin’, so it’s very timely that the society in collaboration with other professional societies updated what are guidelines and rules of road if you’re going to do PCI in ASCs or office based laboratories,” said Dr. Dehmer, who chaired the writing committees of the 2007 and 2014 SCAI expert statements on PCI.
Having this statement is important for centers that don’t have on-site surgical backup, he said. “You couldn’t sustain a PCI operation at a rural hospital on just acute MIs alone. The key thing is that all of this built upon numerous studies both in the U.S. and abroad that showed the safety of doing elective cases – not only STEMIs, but elective PCI – at facilities without on-site surgery.”
CMS pushed the envelope when it decided to reimburse PCIs done in ASCs, Dr. Dehmer said. “That was not based on a lot of data. It was kind of a leap of faith. It’s logical that this should work, but in order for it to work and be safe for pats you have to follow the rules. That’s where SCAI stepped in at this point and said this is a whole new environment and we need to set some ground rules for physicians of who and who should not be having these procures in an office-based lab or an ambulatory surgery center.”
Dr. Grines and Dr. Dehmer have no relevant disclosures.
FROM THE JOURNAL OF SOCIETY FOR CARDIOVASCULAR ANGIOGRAPHY AND INTERVENTIONS
Acute cardiac events common during COVID hospitalization
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
particularly among those with underlying heart disease, and are associated with more severe disease outcomes, a new study suggests.
“We expected to see acute cardiac events occurring among adults hospitalized with COVID-19 but were surprised by how frequently they occurred,” Rebecca C. Woodruff, PhD, MPH, of the U.S. Centers for Disease Control and Prevention, Atlanta, told this news organization.
Overall, she said, “about 1 in 10 adults experienced an acute cardiac event – including heart attacks and acute heart failure – while hospitalized with COVID-19, and this included people with no preexisting heart disease.”
However, she added, “about a quarter of those with underlying heart disease had an acute cardiac event. These patients tended to experience more severe disease outcomes relative to patients hospitalized with COVID-19 who did not experience an acute cardiac event.”
The findings might be relevant to hospitalizations for other viral diseases, “though we can’t say for sure,” she noted. “This study was modeled off a previous study conducted before the COVID-19 pandemic among adults hospitalized with influenza. About 11.7% of [those] adults experienced an acute cardiac event, which was a similar percentage as what we found among patients hospitalized with COVID-19.”
The study was published online in the Journal of the American College of Cardiology.
Underlying cardiac disease key
Dr. Woodruff and colleagues analyzed medical records on a probability sample of 8,460 adults hospitalized with SARS-CoV-2 infection identified from 99 U.S. counties in 14 U.S. states (about 10% of the United States population) from January to November 2021.
Among participants, 11.4% had an acute cardiac event during their hospitalization. The median age was 69 years; 56.5% were men; 48.7%, non-Hispanic White; 33.6%, non-Hispanic Black; 7.4%, Hispanic; and 7.1%, non-Hispanic Asian or Pacific Islander.
As indicated, the prevalence was higher among those with underlying cardiac disease (23.4%), compared with those without (6.2%).
Acute ischemic heart disease (5.5%) and acute heart failure (5.4%) were the most prevalent events; 0.3% of participants had acute myocarditis or pericarditis.
Risk factors varied, depending on underlying cardiac disease status. Those who experienced one or more acute cardiac events had a greater risk for intensive care unit admission (adjusted risk ratio,1.9) and in-hospital death (aRR, 1.7) versus those who did not.
In multivariable analyses, the risk of experiencing acute heart failure was significantly greater among men (aRR, 1.5) and among those with a history of congestive heart failure (aRR, 13.5), atrial fibrillation (aRR, 1.6) or hypertension (aRR,1.3).
Among patients who experienced one or more acute cardiac events, 39.2% required an intensive care unit stay for a median of 5 days. Approximately 22.4% required invasive mechanical ventilation or extracorporeal membrane oxygenation, and 21.1% died while hospitalized.
“Persons at greater risk for experiencing acute cardiac events during COVID-19–associated hospitalizations might benefit from more intensive clinical evaluation and monitoring during hospitalization,” the authors conclude.
The team currently is taking a closer look at acute myocarditis among patients hospitalized with COVID-19, Dr. Woodruff said. Preliminary results were presented at the 2022 annual scientific sessions of the American Heart Association and a paper is forthcoming.
Contemporary data needed
James A. de Lemos, MD, co-chair of the American Heart Association’s COVID-19 CVD Registry Steering Committee and professor of medicine at the University of Texas Southwestern Medical Center, Dallas, said the findings mirror his team’s clinical experience in 2020 and 2021 and echo what was seen in the AHA COVID registry: that is, a 0.3% rate of myocarditis.
“The major caveat is that [the findings] may not be generalizable to contemporary COVID infection, both due to changing viral variants and higher levels of immunity in the population,” he said.
“Rates of COVID hospitalization are markedly lower with the current dominant variants, and we would expect the cardiac risk to be lower as well. I would like to see more contemporary data with current variants, particularly focused on higher risk patients with cardiovascular disease,” Dr. de Lemos added.
In a related editorial, George A. Mensa, MD, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues suggest that the broader impact of the COVID-19 pandemic on human health remains “incompletely examined.”
“The impact of COVID-19 on cardiovascular mortality, in particular, appears to have varied widely, with no large increases seen in a number of the most developed countries but marked increases in hypertensive heart disease mortality seen in the United States in 2021,” they conclude. “The potential contribution of COVID-19 to these deaths, either directly or indirectly, remains to be determined.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
What is the psychological cost of performing CPR?
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
One year ago, as the sun was setting on a late fall day, Andrés Snitcofsky, a 40-year-old designer from Buenos Aires, Argentina, heard harrowing cries for help. It was the niece and the wife of one of his neighbors: a man in his 60s who the women had found “passed out” in the bedroom. “I did CPR for 5 minutes straight until a friend of the victim came in and asked me to stop, telling me that the man had probably been dead for 2 or 3 hours already. But I had no idea because I’d never seen a dead body before,” Mr. Snitcofsky told this news organization. A few minutes later, the ambulance arrived. The doctor confirmed that there was nothing more that could be done.
Mr. Snitcofsky went home. Nobody had asked for his name or address or phone number. … And it wasn’t because they already knew who he was. In fact, there wasn’t any sort of relationship there. Mr. Snitcofsky had only known his neighbors by sight. His actions that day, however, “did not come without a cost. It took me weeks – months, actually – to put myself together again,” he said. The things he saw, the things he heard, everything about that night played over and over in his head. “I had trouble sleeping. I would play out different scenarios in my head. I questioned myself. I second-guessed myself, criticized myself. It’s like some taboo subject. There’s no one to share the experience with, no one who gets it. But with time, I was able to process the event.
“For 2 months, I talked to my psychologist about it all,” he continued. “That really helped me a lot. In addition to therapy, I reached out to a couple I know – they’re both physicians – and to a firefighter who teaches CPR. Their insight and guidance allowed me to get to a point where I was able to understand that what I did was a good thing and that what I did was all that could have been done. But anyone who finds themselves in the position of having to do CPR – they’re going to be affected in many, many ways. It goes beyond the euphoria of seeing a person come back to life. Of that, I’m quite certain.”
We’ve all seen campaigns encouraging people to learn CPR and to be prepared if the need arises. But in training the public (and even health care professionals), not much, if anything, is said about the “collateral damage”: the psychological and emotional consequences of carrying out the procedure. These especially come into play when you don’t know whether the person survived, when your efforts weren’t able to reverse the sudden cardiac arrest, or when the person you gave CPR to was a loved one – a case that may entail immediate therapeutic interventions to minimize or prevent the risk of suffering long-lasting trauma.
In May 2020, popular American activist and educator Kristin Flanary saw someone suffering cardiac arrest. She stepped in and started doing CPR. And she continued doing CPR … for 10 long minutes. The person she was trying to save was her 34-year-old husband, ophthalmologist and comedian Will Flanary. On Twitter, where she’s known as Lady Glaucomflecken, Ms. Flanary recently shared the following message, putting the topic of CPR and automated external defibrillator training front and center.
“Yes, everyone should learn #CPRandAED. But if we are going to ask people to perform such a brutal task, it’s imperative that we also provide them with the info and resources they need to process it mentally and emotionally. It’s traumatic and life changing. It’s irresponsible and unethical to ask people to help in such a brutal and traumatic way and then neglect to help them in return.” In less than a month, the tweet has racked up over 200,000 views.
Doing one’s duty
There are many people who work to promote CPR and strengthen the other links in the chain of survival for out-of-hospital sudden cardiac arrest, such as prompt access to and delivery of early defibrillation. According to them, any negative psychological impact of intervening is temporary and, when compared with the satisfaction of having done one’s duty, quite insignificant – even if the efforts to save a person’s life are not successful.
“In 99.9% of cases, people who have performed CPR feel a sense of satisfaction, even happiness, knowing that they’ve helped. The individuals I’ve spoken with, I’ve never heard any of them say that they felt worse after the event or that they needed to see a psychologist,” said Mario Fitz Maurice, MD, director of the Arrhythmia Council of the Argentine Society of Cardiology and head of Electrophysiology at Rivadavia Hospital in Buenos Aires. He went on to tell this news organization, “Of course, some degree of fear, sadness, or melancholy can remain afterward. But it seems to me, and there are reports saying as much, that, in the end, what stands out in the person’s mind is the fact that they tried to save a life. And for them, there’s joy in knowing this.”
Dr. Fitz Maurice, who is also the director of the National Arrhythmia Institute in Buenos Aires, pointed out that the kind of person who takes CPR classes “has a profile that’s going to allow them to be psychologically involved; they’re the caring person, the one who’s ready and willing to help people.” And he added that, at his hospital, if they can identify the individuals or first responders who have done CPR on a patient, the protocol is to always contact them to offer psychological care and assistance. “But in 99% of cases, they don’t even understand why we’re calling them, they’re extremely happy to have taken part.”
Some studies, though, paint a much different picture, one that shows that providing CPR can be emotionally challenging and have consequences in terms of one’s family and work life. A qualitative study published in 2016 looked into the experiences of 20 lay rescuers in Norway – five were health educated – who had provided CPR to 18 out-of-hospital cardiac arrest (OHCA) victims, 66% of whom survived. The time from experiencing the OHCA incident to participating in the interview ranged from 6 days to 13 years (median 5.5 years). Several participants reported the OHCA incident as a “shocking and terrifying” experience. Tiredness, exhaustion, confusion, and feeling alone about the OHCA experience were individual reactions that could vary in time from days to months. Anxiety and insomnia were also experienced following the incident.
Some lay rescuers described the influence on work and family life, and a few of them described deep sorrow, even several years after the incident. Overall, they reported repetitive self-criticism regarding whether they could have carried out anything else to achieve a better outcome for the cardiac arrest victim. All of them wanted to be informed about the outcome. And four of the lay rescuers needed professional counseling to process the OHCA experience.
In 2020, another qualitative study was conducted, this time in Taiwan. There were nine participants, none of whom were health professionals. Each had provided initial CPR and defibrillation with AED in public locations. Event-to-interview duration was within 1 year and 1-2 years. The major findings from the study were the following:
- The lay rescuers possessed helping traits and high motivation.
- The lay rescuers reported certain aspects of rescue reality that differed much from prior training and expectations, including difficulty in the depth of chest compression, and uncertainties in real emergency situations.
- The lay rescuers gained positive personal fulfillment in sharing their experience and receiving positive feedback from others, and were willing to help next time, although they experienced a short-term negative psychological impact from the event. “Measures should be taken to increase [a] layperson’s confidence and situation awareness, to reduce training-reality discrepancy, and to build up a support system to avoid negative psychological effects.” This was the conclusion of the study team, which was led by Matthew Huei-Ming Ma, MD, PhD. A professor in the department of emergency medicine at National Taiwan University in Taipei, he is also on the board of directors of the Resuscitation Council of Asia.
Potential trauma
In recalling his experience, Mr. Snitcofsky said, “The hardest part of it all was the moment that I stopped giving CPR, that moment of letting go. This became the image that kept coming back to me, the traumatic moment I hadn’t thought about.”
Psychiatrist Daniel Mosca, MD, is the founder and former president of the Argentine Society of Trauma Psychology. He is also the coordinator of the human factors team at the City of Buenos Aires Emergency Medical Care System. “Any event has the potential to be traumatic, all the more so when it’s an event where you come face to face with death and uncertainty. But how a rescuer reacts will depend on their psychological makeup.” Of the individuals who were held for months or years in the jungle as hostages of the Revolutionary Armed Forces of Colombia, “only” half developed symptoms of posttraumatic stress disorder.
Dr. Mosca believes that a comment by Frank Ochberg, MD, speaks to this finding. “In many cases, peritraumatic symptoms are a normal person’s normal response to an abnormal situation.” For a lot of people who have found themselves having to perform CPR, the symptoms associated with the initial acute stress reaction will resolve on their own in 30-90 days. “But if this doesn’t happen, and those symptoms persist, psychotherapeutic or pharmacological intervention will be necessary,” he noted.
“In CPR classes, it would be good for the instructors to talk about the warning signs that people should look out for in themselves and their fellow rescuers. So, for example, insomnia, anxiety, a heightened state of alertness, feeling disconnected from reality,” Dr. Mosca told this news organization.
“Another thing that can help rescuers is letting them know what happened to the person they gave CPR to. This way, they can get closure,” suggested Manlio Márquez Murillo, MD, a cardiologist and electrophysiologist in Mexico. He is also the coordinator of the Alliance Against Sudden Cardiac Death at the Interamerican Society of Cardiology.
“Medical and nursing societies would have to develop a brief protocol or performance standard. The goal would be to ensure that rescuers are asked for their contact information and that someone gets in touch to debrief them and to offer them care. Next would come the treatment part, to resolve any remaining aftereffects,” said in an interview.
For example, a three-stage Lay Responder Support Model (LRSM) was developed and implemented as part of a lay responder support program established in 2014 by the Peel Regional Council in Ontario. The LRSM identifies and engages individuals who witnessed or participated directly or indirectly in an OHCA, inviting them to participate in a debriefing session facilitated by a trained practitioner. Held 24-48 hours post event, the debriefing allows lay responders to contextualize their reaction to the event. The conversation also serves as an opportunity for them to fully articulate their concerns, questions, and thoughts. The facilitator can communicate stress reduction techniques and address psychological first aid needs as they emerge. Approximately 1 week post event, a secondary follow-up occurs. If the lay responder communicates a continuing struggle with symptoms impacting and interfering with everyday life, the facilitator offers a coordinated or facilitated referral for mental health support.
In an article published in the Journal of Cardiac Failure. Ms. Flanary speaks about the three kinds of language that anyone who was either forced to or inspired to perform CPR can use to help process their trauma: words that explain what happened, words that name (eg, “forgotten patients”), and words that validate the experience and allow the person to articulate their feelings. The tools and technologies that organizations and health care professionals provide can help the healing process. Empathy and compassion, too, have a place.
But there are virtually no standardized and proactive initiatives of this kind in much of the world, including Latin America. So, most people who just happened to be in the right place at the right time find that they have to navigate the “after” part all on their own.
Other obstacles
Dr. Márquez Murillo finds it unfortunate that countries in the region have yet to enact “Good Samaritan” laws. If individuals render aid to someone suffering cardiac arrest, then these laws would ensure that they will not be held liable in any way. This is the case in Argentina and Uruguay. So, the fear of things turning into a legal matter may be holding people back from taking action; that fear could also create additional stress for those who end up stepping in to help.
Even with the legal safeguards, exceptional circumstances may arise where rescuers find themselves facing unexpected emotional challenges. In Argentina, Virginia Pérez Antonelli, the 17-year-old who tried in vain to save the life of Fernando Báez Sosa, had to testify at the trial of the eight defendants accused of brutally beating him in January 2020. The press, the public – the attention of an entire country – was focused on her. She had to respond to the defense attorneys who were able to ask whether she was sure that she performed the CPR maneuvers correctly. And a few weeks ago, a medical examiner hired by the defense suggested that “the CPR may have made the situation worse” for the victim. An indignant Dr. Fitz Maurice responded on Twitter: “CPR SAVES LIVES!! Let’s not let a CHEAP AND BASELESS argument destroy all the work that’s been done…!”
Of course, there are consequences that are beyond our control and others that can, in fact, be anticipated and planned for. Dr. Fitz Maurice brought up a preventive approach: Make CPR second nature, teach it in schools, help people overcome their fears. “Cardiac deaths are 200 times more frequent than deaths resulting from fires – and we practice fire drills a lot more than we practice CPR,” he told this news organization. In a society where there is widespread training on the procedure, where people regularly practice the technique, those who have had the experience of giving someone CPR will feel less alone, will be better understood by others.
“On the other hand, beyond the initial impact and the lack of a formal support system, the medium- and long-term outcome for those who acted is also psychologically and emotionally favorable,” said Jorge Bombau, MD, an obstetrician/gynecologist in Buenos Aires. After Dr. Bombau’s 14-year-old son Beltrán suddenly died during a school sports tournament, Dr. Bombau became a prominent advocate spreading the word about CPR.
“I don’t know anyone who regrets doing CPR,” he told this news organization. “There may be a brief period when the person feels distressed or depressed, when they have trouble sleeping. But it’s been proven that doing a good deed improves one’s mood. And what better deed is there than trying to save someone’s life? Whether their efforts were successful or in vain, that person has, at the end of the day, done something meaningful and worthwhile.”
Mr. Snitcofsky shares this sentiment. For several months now, he’s been feeling he’s “in a good place.” And he’s been actively promoting CPR on social media. As he recently posted on Twitter, “I’m here to retweet everything that has to do with getting us all to become familiar with how to do CPR and working up the courage to do it. The training takes no more than a few hours.
“I want to know that, if I ever have an out-of-hospital sudden cardiac arrest, there will be neighbors, friends, or family members around who know how to do CPR. Every person who knows how to do CPR can persuade others, and those of us who’ve had to do CPR in real life are even better candidates for persuading others. And if one day a person ends up needing CPR, I want to step in again and make up for lost time. Here’s hoping it’ll do the job,” he concluded.
It’s the same for Matías Alonso, a journalist in Buenos Aires. On New Year’s Eve 15 years ago, he was at a family dinner when, a few minutes before midnight, he found himself giving CPR to his stepmother’s father. “Unfortunately, he passed away, but I continued doing CPR on him until the ambulance arrived. For some time, I felt a little guilty for not taking charge of the situation from the beginning, and because I had this idea in my head that more people pulled through and recovered. But afterwards, they really thanked me a lot. And that helped me realize that I’d done something. I didn’t stand still when faced with the inevitability of death. I understood that it was good to have tried,” Mr. Alonso told this news organization. “And next time … hopefully there won’t be a next time … but I’m more prepared, and I now know how I can do better.”
Mr. Alonso, Mr. Snitcofsky, Dr. Fitz Maurice, Dr. Mosca, Dr. Bombau, and Dr. Márquez Murillo disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com. This article was translated from Medscape Spanish.
Long QT syndrome overdiagnosis persists
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
Five factors underlie the ongoing overdiagnosis and misdiagnosis of long QT syndrome (LQTS), including temporary QT prolongation following vasovagal syncope, a “pseudo”-positive genetic test result, family history of sudden cardiac death, transient QT prolongation, and misinterpretation of the QTc interval, a new study suggests.
Awareness of these characteristics, which led to a diagnostic reversal in 290 of 1,841 (16%) patients, could reduce the burden of overdiagnosis on the health care system and on patients and families, senior author Michael J. Ackerman, MD, PhD, of Mayo Clinic, Rochester, Minn., and colleagues conclude.
“The findings are a disturbing and disappointing sequel to the paper we published about LQTS overdiagnosis back in 2007, which showed that 2 out of every 5 patients who came to Mayo Clinic for a second opinion left without the diagnosis,” Dr. Ackerman told this news organization.
To date, Dr. Ackerman has reversed the diagnosis for 350 patients, he said.
The consequences of an LQTS diagnosis are “profound,” he noted, including years of unnecessary drug therapy, implantation of a cardioverter defibrillator, disqualification from competitive sports, and emotional stress to the individual and family.
By pointing out the five biggest mistakes his team has seen, he said, “we hope to equip the diagnostician with the means to challenge and assess the veracity of a LQTS diagnosis.”
The study was published online in the Journal of the American College of Cardiology.
Time to do better
Dr. Ackerman and colleagues analyzed electronic medical records on 290 of 1,841 (16%) patients who presented with an outside diagnosis of LQTS but subsequently were dismissed as having normal findings. The mean age of these patients at their first Mayo Clinic evaluation was 22, 60% were female, and the mean QTc interval was 427 ±25 milliseconds.
Overall, 38% of misdiagnoses were the result of misinterpretation of clinical factors; 29%, to diagnostic test misinterpretations; 17%, to an apparently positive genetic test in the context of a weak or absent phenotype; and 16%, to a family history of false LQTS or of sudden cardiac or sudden unexplained death.
More specifically, the most common cause of an LQTS misdiagnosis was QT prolongation following vasovagal syncope, which was misinterpreted as LQTS-attributed syncope.
The second most common cause was an apparently positive genetic test for an LQTS gene that turned out to be a benign or likely benign variant.
The third most common cause was an LQTS diagnosis based solely on a family history of sudden unexplained death (26 patients), QT prolongation (11 patients), or sudden cardiac arrest (9 patients).
The fourth most common cause was an isolated event of QT prolongation (44 patients). The transient QT prolongation was observed under myriad conditions unrelated to LQTS. Yet, 31 patients received a diagnosis based solely on the event.
The fifth most common cause was inclusion of the U-wave in the calculation of the QTc interval (40 patients), leading to an inaccurate interpretation of the electrocardiogram.
Dr. Ackerman noted that these LQTS diagnoses were given by heart-rhythm specialists, and most patients self-referred for a second opinion because a family member questioned the diagnosis after doing their own research.
“It’s time that we step up to the plate and do better,” Dr. Ackerman said. The team’s evaluation of the impact of the misdiagnosis on the patients’ lifestyle and quality of life showed that 45% had been restricted from competitive sports (and subsequently resumed sports activity with no adverse events); 80% had been started on beta-blockers (the drugs were discontinued in 84% as a result of the Mayo Clinic evaluation, whereas 16% opted to continue); and 10 of 22 patients (45%) who received an implanted cardioverter device underwent an extraction of the device without complications.
The authors conclude: “Although missing a patient who truly has LQTS can lead to a tragic outcome, the implications of overdiagnosed LQTS are not trivial and are potentially tragic as well.”
‘Tricky diagnosis’
LQTS specialist Peter Aziz, MD, director of pediatric electrophysiology at the Cleveland Clinic, agreed with these findings.
“Most of us ‘channelopathists’ who see LQTS for a living have a good grasp of the disease, but it can be elusive for others,” he said in an interview. “This is a tricky diagnosis. There are ends of the spectrum where people for sure don’t have it and people for sure do. Most clinicians are able to identify that.”
However, he added, “A lot of patients fall into that gray area where it may not be clear at first, even to an expert. But the expert knows how to do a comprehensive evaluation, examining episodes and symptoms and understanding whether they are relevant to LQTS or completely red herrings, and feeling confident about how they calculate the acute interval on an electrocardiogram.”
“All of these may seem mundane, but without the experience, clinicians are vulnerable to miscalculations,” he said. “That’s why our bias, as channelopathists, is that every patient who has a suspected diagnosis or is being treated for LQTS really should see an expert.”
Similarly, Arthur A.M. Wilde, MD, PhD, of the University of Amsterdam, and Peter J. Schwartz, MD, of IRCCS Istituto Auxologico Italiano, Milan, write in a related editorial that it “has to be kept in mind that both diagnostic scores and risk scores are dynamic and can be modified by time and by appropriate therapy.
“Therefore, to make hasty diagnosis of a disease that requires life-long treatment is inappropriate, especially when this is done without the support of adequate, specific experience.”
No commercial funding or relevant financial relationships were reported.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Novel resuscitation for patients with nonshockable rhythms in cardiac arrest
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine. with a remarkable increase in neurologically intact survival. Welcome, gentlemen.
Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine. with a remarkable increase in neurologically intact survival. Welcome, gentlemen.
Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.
This transcript has been edited for clarity.
Robert D. Glatter, MD: Welcome. I’m Dr Robert Glatter, medical adviser for Medscape Emergency Medicine. with a remarkable increase in neurologically intact survival. Welcome, gentlemen.
Dr. Pepe, I’d like to start off by thanking you for taking time to join us to discuss this novel concept of head-up or what you now refer to as a neuroprotective cardiopulmonary resuscitation (CPR) bundle. Can you define what this entails and why it is referred to as a neuroprotective CPR bundle?
Paul E. Pepe, MD, MPH: CPR has been life saving for 60 years the way we’ve performed it, but probably only in a very small percentage of cases. That’s one of the problems. We have almost a thousand people a day who have sudden cardiac arrest out in the community alone and more in the hospital.
We know that early defibrillation and early CPR can contribute, but it’s still a small percentage of those. About 75%-85% of the cases that we go out to see will have nonshockable rhythms and flatlines. Some cases are what we call “pulseless electrical activity,” meaning that it looks like there is some kind of organized complex, but there is no pulse associated with it.
That’s why it’s a problem, because they don’t come back. Part of the reason why we see poor outcomes is not only that these cases tend to be people who, say, were in ventricular fibrillation and then just went on over time and were not witnessed or resuscitated or had a long response time. They basically either go into flatline or autoconvert into these bizarre rhythms.
The other issue is the way we perform CPR. CPR has been lifesaving, but it only generates about 20% and maybe 15% in some cases of normal blood flow, and particularly, cerebral perfusion pressure. We’ve looked at this nicely in the laboratory.
For example, during chest compressions, we’re hoping during the recoil phase to pull blood down and back into the right heart. The problem is that you’re not only setting a pressure rate up here to the arterial side but also, you’re setting back pressure wave on the venous side. Obviously, the arterial side always wins out, but it’s just not as efficient as it could be, at 20% or 30%.
What does this entail? It entails several independent mechanisms in terms of how they work, but they all do the same thing, which is they help to pull blood out of the brain and back into the right heart by basically manipulating intrathoracic pressure and creating more of a vacuum to get blood back there.
It’s so important that people do quality CPR. You have to have a good release and that helps us suck a little bit of blood and sucks the air in. As soon as the air rushes in, it neutralizes the pressure and there’s no more vacuum and nothing else is happening until the next squeeze.
What we have found is that we can cap the airway just for a second with a little pop-up valve. It acts like when you’re sucking a milkshake through a straw and it creates more of a vacuum in the chest. Just a little pop-up valve that pulls a little bit more blood out of the brain and the rest of the body and into the right heart.
We’ve shown in a human study that, for example, the systolic blood pressure almost doubles. It really goes from 40 mm Hg during standard CPR up to 80 mm Hg, and that would be sustained for 14-15 minutes. That was a nice little study that was done in Milwaukee a few years ago.
The other thing that happens is, if you add on something else, it’s like a toilet plunger. I think many people have seen it; it’s called “active compression-decompression.” It not only compresses, but it decompresses. Where it becomes even more effective is that if you had broken bones or stiff bones as you get older or whatever it may be, as you do the CPR, you’re still getting the push down and then you’re getting the pull out. It helps on several levels. More importantly, when you put the two together, they’re very synergistic.
We, have already done the clinical trial that is the proof of concept, and that was published in The Lancet about 10 years ago. In that study, we found that the combination of those two dramatically improved survival rates by 50%, with 1-year survival neurologically intact. That got us on the right track.
The interesting thing is that someone said, “Can we lift the head up a little bit?” We did a large amount of work in the laboratory over 10 years, fine tuning it. When do you first lift the head? How soon is too soon? It’s probably bad if you just go right to it.
We had to get the pump primed a little bit with these other things to get the flow going better, not only pulling blood out of the brain but now, you have a better flow this way. You have to prime at first for a couple of minutes, and we worked out the timing: Is it 3 or 4 minutes? It seems the timing is right at about 2 minutes, then you gradually elevate the head over about 2 minutes. We’re finding that seems to be the optimal way to do it. About 2 minutes of priming with those other two devices, the adjuncts, and then gradually elevate the head over 2 minutes.
When we do that in the laboratory, we’re getting normalized cerebral perfusion pressures. You’re normalizing the flow back again with that. We’re seeing profound differences in outcome as a result, even in these cases of the nonshockables.
Dr. Glatter: What you’re doing basically is resulting in an increase in cardiac output, essentially. That really is important, especially in these nonshockable rhythms, correct?
Dr. Pepe: Absolutely. As you’re doing this compression and you’re getting these intracranial pulse waves that are going up because they’re colliding up there. It could be even damaging in itself, but we’re seeing these intracranial raises. The intracranial pressure starts going up more and more over time. Also, peripherally in most people, you’re not getting good flow out there; then, your vasculature starts to relax. The arterials are starting to not get oxygen, so they don’t go out.
With this technique where we’re returning the pressure, we’re getting to 40% of normal now with the active compression-decompression CPR plus an impedance threshold device (ACD+ITD CPR) approach. Now, you add this, and you’re almost normalizing. In humans, even in these asystole patients, we’re seeing end-title CO2s which are generally in the 15-20 range with standard CPR are now up with ACD+ITD CPR in the 30%-40% range, where we’re getting through 30 or 40 end-tidal CO2s. Now, we’re seeing even the end-tidal CO2s moving up into the 40s and 50s. We know there’s a surrogate marker telling us that we are generating much better flows not only to the rest of the body, but most importantly, to the brain.
Dr. Glatter: Ryan, could you tell us about the approach in terms of on scene, what you’re doing and how you use the device itself? Maybe you could talk about the backpack that you developed with your fire department?
Ryan P. Quinn, BS, EMS: Our approach has always been to get to the patient quickly, like everybody’s approach on a cardiac arrest when you’re responding. We are an advanced life-support paramedic ambulance service through the fire department – we’re all cross-trained firefighter paramedics. Our first vehicle from the fire department is typically the ambulance. It’s smaller and a little quicker than the fire engine. Two paramedics are going to jump out with two backpacks. One has the automated compressive device (we use the Lucas), and the other one is the sequential patient lifting device, the EleGARD.
Our two paramedics are quick to the patient’s side, and once they make contact with the patient to verify pulseless cardiac arrest, they will unpack. One person will go right to compressions if there’s nobody on compressions already. Sometimes we have a first responder police officer with an automated external defibrillator (AED). We go right to the patient’s side, concentrate on compressions, and within 90 seconds to 2 minutes, we have our bags unpacked, we’ve got the devices turned on, patient lifted up, slid under the device, and we have a supraglottic airway that is placed within 15 seconds already premade with the ITD on top. We have a sealed airway that we can continue to compress with Dr. Pepe’s original discussion of building on what’s previously been shown to work.
Dr. Pepe: Let me make a comment about this. This is so important, what Ryan is saying, because it’s something we found during the study. It’s really a true pit-crew approach. You’re not only getting these materials, which you think you need a medical Sherpa for, but you don’t. They set it up and then when they open it up, it’s all laid out just exactly as you need it. It’s not just how fast you get there; it’s how fast you get this done.
When we look at all cases combined against high-performance systems that had some of the highest survival rates around, when we compare it to those, we found that overall, even if you looked at the ones that had over 20-minute responses, the odds ratios were still three to four times higher. It was impressive.
If you looked at it under 15 minutes, which is really reasonable for most systems that get there by the way, the average time that people start CPR in any system in these studies has been about 8 minutes if you actually start this thing, which takes about 2 minutes more for this new bundle of care with this triad, it’s almost 12-14 times higher in terms of the odds ratio. I’ve never seen anything like that where the higher end is over 100 in terms of your confidence intervals.
Ryan’s system did really well and is one of those with even higher levels of outcomes, mostly because they got it on quickly. It’s like the AED for nonshockables but better because you have a wider range of efficacy where it will work.
Dr. Glatter: When the elapsed time was less than 11 minutes, that seemed to be an inflection point in the study, is that correct? You saw that 11-fold higher incidence in terms of neurologically intact survival, is that correct?
Dr. Pepe: We picked that number because that was the median time to get it on board. Half the people were getting it within that time period. The fact that you have a larger window, we’re talking about 13- almost 14-fold improvements in outcome if it was under 15 minutes. It doesn’t matter about the 11 or the 12. It’s the faster you get it on board, the better off you are.
Dr. Glatter: What’s the next step in the process of doing trials and having implementation on a larger scale based on your Annals of Emergency Medicine study? Where do you go from here?
Dr. Pepe: I’ve come to find out there are many confounding variables. What was the quality of CPR? How did people ventilate? Did they give the breath and hold it? Did they give a large enough breath so that blood can go across the transpulmonary system? There are many confounding variables. That’s why I think, in the future, it’s going to be more of looking at things like propensity score matching because we know all the variables that change outcomes. I think that’s going to be a way for me.
The other thing is that we were looking at only 380 cases here. When this doubles up in numbers, as we accrue more cases around the country of people who are implementing this, these numbers I just quoted are going to go up much higher. Unwitnessed asystole is considered futile, and you just don’t get them back. To be able to get these folks back now, even if it’s a small percentage, and the fact that we know that we’re producing this better flow, is pretty striking.
I’m really impressed, and the main thing is to make sure people are educated about it. Number two is that they understand that it has to be done right. It cannot be done wrong or you’re not going to see the differences. Getting it done right is not only following the procedures, the sequence, and how you do it, but it also has to do with getting there quickly, including assigning the right people to put it on and having well-trained people who know what they’re doing.
Dr. Glatter: In general, the lay public obviously should not attempt this in the field lifting someone’s head up in the sense of trying to do chest compressions. I think that message is important that you just said. It’s not ready for prime time yet in any way. It has to be done right.
Dr. Pepe: Bystanders have to learn CPR – they will buy us time and we’ll have better outcomes when they do that. That’s number one. Number two is that as more and more systems adopt this, you’re going to see more people coming back. If you think about what we’re doing now, if we only get back 5% of these nonshockable vs. less than 1%, it’s 5% of 800 people a day because a thousand people a day die. Several dozens of lives can be saved on a daily basis, coming back neurologically intact. That’s the key thing.
Dr. Glatter: Ryan, can you comment about your experience in the field? Is there anything in terms of your current approach that you think would be ideal to change at this point?
Mr. Quinn: We’ve established that this is the approach that we want to take and we’re just fine tuning it to be more efficient. Using the choreography of which person is going to do which role, we have clearly defined roles and clearly defined command of the scene so we’re not missing anything. Training is extremely important.
Dr. Glatter: Paul, I want to ask you about your anecdotal experience of people waking up quickly and talking after elevating their heads and going through this process. Having people talk about it and waking up is really fascinating. Maybe you can comment further on this.
Dr. Pepe: That’s a great point that you bring up because a 40- to 50-year-old guy who got saved with this approach, when he came around, he said he was hearing what people were saying. When he came out of it, he found out he had been getting CPR for about 25 minutes because he had persistent recurring ventricular fibrillation. He said, “How could I have survived that that long?”
When we told him about the new approach, he added, “Well, that’s like neuroprotective.” He’s right, because in the laboratory, we showed it was neuroprotective and we’re also getting better flows back there. It goes along with everything else, and so we’ve adopted the name because it is.
These are really high-powered systems we are comparing against, and we have the same level of return of spontaneous circulation. The major difference was when you started talking about the neurointact survival. We don’t have enough numbers yet, but next go around, we’re going to look at cerebral performance category (CPC) – CPC1 vs. the CPC2 – which were both considered intact, but CPC1 is actually better. We’re seeing many more of those, anecdotally.
I also wanted to mention that people do bring this up and say, “Well, let’s do a trial.” As far as we’re concerned, the trial’s been done in terms of The Lancet study 10 years ago that showed that the active compression-decompression had tremendously better outcomes. We show in the laboratories that you augment that a little bit. These are all [Food and Drug Administration] approved. You can go out and buy it tomorrow and get it done. I have no conflicts of interest, by the way, with any of this.
To have this device that’s going to have the potential of saving so many more lives is really an exciting breakthrough. More importantly, we’re understanding more now about the physiology of CPR and why it works. It could work much better with the approaches that we’ve been developing over the last 20 years or so.
Dr. Glatter: Absolutely. I want to thank both of you gentlemen. It’s been really an incredible experience to learn more about an advance in resuscitation that could truly be lifesaving. Thank you again for taking time to join us.
Dr. Glatter is an attending physician in the department of emergency medicine, Lenox Hill Hospital, New York. Dr. Pepe is professor, department of management, policy, and community health, University of Texas Health Sciences Center, Houston. Mr. Quinn is EMS Chief, Edina (Minn.) Fire Department. No conflicts of interest were reported.
A version of this article first appeared Jan. 26 on Medscape.com.