Acute Coronary Syndromes

TOPLINE:

The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.

METHODOLOGY:

• Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
• Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
• Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.

TAKEAWAY:

• Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
• These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
• The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
• Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
• There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.

IN PRACTICE:

“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.

“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.

SOURCE:

The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.

LIMITATIONS:

The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.

DISCLOSURES:

Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.

METHODOLOGY:

• Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
• Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
• Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.

TAKEAWAY:

• Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
• These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
• The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
• Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
• There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.

IN PRACTICE:

“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.

“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.

SOURCE:

The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.

LIMITATIONS:

The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.

DISCLOSURES:

Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

The Million Hearts Model, a U.S. Centers for Medicare & Medicaid Services (CMS) initiative that encouraged and paid health care organizations to assess and reduce cardiovascular disease (CVD) risk, reduced first-time myocardial infarction (MI) and strokes among Medicare beneficiaries without significant changes in Medicare spending, a randomized trial finds.

METHODOLOGY:

• Researchers assessed the Million Hearts CVD Risk Reduction Model in a pragmatic, cluster-randomized trial among 342 health care organizations – half in the intervention group and half in the standard care control group.
• Among 218,684 medium- or high-risk Medicare beneficiaries (median age, 72 years), 130,578 were in the intervention group in which Medicare paid for guideline-concordant care including routine CVD risk assessment, and 88,286 were in the standard care group.
• Outcomes included first time CVD events (for instance, MI, stroke, transient ischemic attack), combined first-time CVD events and CVD deaths, and Medicare spending.

TAKEAWAY:

• Over a median follow-up of 4.3 years, the intervention group had a 3.3% lower rate of CVD events than the control group (adjusted hazard ratio, 0.97; 90% confidence interval, 0.93-1.00; P = .09) and a 4.2% lower rate of combined first-time CVD events and CVD deaths (HR, 0.96; 90% CI, 0.93-0.99; P = .02).
• These relative effects represent an absolute re.duction of 0.3 percentage points in the probability of a CVD event over 5 years (7.8% intervention vs 8.1%) and 0.4 percentage points in the probability of a CVD event or CVD death over 5 years (9.3% intervention vs. 9.7% control).
• The intervention group also had a 4.3% lower death rate (HR, 0.96; 90% CI, 0.93-0.98; P = .01; absolute reduction of 0.5 percentage points over 5 years).
• Analyses by cause of death showed the largest relative declines (10.6%) among deaths due to coronary heart disease and CVD.
• There was no significant between-group difference in Medicare spending on CVD events or in overall Medicare Parts A and B spending.

IN PRACTICE:

“The model was unique in paying for overall CVD risk reduction, measured by a novel, longitudinal risk calculator, rather than tying performance-based payments to control of individual risk factors,” the authors write.

“The encouraging findings from the Million Hearts Model suggest that modernized payment models may be an affirmative strategy to [incentivize guideline-concordant CVD preventive care and improve outcomes], though further work is needed to ensure that these models are patient-centric, optimally deployed, and equity-enhancing,” add the editorial writers.

SOURCE:

The study, with first author Laura Blue, PhD, Mathematica, Washington, was published online in JAMA, with an accompanying editorial.

LIMITATIONS:

The main limitation is nonparticipation of many of the organizations (516 were randomly assigned to one of the study groups, 342 participated) and incomplete entry of beneficiary data into the registry, which could have led to systematic differences between the two groups. Bias due to the selective participation of organizations and beneficiaries cannot be ruled out.

DISCLOSURES:

Funding for the study was provided by CMS, Department of Health & Human Services. The authors have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

TOPLINE:

Chronic kidney disease is the strongest predictor of sudden cardiac arrest (SCA) in a population of Hispanic and Latinx patients, new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.

METHODOLOGY:

• The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
• Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
• Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.

TAKEAWAY:

• In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
• Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
• In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.

IN PRACTICE:

“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.

SOURCE:

The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.

LIMITATIONS:

Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.

DISCLOSURES:

The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.

A version of this article first appeared on Medscape.com.

TOPLINE:

Chronic kidney disease is the strongest predictor of sudden cardiac arrest (SCA) in a population of Hispanic and Latinx patients, new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.

METHODOLOGY:

• The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
• Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
• Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.

TAKEAWAY:

• In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
• Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
• In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.

IN PRACTICE:

“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.

SOURCE:

The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.

LIMITATIONS:

Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.

DISCLOSURES:

The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.

A version of this article first appeared on Medscape.com.

TOPLINE:

Chronic kidney disease is the strongest predictor of sudden cardiac arrest (SCA) in a population of Hispanic and Latinx patients, new data show, suggesting early identification of CKD may provide an opportunity to reduce the risk in these groups. Other predictors included heavy drinking, atrial fibrillation, coronary artery disease, heart failure and diabetes.

METHODOLOGY:

• The study included 295 Hispanic or Latinx patients with out-of-hospital SCA from the PRESTO study in Ventura County, California, and 590 frequency-matched controls from the San Diego site of the population-based HCHS/SOL (Hispanic Community Health Survey/Study of Latinos); in both cohorts, men made up 70% of participants, and the median age was about 63 years.
• Researchers collected data on demographics, medical history, and current health conditions. Of note, 51.2% of SCA cases and 8.8% of control participants had CKD, and 20.0% of cases and 0.7% of the control group were on dialysis.
• Pre-SCA echocardiograms were available for 48% of SCA cases and baseline echocardiograms for more than 99% of control participants.

TAKEAWAY:

• In analyses adjusted for age, sex, and clinical variables, predictors significantly associated with higher odds of SCA included: CKD (odds ratio, 7.3; 95% confidence interval, 3.8-14.3; P < .001), heavy drinking (OR, 4.5), stroke (OR, 3.1), atrial fibrillation (OR, 3.7), coronary artery disease (OR, 2.9), heart failure (OR, 2.5), and diabetes (OR, 1.5).
• Hypertension, hyperlipemia, body mass index, and current smoking status were not significantly associated with SCA.
• In adjusted analyses, heart rate (OR, 1.8 per one standard deviation [1-SD] increase), QTc interval (OR, 2.5 per 1-SD increase) and left ventricular ejection fraction (OR, 4.4 per 1-SD decrease) were significantly associated with SCA, suggesting echocardiogram evaluations could help identify Hispanic or Latinx individuals at increased risk for SCA, wrote the authors.

IN PRACTICE:

“Our study, the first to include feasible numbers of Hispanic or Latino individuals, highlights the importance of renal dysfunction as a risk factor for SCA in the community,” the authors wrote, adding that early identification and management of chronic kidney disease could reduce risk for SCA in this population.

SOURCE:

The study was conducted by Kyndaron Reinier, PhD, MPH, Cedars-Sinai Health System, Los Angeles, and colleagues. It was published online in the Journal of the American Heart Association.

LIMITATIONS:

Most participants from the HCHS/SOL study were born outside the United States, compared with about half the SCA cases, which could have influenced cardiovascular disease risk, although results did not change considerably when models were adjusted for place of birth. Study participants were predominantly of Mexican heritage, so results may not be generalizable to Hispanic or Latinx individuals from other regions. As medical history was assessed differently in the two studies, there could be some error in estimating the strength of associations. Results from echocardiographic data should be viewed as hypothesis generating because of the potential for residual bias.

DISCLOSURES:

The Ventura PRESTO study was funded, in part, by the National Institutes of Health, and National Heart, Lung, and Blood Institute. The HCHS/SOL was carried out as a collaborative study supported by contracts from the NHLBI.

A version of this article first appeared on Medscape.com.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

In a large prospective study, a graded higher risk of all-cause mortality and mortality from cardiovascular disease (CVD) and ischemic heart disease (IHD) emerged in adults with moderate to severe depressive symptoms, compared with those with no such symptoms.

Participants with mild depressive symptoms had a 35%-49% higher risk of all-cause and CVD mortality, respectively, while for those with moderate to severe depressive symptoms, the risk of all-cause, CVD, and IHD mortality was 62%, 79%, and 121% higher, respectively.

Dr. Zefeng Zhang, CDC

“This information highlights the importance for clinicians to identify patients with depressive symptoms and help them engage in treatment,” lead author Zefeng Zhang, MD, PhD, of the division for heart disease and stroke prevention at the U.S. Centers for Disease Control and Prevention, Atlanta, said in an interview.

The study appears in JAMA Network Open.

A nonclassic risk factor for CVD death

This graded positive association between depressive symptoms and CVD death was observed in data from the National Health and Nutrition Examination Survey 2005-2018, which were linked with the National Death Index through 2019 for adults aged 20 and older. Data analysis occurred from March 1 to May 26, 2023. According to the authors, their analyses extend findings from previous research by assessing these associations in a large, diverse, and nationally representative sample. Using more nuanced CVD-related causes of death, depressive symptoms emerged as a nontraditional risk factor for CVD mortality.

The study

In a total cohort of 23,694, about half male, mean overall age 44.7 years, prevalences of mild and moderate to severe depression were 14.9% and 7.2%, respectively, with depressive symptoms assessed by the nine-item Patient Health Questionnaire asking about symptoms over the past 2 weeks.

Adults with depression had significantly lower CV health scores in six of the American Heart Association Life’s Essential 8 metrics for heart health. For all-cause mortality, hazard ratios were 1.35 (95% confidence interval, 1.07-1.72) for mild depressive symptoms vs. none and 1.62 (95% CI, 1.24-2.12) for moderate to severe depressive symptoms vs. none.

The corresponding hazard ratios were 1.49 (95% CI, 1.11-2.0) and 1.79 (95% CI,1.22-2.62) for CVD mortality and 0.96 (95% CI, 0.58-1.60) and 2.21 (95% CI, 1.24-3.91) for IHD death, with associations largely consistent across subgroups.

At the highest severity of depressive symptoms (almost daily for past 2 weeks), feeling tired or having little energy, poor appetite or overeating, and having little interest in doing things were significantly associated with all-cause and CVD mortality after adjusting for potential confounders.

Approximately 11%-16% of the positive associations could be explained by lifestyle factors such as excess alcohol consumption, overeating, and inactivity as per the AHA’s Life’s Essential 8 metrics.

“Taken together with the body of literature on associations between depression and CVD mortality, these findings can support public health efforts to develop a comprehensive, nationwide strategy to improve well-being, including both mental and cardiovascular health,” Dr. Zhang and associates wrote.

This research was funded by the U.S. Centers for Disease Control and Prevention. The authors had no conflicts of interest to disclose.

Among “bi-risk” patients with acute coronary syndrome (ACS) who received a stent and completed 9-12 months of dual-antiplatelet therapy (DAPT), those who de-escalated therapy to clopidogrel alone as opposed to continuing on clopidogrel and aspirin for 9 months had 25% less bleeding without increased ischemic risk.

The findings are from the OPT-BIRISK trial in more than 7,700 patients in China deemed “bi-risk” because they had both a high risk of clinically relevant bleeding and a high risk of major adverse cardiac and cerebral events (MACCE).

Yaling Han, MD, from General Hospital of Northern Theater Command in Shenyang, China, presented the trial in a hotline session at the annual congress of the  European Society of Cardiology.

The results provide evidence for this treatment strategy from “a large cohort seen in clinical practice in whom the question of continuing DAPT vs. deescalating to clopidogrel monotherapy at this time period has not previously been addressed,” Dr. Han said in an interview.

She acknowledged that the findings may not be generalizable to non-Asian cohorts. Also, these patients were event-free after 9 months on DAPT, so they were relatively stable. Moreover, the finding that clopidogrel monotherapy was superior to DAPT for MACCE is only hypothesis-generating.

Renato D. Lopes, MD, PhD, Duke University, Durham, N.C., the assigned discussant at the session, congratulated the authors “for an important trial in the understudied East Asian population. The OPT-BIRISK trial adds information to the complex puzzle of antithrombotic therapy after ACS,” he said.

However, he brought up a few points that should be taken into consideration when interpreting this trial, including the ones noted by Dr. Han.

In an interview, Dr. Lopes cautioned that OPT-BIRISK tested an antiplatelet strategy “in challenging patients at increased risk for bleeding and ischemic events, but I don’t think we can say this is truly a high-risk population.” Invited to reply, Dr. Han conceded that these patients constituted a relatively low-risk subset of bi-risk patients.
 

Double-edged sword

“Antiplatelet therapy is a double-edged sword: it reduces ischemic risk but increases bleeding risk. Optimal antiplatelet therapy for bi-risk ACS patients remains a clinical challenge, and unsolved problem for the cardiovascular physician,” Dr. Han said in a press briefing.

The rationale and design of OPT-BIRISK were published in the American Heart Journal in 2020.

Between February 2018 and December 2020, the researchers enrolled and randomly assigned 7,758 bi-risk patients in 101 centers in China who had completed 9-12 months of DAPT (aspirin plus either clopidogrel or ticagrelor) after drug-eluting stent implantation for ACS.

The patients were randomly assigned to receive either clopidogrel plus aspirin or clopidogrel plus placebo for 9 months, followed by 3 months of aspirin.

The primary endpoint was clinically relevant Bleeding Academic Research Consortium (BARC) types 2, 3, or 5 bleeding, at 9 months after randomization.

Key secondary endpoints were MACCE (all-cause mortality, MI, stroke, or clinically driven revascularization), individual components of MACCE, any bleeding, and stent thrombosis at 9 months after randomization.

The patient criteria for having bi-risk ACS were:

• < 65 years old with at least one high-bleeding risk criterion and at least one high-ischemia risk criterion.
• 65-78 years old with at least one high-bleeding risk criterion or at least one high-ischemia risk criterion.
• > 75 years old.

The high bleeding risk criteria were female gender, iron deficiency anemia, stroke, taking a type 2 diabetes medication, and chronic kidney disease.

The high ischemic risk criteria included troponin-positive ACS, previous stent thrombosis, previous CV events (MI, stroke, peripheral artery disease [PAD], percutaneous coronary intervention [PCI]), on a type 2 diabetes medication, chronic kidney disease, and certain lesion characteristics.

The patients had a mean age of about 65 years and 41% were female. 

About half (52%) had type 2 diabetes, 18% had previous MI, and 15% had previous ischemic stroke. The ACS was mainly unstable angina (62%), followed by NSTEMI (17%) or STEMI (21%).

The patients had a mean high ischemic risk criteria of 3.2 and a mean high bleeding risk criteria of 1.4.

The initial DAPT treatment was aspirin and clopidogrel in three quarters of the patients and aspirin and ticagrelor in the remaining patients.

At 9 months, the primary endpoint of BARC type 2-5 bleeding occurred in 2.5% of patients in the clopidogrel plus placebo group and in 3.3% of patients in the clopidogrel plus aspirin group (hazard ratio, 0.75; 95% confidence interval, 0.57-0.97, P = .03).

“The bleeding results are not surprising,” Dr. Lopes said. Monotherapy vs. DAPT will cause less bleeding, Dr. Han agreed.

At 9 months, MACCE occurred in 2.6% of patients in the clopidogrel plus placebo group and in 3.5% of patients in the clopidogrel plus aspirin group (HR, 0.74; 95% CI, 0.57-0.96, P = .02).

Interpreting this latter finding as “reduced risk” of MACCE “is a stretch,” Dr. Lopes cautioned.

A potential explanation for this finding in the trial is that in the comparison group (aspirin plus clopidogrel), when patients had bleeding, they might have stopped all antiplatelet therapy, and this may have led to more ischemic events, he speculated.

“The observed reduction in MACCE is plausible,” Dr. Han said. “However, according to study protocol, we assumed that clopidogrel monotherapy would be noninferior to DAPT on the risk of MACCE. The superiority of clopidogrel alone vs. DAPT on MACCE should therefore be hypothesis-generating.”

“The increased rate of MACCE in the clopidogrel plus aspirin group was surprising,” she said in a press release from the ESC, “and may be because hemorrhagic events, which are more common with ongoing DAPT, could be associated with an adrenergic state with increased platelet aggregation due to hypotension, remedial procedures to treat bleeding, and the cessation of anti-ischemic medications.”
 

A low-risk subset of bi-risk patients, commonly seen in clinical practice

At the time of the index ACS, more than 60% of the patients had unstable angina, Dr. Lopes observed, “and we know these patients are lower risk.” Also, more than 1,000 of the patients did not have at least one high-risk factor for bleeding or ischemia. Moreover, these patients had not had any clinical events in the past 9-12 months on DAPT, “so they were not truly high risk when they were randomized.

“Patients aged 75 years and above are definitely bi-risk (even without any bleeding/ischemic criteria), especially post ACS, according to much literature,” Dr. Han said.

“Although patients met the bi-risk criteria for increased ischemia and bleeding at the time of index ACS and PCI, they were free from major events for at least 6 months on DAPT, thus constituting a relatively low-risk subset of bi-risk patients,” she conceded.

“Nonetheless, these patients (mean age nearly 65 years, 41% female, 52% diabetes, 18% MI history and 15% ischemic stroke history in bi-risk study) represent a large cohort seen in clinical practice,” she said. And “according to a real-world, nationwide registry from China (the OPT-CAD study), unstable angina accounted for about 50% of all ACS patients.”

There have been more data with shorter times for stopping aspirin, so it’s difficult to reconcile those studies with data from OPT-BIRISK, according to Dr. Lopes.

For example, the 2019 TWILIGHT study in patients undergoing PCI at high risk for bleeding showed that it seems to be safe to stop aspirin after 3 months and continue ticagrelor, without an increase in ischemic events.

“The question is almost in the wrong time,” he said, noting that the field is moving in the direction of stopping aspirin earlier, according to five or six recently published trials.

It is hard to generalize from an Asian population, he agreed. “In the U.S., we have other data that suggests that for high-risk patients, you can stop aspirin earlier than 9 months. That’s what most practices are doing.”

“When you look at different drugs, different doses, different duration,” Dr. Lopes summarized, “you have thousands of different permutations,” for antiplatelet therapy strategies. “Every time we have some data in large studies it adds a piece to the puzzle.”

The study was funded by the National Key Research and Development Project in China, and by a grant from Sanofi-Aventis. Dr. Han reports no relevant financial relationships. Disclosures for the other coauthors can be found with the original article.

A version of this article first appeared on Medscape.com.

Among “bi-risk” patients with acute coronary syndrome (ACS) who received a stent and completed 9-12 months of dual-antiplatelet therapy (DAPT), those who de-escalated therapy to clopidogrel alone as opposed to continuing on clopidogrel and aspirin for 9 months had 25% less bleeding without increased ischemic risk.

The findings are from the OPT-BIRISK trial in more than 7,700 patients in China deemed “bi-risk” because they had both a high risk of clinically relevant bleeding and a high risk of major adverse cardiac and cerebral events (MACCE).

Yaling Han, MD, from General Hospital of Northern Theater Command in Shenyang, China, presented the trial in a hotline session at the annual congress of the  European Society of Cardiology.

The results provide evidence for this treatment strategy from “a large cohort seen in clinical practice in whom the question of continuing DAPT vs. deescalating to clopidogrel monotherapy at this time period has not previously been addressed,” Dr. Han said in an interview.

She acknowledged that the findings may not be generalizable to non-Asian cohorts. Also, these patients were event-free after 9 months on DAPT, so they were relatively stable. Moreover, the finding that clopidogrel monotherapy was superior to DAPT for MACCE is only hypothesis-generating.

Renato D. Lopes, MD, PhD, Duke University, Durham, N.C., the assigned discussant at the session, congratulated the authors “for an important trial in the understudied East Asian population. The OPT-BIRISK trial adds information to the complex puzzle of antithrombotic therapy after ACS,” he said.

However, he brought up a few points that should be taken into consideration when interpreting this trial, including the ones noted by Dr. Han.

In an interview, Dr. Lopes cautioned that OPT-BIRISK tested an antiplatelet strategy “in challenging patients at increased risk for bleeding and ischemic events, but I don’t think we can say this is truly a high-risk population.” Invited to reply, Dr. Han conceded that these patients constituted a relatively low-risk subset of bi-risk patients.
 

Double-edged sword

“Antiplatelet therapy is a double-edged sword: it reduces ischemic risk but increases bleeding risk. Optimal antiplatelet therapy for bi-risk ACS patients remains a clinical challenge, and unsolved problem for the cardiovascular physician,” Dr. Han said in a press briefing.

The rationale and design of OPT-BIRISK were published in the American Heart Journal in 2020.

Between February 2018 and December 2020, the researchers enrolled and randomly assigned 7,758 bi-risk patients in 101 centers in China who had completed 9-12 months of DAPT (aspirin plus either clopidogrel or ticagrelor) after drug-eluting stent implantation for ACS.

The patients were randomly assigned to receive either clopidogrel plus aspirin or clopidogrel plus placebo for 9 months, followed by 3 months of aspirin.

The primary endpoint was clinically relevant Bleeding Academic Research Consortium (BARC) types 2, 3, or 5 bleeding, at 9 months after randomization.

Key secondary endpoints were MACCE (all-cause mortality, MI, stroke, or clinically driven revascularization), individual components of MACCE, any bleeding, and stent thrombosis at 9 months after randomization.

The patient criteria for having bi-risk ACS were:

• < 65 years old with at least one high-bleeding risk criterion and at least one high-ischemia risk criterion.
• 65-78 years old with at least one high-bleeding risk criterion or at least one high-ischemia risk criterion.
• > 75 years old.

The high bleeding risk criteria were female gender, iron deficiency anemia, stroke, taking a type 2 diabetes medication, and chronic kidney disease.

The high ischemic risk criteria included troponin-positive ACS, previous stent thrombosis, previous CV events (MI, stroke, peripheral artery disease [PAD], percutaneous coronary intervention [PCI]), on a type 2 diabetes medication, chronic kidney disease, and certain lesion characteristics.

The patients had a mean age of about 65 years and 41% were female. 

About half (52%) had type 2 diabetes, 18% had previous MI, and 15% had previous ischemic stroke. The ACS was mainly unstable angina (62%), followed by NSTEMI (17%) or STEMI (21%).

The patients had a mean high ischemic risk criteria of 3.2 and a mean high bleeding risk criteria of 1.4.

The initial DAPT treatment was aspirin and clopidogrel in three quarters of the patients and aspirin and ticagrelor in the remaining patients.

At 9 months, the primary endpoint of BARC type 2-5 bleeding occurred in 2.5% of patients in the clopidogrel plus placebo group and in 3.3% of patients in the clopidogrel plus aspirin group (hazard ratio, 0.75; 95% confidence interval, 0.57-0.97, P = .03).

“The bleeding results are not surprising,” Dr. Lopes said. Monotherapy vs. DAPT will cause less bleeding, Dr. Han agreed.

At 9 months, MACCE occurred in 2.6% of patients in the clopidogrel plus placebo group and in 3.5% of patients in the clopidogrel plus aspirin group (HR, 0.74; 95% CI, 0.57-0.96, P = .02).

Interpreting this latter finding as “reduced risk” of MACCE “is a stretch,” Dr. Lopes cautioned.

A potential explanation for this finding in the trial is that in the comparison group (aspirin plus clopidogrel), when patients had bleeding, they might have stopped all antiplatelet therapy, and this may have led to more ischemic events, he speculated.

“The observed reduction in MACCE is plausible,” Dr. Han said. “However, according to study protocol, we assumed that clopidogrel monotherapy would be noninferior to DAPT on the risk of MACCE. The superiority of clopidogrel alone vs. DAPT on MACCE should therefore be hypothesis-generating.”

“The increased rate of MACCE in the clopidogrel plus aspirin group was surprising,” she said in a press release from the ESC, “and may be because hemorrhagic events, which are more common with ongoing DAPT, could be associated with an adrenergic state with increased platelet aggregation due to hypotension, remedial procedures to treat bleeding, and the cessation of anti-ischemic medications.”
 

A low-risk subset of bi-risk patients, commonly seen in clinical practice

At the time of the index ACS, more than 60% of the patients had unstable angina, Dr. Lopes observed, “and we know these patients are lower risk.” Also, more than 1,000 of the patients did not have at least one high-risk factor for bleeding or ischemia. Moreover, these patients had not had any clinical events in the past 9-12 months on DAPT, “so they were not truly high risk when they were randomized.

“Patients aged 75 years and above are definitely bi-risk (even without any bleeding/ischemic criteria), especially post ACS, according to much literature,” Dr. Han said.

“Although patients met the bi-risk criteria for increased ischemia and bleeding at the time of index ACS and PCI, they were free from major events for at least 6 months on DAPT, thus constituting a relatively low-risk subset of bi-risk patients,” she conceded.

“Nonetheless, these patients (mean age nearly 65 years, 41% female, 52% diabetes, 18% MI history and 15% ischemic stroke history in bi-risk study) represent a large cohort seen in clinical practice,” she said. And “according to a real-world, nationwide registry from China (the OPT-CAD study), unstable angina accounted for about 50% of all ACS patients.”

There have been more data with shorter times for stopping aspirin, so it’s difficult to reconcile those studies with data from OPT-BIRISK, according to Dr. Lopes.

For example, the 2019 TWILIGHT study in patients undergoing PCI at high risk for bleeding showed that it seems to be safe to stop aspirin after 3 months and continue ticagrelor, without an increase in ischemic events.

“The question is almost in the wrong time,” he said, noting that the field is moving in the direction of stopping aspirin earlier, according to five or six recently published trials.

It is hard to generalize from an Asian population, he agreed. “In the U.S., we have other data that suggests that for high-risk patients, you can stop aspirin earlier than 9 months. That’s what most practices are doing.”

“When you look at different drugs, different doses, different duration,” Dr. Lopes summarized, “you have thousands of different permutations,” for antiplatelet therapy strategies. “Every time we have some data in large studies it adds a piece to the puzzle.”

The study was funded by the National Key Research and Development Project in China, and by a grant from Sanofi-Aventis. Dr. Han reports no relevant financial relationships. Disclosures for the other coauthors can be found with the original article.

A version of this article first appeared on Medscape.com.

Among “bi-risk” patients with acute coronary syndrome (ACS) who received a stent and completed 9-12 months of dual-antiplatelet therapy (DAPT), those who de-escalated therapy to clopidogrel alone as opposed to continuing on clopidogrel and aspirin for 9 months had 25% less bleeding without increased ischemic risk.

The findings are from the OPT-BIRISK trial in more than 7,700 patients in China deemed “bi-risk” because they had both a high risk of clinically relevant bleeding and a high risk of major adverse cardiac and cerebral events (MACCE).

Yaling Han, MD, from General Hospital of Northern Theater Command in Shenyang, China, presented the trial in a hotline session at the annual congress of the  European Society of Cardiology.

The results provide evidence for this treatment strategy from “a large cohort seen in clinical practice in whom the question of continuing DAPT vs. deescalating to clopidogrel monotherapy at this time period has not previously been addressed,” Dr. Han said in an interview.

She acknowledged that the findings may not be generalizable to non-Asian cohorts. Also, these patients were event-free after 9 months on DAPT, so they were relatively stable. Moreover, the finding that clopidogrel monotherapy was superior to DAPT for MACCE is only hypothesis-generating.

Renato D. Lopes, MD, PhD, Duke University, Durham, N.C., the assigned discussant at the session, congratulated the authors “for an important trial in the understudied East Asian population. The OPT-BIRISK trial adds information to the complex puzzle of antithrombotic therapy after ACS,” he said.

However, he brought up a few points that should be taken into consideration when interpreting this trial, including the ones noted by Dr. Han.

In an interview, Dr. Lopes cautioned that OPT-BIRISK tested an antiplatelet strategy “in challenging patients at increased risk for bleeding and ischemic events, but I don’t think we can say this is truly a high-risk population.” Invited to reply, Dr. Han conceded that these patients constituted a relatively low-risk subset of bi-risk patients.
 

Double-edged sword

“Antiplatelet therapy is a double-edged sword: it reduces ischemic risk but increases bleeding risk. Optimal antiplatelet therapy for bi-risk ACS patients remains a clinical challenge, and unsolved problem for the cardiovascular physician,” Dr. Han said in a press briefing.

The rationale and design of OPT-BIRISK were published in the American Heart Journal in 2020.

Between February 2018 and December 2020, the researchers enrolled and randomly assigned 7,758 bi-risk patients in 101 centers in China who had completed 9-12 months of DAPT (aspirin plus either clopidogrel or ticagrelor) after drug-eluting stent implantation for ACS.

The patients were randomly assigned to receive either clopidogrel plus aspirin or clopidogrel plus placebo for 9 months, followed by 3 months of aspirin.

The primary endpoint was clinically relevant Bleeding Academic Research Consortium (BARC) types 2, 3, or 5 bleeding, at 9 months after randomization.

Key secondary endpoints were MACCE (all-cause mortality, MI, stroke, or clinically driven revascularization), individual components of MACCE, any bleeding, and stent thrombosis at 9 months after randomization.

The patient criteria for having bi-risk ACS were:

• < 65 years old with at least one high-bleeding risk criterion and at least one high-ischemia risk criterion.
• 65-78 years old with at least one high-bleeding risk criterion or at least one high-ischemia risk criterion.
• > 75 years old.

The high bleeding risk criteria were female gender, iron deficiency anemia, stroke, taking a type 2 diabetes medication, and chronic kidney disease.

The high ischemic risk criteria included troponin-positive ACS, previous stent thrombosis, previous CV events (MI, stroke, peripheral artery disease [PAD], percutaneous coronary intervention [PCI]), on a type 2 diabetes medication, chronic kidney disease, and certain lesion characteristics.

The patients had a mean age of about 65 years and 41% were female. 

About half (52%) had type 2 diabetes, 18% had previous MI, and 15% had previous ischemic stroke. The ACS was mainly unstable angina (62%), followed by NSTEMI (17%) or STEMI (21%).

The patients had a mean high ischemic risk criteria of 3.2 and a mean high bleeding risk criteria of 1.4.

The initial DAPT treatment was aspirin and clopidogrel in three quarters of the patients and aspirin and ticagrelor in the remaining patients.

At 9 months, the primary endpoint of BARC type 2-5 bleeding occurred in 2.5% of patients in the clopidogrel plus placebo group and in 3.3% of patients in the clopidogrel plus aspirin group (hazard ratio, 0.75; 95% confidence interval, 0.57-0.97, P = .03).

“The bleeding results are not surprising,” Dr. Lopes said. Monotherapy vs. DAPT will cause less bleeding, Dr. Han agreed.

At 9 months, MACCE occurred in 2.6% of patients in the clopidogrel plus placebo group and in 3.5% of patients in the clopidogrel plus aspirin group (HR, 0.74; 95% CI, 0.57-0.96, P = .02).

Interpreting this latter finding as “reduced risk” of MACCE “is a stretch,” Dr. Lopes cautioned.

A potential explanation for this finding in the trial is that in the comparison group (aspirin plus clopidogrel), when patients had bleeding, they might have stopped all antiplatelet therapy, and this may have led to more ischemic events, he speculated.

“The observed reduction in MACCE is plausible,” Dr. Han said. “However, according to study protocol, we assumed that clopidogrel monotherapy would be noninferior to DAPT on the risk of MACCE. The superiority of clopidogrel alone vs. DAPT on MACCE should therefore be hypothesis-generating.”

“The increased rate of MACCE in the clopidogrel plus aspirin group was surprising,” she said in a press release from the ESC, “and may be because hemorrhagic events, which are more common with ongoing DAPT, could be associated with an adrenergic state with increased platelet aggregation due to hypotension, remedial procedures to treat bleeding, and the cessation of anti-ischemic medications.”
 

A low-risk subset of bi-risk patients, commonly seen in clinical practice

At the time of the index ACS, more than 60% of the patients had unstable angina, Dr. Lopes observed, “and we know these patients are lower risk.” Also, more than 1,000 of the patients did not have at least one high-risk factor for bleeding or ischemia. Moreover, these patients had not had any clinical events in the past 9-12 months on DAPT, “so they were not truly high risk when they were randomized.

“Patients aged 75 years and above are definitely bi-risk (even without any bleeding/ischemic criteria), especially post ACS, according to much literature,” Dr. Han said.

“Although patients met the bi-risk criteria for increased ischemia and bleeding at the time of index ACS and PCI, they were free from major events for at least 6 months on DAPT, thus constituting a relatively low-risk subset of bi-risk patients,” she conceded.

“Nonetheless, these patients (mean age nearly 65 years, 41% female, 52% diabetes, 18% MI history and 15% ischemic stroke history in bi-risk study) represent a large cohort seen in clinical practice,” she said. And “according to a real-world, nationwide registry from China (the OPT-CAD study), unstable angina accounted for about 50% of all ACS patients.”

There have been more data with shorter times for stopping aspirin, so it’s difficult to reconcile those studies with data from OPT-BIRISK, according to Dr. Lopes.

For example, the 2019 TWILIGHT study in patients undergoing PCI at high risk for bleeding showed that it seems to be safe to stop aspirin after 3 months and continue ticagrelor, without an increase in ischemic events.

“The question is almost in the wrong time,” he said, noting that the field is moving in the direction of stopping aspirin earlier, according to five or six recently published trials.

It is hard to generalize from an Asian population, he agreed. “In the U.S., we have other data that suggests that for high-risk patients, you can stop aspirin earlier than 9 months. That’s what most practices are doing.”

“When you look at different drugs, different doses, different duration,” Dr. Lopes summarized, “you have thousands of different permutations,” for antiplatelet therapy strategies. “Every time we have some data in large studies it adds a piece to the puzzle.”

The study was funded by the National Key Research and Development Project in China, and by a grant from Sanofi-Aventis. Dr. Han reports no relevant financial relationships. Disclosures for the other coauthors can be found with the original article.

A version of this article first appeared on Medscape.com.

Use of continuous positive-airway pressure devices for at least 4 hours a day was associated with a reduced risk of major adverse cardiac and cerebrovascular events in adults with cardiovascular disease and obstructive sleep apnea, based on data from more than 4,000 individuals.

Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular diseases, but the association between management of OSA with a continuous positive-airway pressure device (CPAP) and major adverse cardiac or cerebrovascular events (MACCEs) remains unclear, wrote Manuel Sánchez-de-la-Torre, PhD, of the University of Lleida, Spain, and colleagues.

In a meta-analysis published in JAMA, the researchers reviewed data from 4,186 individuals with a mean age of 61.2 years; 82.1% were men. The study population included 2,097 patients who used CPAP and 2,089 who did not. The mean apnea-hypopnea index (AHI) was 31.2 events per hour, and OSA was defined as an oxygen desaturation index of 12 events or more per hour or an AHI of 15 events or more per hour. The composite primary outcome included the first MACCE, or death from cardiovascular causes, myocardial infarction, stroke, revascularization procedure, hospital admission for heart failure, hospital admission for unstable angina, or hospital admission for transient ischemic attack. Each of these components was a secondary endpoint.

Overall, the primary outcome of MACCE was similar for CPAP and non-CPAP using patients (hazard ratio, 1.01) with a total of 349 MACCE events in the CPAP group and 342 in the non-CPAP group. The mean adherence to CPAP was 3.1 hours per day. A total of 38.5% of patients in the CPAP group met the criteria for good adherence, defined as a mean of 4 or more hours per day.

However, as defined, good adherence to CPAP significantly reduced the risk of MACCE, compared with no CPAP use (HR, 0.69), and a sensitivity analysis showed a significant risk reduction, compared with patients who did not meet the criteria for good adherence (HR, 0.55; P = .005).

“Adherence to treatment is complex to determine and there are other potential factors that could affect patient adherence, such as health education, motivation, attitude, self-efficacy, psychosocial factors, and other health care system–related features,” the researchers wrote in their discussion.

The findings were limited by several factors including the evaluation only of CPAP as a treatment for OSA, and the inability to assess separate components of the composite endpoint, the researchers noted. Other limitations included the relatively small number of female patients, reliance mainly on at-home sleep apnea tests, and the potential for selection bias, they said.

However, the results suggest that CPAP adherence is important to prevention of secondary cardiovascular outcomes in OSA patients, and that implementation of specific and personalized strategies to improve adherence to treatment should be a clinical priority, they concluded.

The study was funded by the Instituto de Salud Carlos III, the European Union and FEDER, IRBLleida–Fundació Dr Pifarré, SEPAR, ResMed Ltd. (Australia), Associació Lleidatana de Respiratori, and CIBERES. Dr Sánchez-de-la-Torre also disclosed financial support from a Ramón y Cajal grant.

Use of continuous positive-airway pressure devices for at least 4 hours a day was associated with a reduced risk of major adverse cardiac and cerebrovascular events in adults with cardiovascular disease and obstructive sleep apnea, based on data from more than 4,000 individuals.

Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular diseases, but the association between management of OSA with a continuous positive-airway pressure device (CPAP) and major adverse cardiac or cerebrovascular events (MACCEs) remains unclear, wrote Manuel Sánchez-de-la-Torre, PhD, of the University of Lleida, Spain, and colleagues.

In a meta-analysis published in JAMA, the researchers reviewed data from 4,186 individuals with a mean age of 61.2 years; 82.1% were men. The study population included 2,097 patients who used CPAP and 2,089 who did not. The mean apnea-hypopnea index (AHI) was 31.2 events per hour, and OSA was defined as an oxygen desaturation index of 12 events or more per hour or an AHI of 15 events or more per hour. The composite primary outcome included the first MACCE, or death from cardiovascular causes, myocardial infarction, stroke, revascularization procedure, hospital admission for heart failure, hospital admission for unstable angina, or hospital admission for transient ischemic attack. Each of these components was a secondary endpoint.

Overall, the primary outcome of MACCE was similar for CPAP and non-CPAP using patients (hazard ratio, 1.01) with a total of 349 MACCE events in the CPAP group and 342 in the non-CPAP group. The mean adherence to CPAP was 3.1 hours per day. A total of 38.5% of patients in the CPAP group met the criteria for good adherence, defined as a mean of 4 or more hours per day.

However, as defined, good adherence to CPAP significantly reduced the risk of MACCE, compared with no CPAP use (HR, 0.69), and a sensitivity analysis showed a significant risk reduction, compared with patients who did not meet the criteria for good adherence (HR, 0.55; P = .005).

“Adherence to treatment is complex to determine and there are other potential factors that could affect patient adherence, such as health education, motivation, attitude, self-efficacy, psychosocial factors, and other health care system–related features,” the researchers wrote in their discussion.

The findings were limited by several factors including the evaluation only of CPAP as a treatment for OSA, and the inability to assess separate components of the composite endpoint, the researchers noted. Other limitations included the relatively small number of female patients, reliance mainly on at-home sleep apnea tests, and the potential for selection bias, they said.

However, the results suggest that CPAP adherence is important to prevention of secondary cardiovascular outcomes in OSA patients, and that implementation of specific and personalized strategies to improve adherence to treatment should be a clinical priority, they concluded.

The study was funded by the Instituto de Salud Carlos III, the European Union and FEDER, IRBLleida–Fundació Dr Pifarré, SEPAR, ResMed Ltd. (Australia), Associació Lleidatana de Respiratori, and CIBERES. Dr Sánchez-de-la-Torre also disclosed financial support from a Ramón y Cajal grant.

Use of continuous positive-airway pressure devices for at least 4 hours a day was associated with a reduced risk of major adverse cardiac and cerebrovascular events in adults with cardiovascular disease and obstructive sleep apnea, based on data from more than 4,000 individuals.

Obstructive sleep apnea (OSA) is associated with an increased risk of cardiovascular diseases, but the association between management of OSA with a continuous positive-airway pressure device (CPAP) and major adverse cardiac or cerebrovascular events (MACCEs) remains unclear, wrote Manuel Sánchez-de-la-Torre, PhD, of the University of Lleida, Spain, and colleagues.

In a meta-analysis published in JAMA, the researchers reviewed data from 4,186 individuals with a mean age of 61.2 years; 82.1% were men. The study population included 2,097 patients who used CPAP and 2,089 who did not. The mean apnea-hypopnea index (AHI) was 31.2 events per hour, and OSA was defined as an oxygen desaturation index of 12 events or more per hour or an AHI of 15 events or more per hour. The composite primary outcome included the first MACCE, or death from cardiovascular causes, myocardial infarction, stroke, revascularization procedure, hospital admission for heart failure, hospital admission for unstable angina, or hospital admission for transient ischemic attack. Each of these components was a secondary endpoint.

Overall, the primary outcome of MACCE was similar for CPAP and non-CPAP using patients (hazard ratio, 1.01) with a total of 349 MACCE events in the CPAP group and 342 in the non-CPAP group. The mean adherence to CPAP was 3.1 hours per day. A total of 38.5% of patients in the CPAP group met the criteria for good adherence, defined as a mean of 4 or more hours per day.

However, as defined, good adherence to CPAP significantly reduced the risk of MACCE, compared with no CPAP use (HR, 0.69), and a sensitivity analysis showed a significant risk reduction, compared with patients who did not meet the criteria for good adherence (HR, 0.55; P = .005).

“Adherence to treatment is complex to determine and there are other potential factors that could affect patient adherence, such as health education, motivation, attitude, self-efficacy, psychosocial factors, and other health care system–related features,” the researchers wrote in their discussion.

The findings were limited by several factors including the evaluation only of CPAP as a treatment for OSA, and the inability to assess separate components of the composite endpoint, the researchers noted. Other limitations included the relatively small number of female patients, reliance mainly on at-home sleep apnea tests, and the potential for selection bias, they said.

However, the results suggest that CPAP adherence is important to prevention of secondary cardiovascular outcomes in OSA patients, and that implementation of specific and personalized strategies to improve adherence to treatment should be a clinical priority, they concluded.

The study was funded by the Instituto de Salud Carlos III, the European Union and FEDER, IRBLleida–Fundació Dr Pifarré, SEPAR, ResMed Ltd. (Australia), Associació Lleidatana de Respiratori, and CIBERES. Dr Sánchez-de-la-Torre also disclosed financial support from a Ramón y Cajal grant.

The American Heart Association has released a focused update on managing patients with cardiac arrest or life-threatening toxicity due to poisoning.

The update reflects treatment advances and new knowledge, including the use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) for patients whose condition is refractory to poison antidotes and other therapies.

The new guidelines are designed primarily for North American health care professionals who treat adults and children who are critically ill because of poisoning, including intentional and unintentional drug overdose, chemical exposure, and drug-drug interactions, the authors note.

Published online in Circulation, the update was endorsed by the American Academy of Pediatrics.
 

‘Nearly miraculous’

“It’s been 13 years since the poisoning treatment guidelines had a comprehensive update,” lead author Eric J. Lavonas, MD, professor of emergency medicine at Denver Health and the Rocky Mountain Poison and Drug Center, Colo., told this news organization. “In that time, we’ve learned a lot about how to best use antidotes and other treatments to save the most critically poisoned patients.”

Highlighting a few key points from the update, he said, “For those rare situations when antidotes aren’t enough, the new guidelines include the use of heart-lung machines (VA-ECMO) for patients with beta-blocker, calcium channel blocker, or sodium channel blocker poisoning causing cardiogenic shock.”

Furthermore, he said, “High-dose insulin treatment for patients with beta-blocker and calcium channel blocker poisoning [also recommended in the update] has really become mainstream. The doses are up to 10 times higher than the amount used to treat diabetic emergencies.

“Some excellent science has shown that giving IV lipid emulsion can save the life of someone with an accidental overdose of local anesthetic medications, particularly bupivacaine,” he added. “The result is sometimes nearly miraculous.

“But when this treatment is extended to poisoning from other medications, it often doesn’t work as well, and in some situations may make things worse,” he said. “The issue may be that giving lipids increases absorption of drug from the stomach and intestines, which can be dangerous when the patient took an overdose of pills.”
 

Low level of evidence

The guidelines were compiled by the Critical Poisoning Writing Group, which includes experts from emergency medicine, pediatrics, medical toxicology, pharmacology, critical care, emergency medical services, education, research, and nursing. Group members were appointed by the AHA Emergency Cardiovascular Care Science Subcommittee and were approved by the AHA Manuscript Oversight Committee.

First and foremost, the group recommends timely consultation with a medical toxicologist, a clinical toxicologist, or a regional poison center to facilitate rapid, effective therapy, because treatment of cardiac arrest and toxicity from poisoning often requires treatments that most clinicians don’t use frequently.

Other key points include the following:

• Naloxone administration may reverse respiratory arrest due to opioid overdose, preventing progression to cardiac arrest.
• Give high-dose insulin therapy early in the treatment of patients with beta-blocker and calcium channel blocker poisoning, Dr. Lavonas noted.
• Standard advanced life support plus sodium bicarbonate is appropriate for life-threatening dysrhythmias caused by cocaine or other sodium channel blockers.
• If cyanide poisoning is suspected, clinicians should not wait for confirmatory testing; treatment should begin immediately with hydroxocobalamin (preferred) or sodium nitrite plus sodium thiosulfate.
• Digoxin-specific immune antibody fragments can reverse life-threatening dysrhythmias from digoxin poisoning.
• Use of 20% intravenous lipid emulsion can be efficacious in the resuscitation of life-threatening local anesthetic toxicity, especially from bupivacaine, Dr. Lavonas indicated.
• Sedation is recommended for patients with severe agitation from sympathomimetic poisoning to manage hyperthermia and acidosis, prevent rhabdomyolysis and injury, and allow evaluation for other life-threatening conditions.
• Although flumazenil reverses central nervous system and respiratory depression from benzodiazepine poisoning, risks and contraindications, provided in the guidelines, limit its use.
• VA-ECMO can be lifesaving for patients with cardiogenic shock or dysrhythmias that are refractory to other treatments.

“Unfortunately, despite improvements in the design and funding support for resuscitation research, the overall certainty of the evidence base for resuscitation science and management of critical poisoning is low,” the group acknowledges.

Of the 73 guideline recommendations, only 2 are supported by level A evidence; 3 are supported by level B-randomized evidence, 12 by level B-nonrandomized evidence, and the rest by level C evidence.

“Accordingly, the strength of recommendations is weaker than optimal,” they write. “Clinical trials in resuscitation and the management of critical poisoning are sorely needed.”
 

‘Don’t go it alone!’

“Most critical poisonings are pretty uncommon, and each patient is different,” Dr. Lavonas said. “Even in the emergency department or ICU, most physicians will treat a patient who is critically ill with any given poison less than once a year. The antidotes and medication doses needed to effectively treat these patients are often very different than everyday medical practice.

“Don’t try to go it alone!” he urges. “Poisoning cases are complex, and the treatments work best when they are implemented quickly and assertively. A toxicologist can help sort through complex situations and get effective treatment started without delay.”

Every certified poison center has a medical toxicologist or clinical toxicologist on call 24/7 to give advice to physicians and hospitals about patients who are critically ill after being poisoned, he added. “Everyone in the U.S. has access to a poison center by calling one number: 1-800-222-1222.”

Dr. Lavonas has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The American Heart Association has released a focused update on managing patients with cardiac arrest or life-threatening toxicity due to poisoning.

The update reflects treatment advances and new knowledge, including the use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) for patients whose condition is refractory to poison antidotes and other therapies.

The new guidelines are designed primarily for North American health care professionals who treat adults and children who are critically ill because of poisoning, including intentional and unintentional drug overdose, chemical exposure, and drug-drug interactions, the authors note.

Published online in Circulation, the update was endorsed by the American Academy of Pediatrics.
 

‘Nearly miraculous’

“It’s been 13 years since the poisoning treatment guidelines had a comprehensive update,” lead author Eric J. Lavonas, MD, professor of emergency medicine at Denver Health and the Rocky Mountain Poison and Drug Center, Colo., told this news organization. “In that time, we’ve learned a lot about how to best use antidotes and other treatments to save the most critically poisoned patients.”

Highlighting a few key points from the update, he said, “For those rare situations when antidotes aren’t enough, the new guidelines include the use of heart-lung machines (VA-ECMO) for patients with beta-blocker, calcium channel blocker, or sodium channel blocker poisoning causing cardiogenic shock.”

Furthermore, he said, “High-dose insulin treatment for patients with beta-blocker and calcium channel blocker poisoning [also recommended in the update] has really become mainstream. The doses are up to 10 times higher than the amount used to treat diabetic emergencies.

“Some excellent science has shown that giving IV lipid emulsion can save the life of someone with an accidental overdose of local anesthetic medications, particularly bupivacaine,” he added. “The result is sometimes nearly miraculous.

“But when this treatment is extended to poisoning from other medications, it often doesn’t work as well, and in some situations may make things worse,” he said. “The issue may be that giving lipids increases absorption of drug from the stomach and intestines, which can be dangerous when the patient took an overdose of pills.”
 

Low level of evidence

The guidelines were compiled by the Critical Poisoning Writing Group, which includes experts from emergency medicine, pediatrics, medical toxicology, pharmacology, critical care, emergency medical services, education, research, and nursing. Group members were appointed by the AHA Emergency Cardiovascular Care Science Subcommittee and were approved by the AHA Manuscript Oversight Committee.

First and foremost, the group recommends timely consultation with a medical toxicologist, a clinical toxicologist, or a regional poison center to facilitate rapid, effective therapy, because treatment of cardiac arrest and toxicity from poisoning often requires treatments that most clinicians don’t use frequently.

Other key points include the following:

• Naloxone administration may reverse respiratory arrest due to opioid overdose, preventing progression to cardiac arrest.
• Give high-dose insulin therapy early in the treatment of patients with beta-blocker and calcium channel blocker poisoning, Dr. Lavonas noted.
• Standard advanced life support plus sodium bicarbonate is appropriate for life-threatening dysrhythmias caused by cocaine or other sodium channel blockers.
• If cyanide poisoning is suspected, clinicians should not wait for confirmatory testing; treatment should begin immediately with hydroxocobalamin (preferred) or sodium nitrite plus sodium thiosulfate.
• Digoxin-specific immune antibody fragments can reverse life-threatening dysrhythmias from digoxin poisoning.
• Use of 20% intravenous lipid emulsion can be efficacious in the resuscitation of life-threatening local anesthetic toxicity, especially from bupivacaine, Dr. Lavonas indicated.
• Sedation is recommended for patients with severe agitation from sympathomimetic poisoning to manage hyperthermia and acidosis, prevent rhabdomyolysis and injury, and allow evaluation for other life-threatening conditions.
• Although flumazenil reverses central nervous system and respiratory depression from benzodiazepine poisoning, risks and contraindications, provided in the guidelines, limit its use.
• VA-ECMO can be lifesaving for patients with cardiogenic shock or dysrhythmias that are refractory to other treatments.

“Unfortunately, despite improvements in the design and funding support for resuscitation research, the overall certainty of the evidence base for resuscitation science and management of critical poisoning is low,” the group acknowledges.

Of the 73 guideline recommendations, only 2 are supported by level A evidence; 3 are supported by level B-randomized evidence, 12 by level B-nonrandomized evidence, and the rest by level C evidence.

“Accordingly, the strength of recommendations is weaker than optimal,” they write. “Clinical trials in resuscitation and the management of critical poisoning are sorely needed.”
 

‘Don’t go it alone!’

“Most critical poisonings are pretty uncommon, and each patient is different,” Dr. Lavonas said. “Even in the emergency department or ICU, most physicians will treat a patient who is critically ill with any given poison less than once a year. The antidotes and medication doses needed to effectively treat these patients are often very different than everyday medical practice.

“Don’t try to go it alone!” he urges. “Poisoning cases are complex, and the treatments work best when they are implemented quickly and assertively. A toxicologist can help sort through complex situations and get effective treatment started without delay.”

Every certified poison center has a medical toxicologist or clinical toxicologist on call 24/7 to give advice to physicians and hospitals about patients who are critically ill after being poisoned, he added. “Everyone in the U.S. has access to a poison center by calling one number: 1-800-222-1222.”

Dr. Lavonas has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

The American Heart Association has released a focused update on managing patients with cardiac arrest or life-threatening toxicity due to poisoning.

The update reflects treatment advances and new knowledge, including the use of venoarterial extracorporeal membrane oxygenation (VA-ECMO) for patients whose condition is refractory to poison antidotes and other therapies.

The new guidelines are designed primarily for North American health care professionals who treat adults and children who are critically ill because of poisoning, including intentional and unintentional drug overdose, chemical exposure, and drug-drug interactions, the authors note.

Published online in Circulation, the update was endorsed by the American Academy of Pediatrics.
 

‘Nearly miraculous’

“It’s been 13 years since the poisoning treatment guidelines had a comprehensive update,” lead author Eric J. Lavonas, MD, professor of emergency medicine at Denver Health and the Rocky Mountain Poison and Drug Center, Colo., told this news organization. “In that time, we’ve learned a lot about how to best use antidotes and other treatments to save the most critically poisoned patients.”

Highlighting a few key points from the update, he said, “For those rare situations when antidotes aren’t enough, the new guidelines include the use of heart-lung machines (VA-ECMO) for patients with beta-blocker, calcium channel blocker, or sodium channel blocker poisoning causing cardiogenic shock.”

Furthermore, he said, “High-dose insulin treatment for patients with beta-blocker and calcium channel blocker poisoning [also recommended in the update] has really become mainstream. The doses are up to 10 times higher than the amount used to treat diabetic emergencies.

“Some excellent science has shown that giving IV lipid emulsion can save the life of someone with an accidental overdose of local anesthetic medications, particularly bupivacaine,” he added. “The result is sometimes nearly miraculous.

“But when this treatment is extended to poisoning from other medications, it often doesn’t work as well, and in some situations may make things worse,” he said. “The issue may be that giving lipids increases absorption of drug from the stomach and intestines, which can be dangerous when the patient took an overdose of pills.”
 

Low level of evidence

The guidelines were compiled by the Critical Poisoning Writing Group, which includes experts from emergency medicine, pediatrics, medical toxicology, pharmacology, critical care, emergency medical services, education, research, and nursing. Group members were appointed by the AHA Emergency Cardiovascular Care Science Subcommittee and were approved by the AHA Manuscript Oversight Committee.

First and foremost, the group recommends timely consultation with a medical toxicologist, a clinical toxicologist, or a regional poison center to facilitate rapid, effective therapy, because treatment of cardiac arrest and toxicity from poisoning often requires treatments that most clinicians don’t use frequently.

Other key points include the following:

• Naloxone administration may reverse respiratory arrest due to opioid overdose, preventing progression to cardiac arrest.
• Give high-dose insulin therapy early in the treatment of patients with beta-blocker and calcium channel blocker poisoning, Dr. Lavonas noted.
• Standard advanced life support plus sodium bicarbonate is appropriate for life-threatening dysrhythmias caused by cocaine or other sodium channel blockers.
• If cyanide poisoning is suspected, clinicians should not wait for confirmatory testing; treatment should begin immediately with hydroxocobalamin (preferred) or sodium nitrite plus sodium thiosulfate.
• Digoxin-specific immune antibody fragments can reverse life-threatening dysrhythmias from digoxin poisoning.
• Use of 20% intravenous lipid emulsion can be efficacious in the resuscitation of life-threatening local anesthetic toxicity, especially from bupivacaine, Dr. Lavonas indicated.
• Sedation is recommended for patients with severe agitation from sympathomimetic poisoning to manage hyperthermia and acidosis, prevent rhabdomyolysis and injury, and allow evaluation for other life-threatening conditions.
• Although flumazenil reverses central nervous system and respiratory depression from benzodiazepine poisoning, risks and contraindications, provided in the guidelines, limit its use.
• VA-ECMO can be lifesaving for patients with cardiogenic shock or dysrhythmias that are refractory to other treatments.

“Unfortunately, despite improvements in the design and funding support for resuscitation research, the overall certainty of the evidence base for resuscitation science and management of critical poisoning is low,” the group acknowledges.

Of the 73 guideline recommendations, only 2 are supported by level A evidence; 3 are supported by level B-randomized evidence, 12 by level B-nonrandomized evidence, and the rest by level C evidence.

“Accordingly, the strength of recommendations is weaker than optimal,” they write. “Clinical trials in resuscitation and the management of critical poisoning are sorely needed.”
 

‘Don’t go it alone!’

“Most critical poisonings are pretty uncommon, and each patient is different,” Dr. Lavonas said. “Even in the emergency department or ICU, most physicians will treat a patient who is critically ill with any given poison less than once a year. The antidotes and medication doses needed to effectively treat these patients are often very different than everyday medical practice.

“Don’t try to go it alone!” he urges. “Poisoning cases are complex, and the treatments work best when they are implemented quickly and assertively. A toxicologist can help sort through complex situations and get effective treatment started without delay.”

Every certified poison center has a medical toxicologist or clinical toxicologist on call 24/7 to give advice to physicians and hospitals about patients who are critically ill after being poisoned, he added. “Everyone in the U.S. has access to a poison center by calling one number: 1-800-222-1222.”

Dr. Lavonas has disclosed no relevant financial relationships.

A version of this article appeared on Medscape.com.

Moving from one residence to another after an acute myocardial infarction (AMI) significantly increases the risk for death or transition to a long-term care facility as an end-of-life measure, data suggest.

In a prospective study that followed more than 3,000 patients with AMI over 2 decades, each residential move was associated with a 12% higher rate of death.

“This study determined that residential mobility was more important than any other social factor that we studied,” investigator David Alter, MD, PhD, chair of cardiovascular and metabolic research at the University Health Network–Toronto Rehabilitation Institute and associate professor of medicine at the University of Toronto, said in an interview.

The results were published online in the Canadian Journal of Cardiology.
 

Moving and mortality

“There’s been very little work, surprisingly, on what happens when individuals move from community to community,” said Dr. Alter. “It is that movement from community to community that is a factor within the social context that needs to be explored better. To the best of our knowledge, up until our study, it has been studied very briefly in the literature.”

The prospective cohort study sample included 3,369 patients who had an AMI between Dec. 1, 1999, and March 30, 2023. The investigators followed participants until death or the last available follow-up date of March 30, 2020. They defined a residential move as a relocation from one postal code region to another.

The investigators drew data from multiple sources, including the prospective, observational Socio-Economic Status and Acute Myocardial Infarction study, which encompassed more than 35,000 patient life-years following hospitalization for a first heart attack in Ontario. Mortality data were collected from the Ontario Registered Persons Data Base. Other sources included Statistics Canada for information on neighborhood income, the Canadian Institutes for Health Information for patients’ clinical factors and comorbidities, and the Ontario Health Insurance Plan (OHIP) database for physician visits. Information on long-term care admissions came from the Continuous Care Reporting System-Long Term Care, OHIP, and the Ontario Drugs Benefit databases, the latter of which also provided information on medication prescriptions for individuals aged 65 years and older.

Patients’ ages ranged from 19 to 101 years (median age, 65 years). About 69% of patients were men. Of the study population, 1,828 patients (54.3%) had at least one residential move during the study period. Approximately 87% died in the community or moved from home into a long-term care facility as an end-of-life destination. Overall, 84.8% of patients who were admitted to long-term care facilities died.

The study also tracked the socioeconomic status of persons living in the postal code regions from and to which patients moved. About 32% of patients moved to a neighborhood with a lower socioeconomic status, and 30.5% moved to an area with a higher socioeconomic status.

Each residential move was associated with a 12% higher rate of death and a 26% higher rate of long-term institutionalization for end-of-life care. In unadjusted analyses, the rate of death was almost double for those who moved more frequently: 44.3% for those who moved two or more times versus 24.8% for those who moved once in 10 years.

Accounting for a multitude of variables, such as the socioeconomic status of areas that patients moved between, is a strength of the study, said Dr. Alter. But the study lacked information about why people moved.

“Where this study has a huge amount of strength is that it was designed specifically to really understand a patient’s clinical and psychosocial profile at the start of their journey, their first AMI. But the fact that we took it from heart attack onward is also a strength because it characterizes and anchors a clinical context in which we were following patients out,” said Dr. Alter.
 

‘An important marker’

In a comment, Paul Oh, MD, medical director of the cardiovascular disease prevention and rehabilitation program at University Health Network, said: “This is a very well-designed study and analysis from a cohort that has provided important insights about the role of socioeconomic factors and long-term outcomes post MI over many years.” Dr. Oh did not participate in the study.

“A few covariates that could impact on outcomes, like institutionalization, were not available to include in adjusted analyses – e.g., functional status, frailty, mild cognitive changes, and availability of social supports in the home,” he said.

The findings add another variable that cardiologists who care for post-MI patients need to be aware of, Dr. Oh added. “Clinicians need better awareness that the need to change residence is an important marker of changing health status and may portend end-of-life events in the near future. The need to change residence can signal an important change in physical, cognitive, and social circumstances that needs to be further explored during clinical encounters, with the goal of identifying and addressing any potentially reversible issues and identifying additional supports that may help that individual continue to live independently in their own home.”

The study was supported by ICES, which receives funding from the Ontario Ministry of Health. The investigators disclosed no relevant financial relationships. Dr. Oh serves on research boards for Lilly and Novartis and receives research funding from Apple.

A version of this article first appeared on Medscape.com.

Moving from one residence to another after an acute myocardial infarction (AMI) significantly increases the risk for death or transition to a long-term care facility as an end-of-life measure, data suggest.

In a prospective study that followed more than 3,000 patients with AMI over 2 decades, each residential move was associated with a 12% higher rate of death.

“This study determined that residential mobility was more important than any other social factor that we studied,” investigator David Alter, MD, PhD, chair of cardiovascular and metabolic research at the University Health Network–Toronto Rehabilitation Institute and associate professor of medicine at the University of Toronto, said in an interview.

The results were published online in the Canadian Journal of Cardiology.
 

Moving and mortality

“There’s been very little work, surprisingly, on what happens when individuals move from community to community,” said Dr. Alter. “It is that movement from community to community that is a factor within the social context that needs to be explored better. To the best of our knowledge, up until our study, it has been studied very briefly in the literature.”

The prospective cohort study sample included 3,369 patients who had an AMI between Dec. 1, 1999, and March 30, 2023. The investigators followed participants until death or the last available follow-up date of March 30, 2020. They defined a residential move as a relocation from one postal code region to another.

The investigators drew data from multiple sources, including the prospective, observational Socio-Economic Status and Acute Myocardial Infarction study, which encompassed more than 35,000 patient life-years following hospitalization for a first heart attack in Ontario. Mortality data were collected from the Ontario Registered Persons Data Base. Other sources included Statistics Canada for information on neighborhood income, the Canadian Institutes for Health Information for patients’ clinical factors and comorbidities, and the Ontario Health Insurance Plan (OHIP) database for physician visits. Information on long-term care admissions came from the Continuous Care Reporting System-Long Term Care, OHIP, and the Ontario Drugs Benefit databases, the latter of which also provided information on medication prescriptions for individuals aged 65 years and older.

Patients’ ages ranged from 19 to 101 years (median age, 65 years). About 69% of patients were men. Of the study population, 1,828 patients (54.3%) had at least one residential move during the study period. Approximately 87% died in the community or moved from home into a long-term care facility as an end-of-life destination. Overall, 84.8% of patients who were admitted to long-term care facilities died.

The study also tracked the socioeconomic status of persons living in the postal code regions from and to which patients moved. About 32% of patients moved to a neighborhood with a lower socioeconomic status, and 30.5% moved to an area with a higher socioeconomic status.

Each residential move was associated with a 12% higher rate of death and a 26% higher rate of long-term institutionalization for end-of-life care. In unadjusted analyses, the rate of death was almost double for those who moved more frequently: 44.3% for those who moved two or more times versus 24.8% for those who moved once in 10 years.

Accounting for a multitude of variables, such as the socioeconomic status of areas that patients moved between, is a strength of the study, said Dr. Alter. But the study lacked information about why people moved.

“Where this study has a huge amount of strength is that it was designed specifically to really understand a patient’s clinical and psychosocial profile at the start of their journey, their first AMI. But the fact that we took it from heart attack onward is also a strength because it characterizes and anchors a clinical context in which we were following patients out,” said Dr. Alter.
 

‘An important marker’

In a comment, Paul Oh, MD, medical director of the cardiovascular disease prevention and rehabilitation program at University Health Network, said: “This is a very well-designed study and analysis from a cohort that has provided important insights about the role of socioeconomic factors and long-term outcomes post MI over many years.” Dr. Oh did not participate in the study.

“A few covariates that could impact on outcomes, like institutionalization, were not available to include in adjusted analyses – e.g., functional status, frailty, mild cognitive changes, and availability of social supports in the home,” he said.

The findings add another variable that cardiologists who care for post-MI patients need to be aware of, Dr. Oh added. “Clinicians need better awareness that the need to change residence is an important marker of changing health status and may portend end-of-life events in the near future. The need to change residence can signal an important change in physical, cognitive, and social circumstances that needs to be further explored during clinical encounters, with the goal of identifying and addressing any potentially reversible issues and identifying additional supports that may help that individual continue to live independently in their own home.”

The study was supported by ICES, which receives funding from the Ontario Ministry of Health. The investigators disclosed no relevant financial relationships. Dr. Oh serves on research boards for Lilly and Novartis and receives research funding from Apple.

A version of this article first appeared on Medscape.com.

Moving from one residence to another after an acute myocardial infarction (AMI) significantly increases the risk for death or transition to a long-term care facility as an end-of-life measure, data suggest.

In a prospective study that followed more than 3,000 patients with AMI over 2 decades, each residential move was associated with a 12% higher rate of death.

“This study determined that residential mobility was more important than any other social factor that we studied,” investigator David Alter, MD, PhD, chair of cardiovascular and metabolic research at the University Health Network–Toronto Rehabilitation Institute and associate professor of medicine at the University of Toronto, said in an interview.

The results were published online in the Canadian Journal of Cardiology.
 

Moving and mortality

“There’s been very little work, surprisingly, on what happens when individuals move from community to community,” said Dr. Alter. “It is that movement from community to community that is a factor within the social context that needs to be explored better. To the best of our knowledge, up until our study, it has been studied very briefly in the literature.”

The prospective cohort study sample included 3,369 patients who had an AMI between Dec. 1, 1999, and March 30, 2023. The investigators followed participants until death or the last available follow-up date of March 30, 2020. They defined a residential move as a relocation from one postal code region to another.

The investigators drew data from multiple sources, including the prospective, observational Socio-Economic Status and Acute Myocardial Infarction study, which encompassed more than 35,000 patient life-years following hospitalization for a first heart attack in Ontario. Mortality data were collected from the Ontario Registered Persons Data Base. Other sources included Statistics Canada for information on neighborhood income, the Canadian Institutes for Health Information for patients’ clinical factors and comorbidities, and the Ontario Health Insurance Plan (OHIP) database for physician visits. Information on long-term care admissions came from the Continuous Care Reporting System-Long Term Care, OHIP, and the Ontario Drugs Benefit databases, the latter of which also provided information on medication prescriptions for individuals aged 65 years and older.

Patients’ ages ranged from 19 to 101 years (median age, 65 years). About 69% of patients were men. Of the study population, 1,828 patients (54.3%) had at least one residential move during the study period. Approximately 87% died in the community or moved from home into a long-term care facility as an end-of-life destination. Overall, 84.8% of patients who were admitted to long-term care facilities died.

The study also tracked the socioeconomic status of persons living in the postal code regions from and to which patients moved. About 32% of patients moved to a neighborhood with a lower socioeconomic status, and 30.5% moved to an area with a higher socioeconomic status.

Each residential move was associated with a 12% higher rate of death and a 26% higher rate of long-term institutionalization for end-of-life care. In unadjusted analyses, the rate of death was almost double for those who moved more frequently: 44.3% for those who moved two or more times versus 24.8% for those who moved once in 10 years.

Accounting for a multitude of variables, such as the socioeconomic status of areas that patients moved between, is a strength of the study, said Dr. Alter. But the study lacked information about why people moved.

“Where this study has a huge amount of strength is that it was designed specifically to really understand a patient’s clinical and psychosocial profile at the start of their journey, their first AMI. But the fact that we took it from heart attack onward is also a strength because it characterizes and anchors a clinical context in which we were following patients out,” said Dr. Alter.
 

‘An important marker’

In a comment, Paul Oh, MD, medical director of the cardiovascular disease prevention and rehabilitation program at University Health Network, said: “This is a very well-designed study and analysis from a cohort that has provided important insights about the role of socioeconomic factors and long-term outcomes post MI over many years.” Dr. Oh did not participate in the study.

“A few covariates that could impact on outcomes, like institutionalization, were not available to include in adjusted analyses – e.g., functional status, frailty, mild cognitive changes, and availability of social supports in the home,” he said.

The findings add another variable that cardiologists who care for post-MI patients need to be aware of, Dr. Oh added. “Clinicians need better awareness that the need to change residence is an important marker of changing health status and may portend end-of-life events in the near future. The need to change residence can signal an important change in physical, cognitive, and social circumstances that needs to be further explored during clinical encounters, with the goal of identifying and addressing any potentially reversible issues and identifying additional supports that may help that individual continue to live independently in their own home.”

The study was supported by ICES, which receives funding from the Ontario Ministry of Health. The investigators disclosed no relevant financial relationships. Dr. Oh serves on research boards for Lilly and Novartis and receives research funding from Apple.

A version of this article first appeared on Medscape.com.

TOPLINE:

Women who use cocaine, cannabis, or other substances during pregnancy have increased risks of acute cardiovascular (CV) events while in the hospital for delivery, including more than double the risk of maternal mortality, a new study shows.

METHODOLOGY:

• Using the National Inpatient Sample database to identify hospital deliveries between 2004 and 2018 and diagnostic codes to identify maternal substance use, researchers compared 955,531 pregnancies with accompanying substance use – the most common substances being cannabis and opioids, followed by stimulants – to over 60 million pregnancies in which there was no substance use.
• The primary outcome was any CV event, including acute myocardial infarction, stroke, arrhythmia, endocarditis, any acute cardiomyopathy or heart failure, or cardiac arrest; other outcomes included maternal mortality and major adverse cardiac events (MACE).

TAKEAWAY:

• Deliveries complicated by substance use increased from 1,126 per 100,000 deliveries in 2004 to 1,547 per 100,000 in 2018, peaking at 2,187 per 100,000 in 2014.
• After the researchers controlled for patient demographics and CVD risk factors, results showed that pregnant women who used any substance (cannabis, opioids, methamphetamine, alcohol, tobacco, or cocaine) were more likely to experience a CVD event (adjusted odds ratio [aOR], 1.61; 95% confidence interval [CI], 1.53-1.70; P < .001), MACE (aOR, 1.53; 95% CI, 1.46-1.61; P < .001), or maternal mortality (aOR, 2.65; 95% CI, 2.15-3.25; P < .001) during hospitalization for delivery.
• Those using amphetamine/methamphetamine had ninefold higher odds of cardiomyopathy or heart failure and more than sevenfold higher odds of cardiac arrest.

IN PRACTICE:

“For the wellbeing of pregnant women and their children, substance use needs to be considered an independent risk factor for CV events in pregnancy,” the authors wrote. They called for prenatal assessments by a multidisciplinary cardio-obstetrics team to try to decrease cardiac complications.

In an accompanying editorial by Abha Khandelwal, MD, department of medicine, Stanford (Calif.) University, and others, the authors said the findings “highlight the critical support required during pregnancy and postpartum” for substance users, which should include comprehensive medical care and social services as well as access to addiction medicine and treatment of co-occurring mental health disorders.

SOURCE:

The study was carried out by Kari Evans, MD, division of maternal fetal medicine, department of obstetrics and gynecology, University of Arizona, Phoenix. It was published online in the Journal of the American College of Cardiology: Advances.

LIMITATIONS:

Use of administrative databases may have resulted in underreporting of diagnoses. The researchers could not assess the association of dose, duration, method, or timing of use for any substance with CV events. They also could not examine the effect of vaping on maternal CV events or differentiate hospitalizations for delivery that were complicated by CV events from hospitalizations for CV events that prompted delivery. The data did not reflect the postpartum period, during which a high rate of adverse CV events occurs.

DISCLOSURES:

The authors and editorial writers have no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women who use cocaine, cannabis, or other substances during pregnancy have increased risks of acute cardiovascular (CV) events while in the hospital for delivery, including more than double the risk of maternal mortality, a new study shows.

METHODOLOGY:

• Using the National Inpatient Sample database to identify hospital deliveries between 2004 and 2018 and diagnostic codes to identify maternal substance use, researchers compared 955,531 pregnancies with accompanying substance use – the most common substances being cannabis and opioids, followed by stimulants – to over 60 million pregnancies in which there was no substance use.
• The primary outcome was any CV event, including acute myocardial infarction, stroke, arrhythmia, endocarditis, any acute cardiomyopathy or heart failure, or cardiac arrest; other outcomes included maternal mortality and major adverse cardiac events (MACE).

TAKEAWAY:

• Deliveries complicated by substance use increased from 1,126 per 100,000 deliveries in 2004 to 1,547 per 100,000 in 2018, peaking at 2,187 per 100,000 in 2014.
• After the researchers controlled for patient demographics and CVD risk factors, results showed that pregnant women who used any substance (cannabis, opioids, methamphetamine, alcohol, tobacco, or cocaine) were more likely to experience a CVD event (adjusted odds ratio [aOR], 1.61; 95% confidence interval [CI], 1.53-1.70; P < .001), MACE (aOR, 1.53; 95% CI, 1.46-1.61; P < .001), or maternal mortality (aOR, 2.65; 95% CI, 2.15-3.25; P < .001) during hospitalization for delivery.
• Those using amphetamine/methamphetamine had ninefold higher odds of cardiomyopathy or heart failure and more than sevenfold higher odds of cardiac arrest.

IN PRACTICE:

“For the wellbeing of pregnant women and their children, substance use needs to be considered an independent risk factor for CV events in pregnancy,” the authors wrote. They called for prenatal assessments by a multidisciplinary cardio-obstetrics team to try to decrease cardiac complications.

In an accompanying editorial by Abha Khandelwal, MD, department of medicine, Stanford (Calif.) University, and others, the authors said the findings “highlight the critical support required during pregnancy and postpartum” for substance users, which should include comprehensive medical care and social services as well as access to addiction medicine and treatment of co-occurring mental health disorders.

SOURCE:

The study was carried out by Kari Evans, MD, division of maternal fetal medicine, department of obstetrics and gynecology, University of Arizona, Phoenix. It was published online in the Journal of the American College of Cardiology: Advances.

LIMITATIONS:

Use of administrative databases may have resulted in underreporting of diagnoses. The researchers could not assess the association of dose, duration, method, or timing of use for any substance with CV events. They also could not examine the effect of vaping on maternal CV events or differentiate hospitalizations for delivery that were complicated by CV events from hospitalizations for CV events that prompted delivery. The data did not reflect the postpartum period, during which a high rate of adverse CV events occurs.

DISCLOSURES:

The authors and editorial writers have no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

TOPLINE:

Women who use cocaine, cannabis, or other substances during pregnancy have increased risks of acute cardiovascular (CV) events while in the hospital for delivery, including more than double the risk of maternal mortality, a new study shows.

METHODOLOGY:

• Using the National Inpatient Sample database to identify hospital deliveries between 2004 and 2018 and diagnostic codes to identify maternal substance use, researchers compared 955,531 pregnancies with accompanying substance use – the most common substances being cannabis and opioids, followed by stimulants – to over 60 million pregnancies in which there was no substance use.
• The primary outcome was any CV event, including acute myocardial infarction, stroke, arrhythmia, endocarditis, any acute cardiomyopathy or heart failure, or cardiac arrest; other outcomes included maternal mortality and major adverse cardiac events (MACE).

TAKEAWAY:

• Deliveries complicated by substance use increased from 1,126 per 100,000 deliveries in 2004 to 1,547 per 100,000 in 2018, peaking at 2,187 per 100,000 in 2014.
• After the researchers controlled for patient demographics and CVD risk factors, results showed that pregnant women who used any substance (cannabis, opioids, methamphetamine, alcohol, tobacco, or cocaine) were more likely to experience a CVD event (adjusted odds ratio [aOR], 1.61; 95% confidence interval [CI], 1.53-1.70; P < .001), MACE (aOR, 1.53; 95% CI, 1.46-1.61; P < .001), or maternal mortality (aOR, 2.65; 95% CI, 2.15-3.25; P < .001) during hospitalization for delivery.
• Those using amphetamine/methamphetamine had ninefold higher odds of cardiomyopathy or heart failure and more than sevenfold higher odds of cardiac arrest.

IN PRACTICE:

“For the wellbeing of pregnant women and their children, substance use needs to be considered an independent risk factor for CV events in pregnancy,” the authors wrote. They called for prenatal assessments by a multidisciplinary cardio-obstetrics team to try to decrease cardiac complications.

In an accompanying editorial by Abha Khandelwal, MD, department of medicine, Stanford (Calif.) University, and others, the authors said the findings “highlight the critical support required during pregnancy and postpartum” for substance users, which should include comprehensive medical care and social services as well as access to addiction medicine and treatment of co-occurring mental health disorders.

SOURCE:

The study was carried out by Kari Evans, MD, division of maternal fetal medicine, department of obstetrics and gynecology, University of Arizona, Phoenix. It was published online in the Journal of the American College of Cardiology: Advances.

LIMITATIONS:

Use of administrative databases may have resulted in underreporting of diagnoses. The researchers could not assess the association of dose, duration, method, or timing of use for any substance with CV events. They also could not examine the effect of vaping on maternal CV events or differentiate hospitalizations for delivery that were complicated by CV events from hospitalizations for CV events that prompted delivery. The data did not reflect the postpartum period, during which a high rate of adverse CV events occurs.

DISCLOSURES:

The authors and editorial writers have no relevant conflicts of interest.
 

A version of this article appeared on Medscape.com.

Recorded Aug. 26, 2023. This transcript has been edited for clarity.

Robert A. Harrington, MD: I’m here with my good friend, Manesh Patel, from Duke University. We’re at the European Society of Cardiology (ESC) congress in Amsterdam, and I pulled Manesh into the studio for a conversation about something that’s really topical right now: sudden cardiac death in athletes.

What I hope to do [in this interview] is really pick Manesh’s brain on how we are thinking about this. Are we going to think about treatment issues? Are we going to think about prevention issues? Are we thinking about screening? We’ll try to make it practical.

Dr. Manesh Patel is chief of cardiovascular medicine at Duke University and also the director of the Duke Heart Center. Manesh, thanks for joining me here.
 

Bronny James and Damar Hamlin

Manesh R. Patel, MD: Excited to be here, Bob. Always.

Harrington: [Recently,] a news article comes out about the cause of Bronny James’ sudden cardiac death. Let me put this into a bigger societal context.

Last winter, Damar Hamlin, from the Buffalo Bills, suffered a traumatic injury on the field, and with that, had cardiac arrest. He’s back playing football – great to see. You and I are involved with the American Heart Association. He’s been very supportive of our efforts around things like CPR. He’s been terrific. It’s great to see him playing.

We know a little less about Bronny James. The news articles say the cause is both functional and anatomical, and it seems to be congenital, but we don’t have any details beyond this. Let’s not focus on the people; let’s focus on the topic.

Patel: I’m excited that we’re having the conversation. First and foremost, we’re excited that, with what we’ve seen on a national stage, these two individuals are doing well. They survived sudden cardiac death, which is a testament to all the things that we’ll talk about.

There are many important questions, like, is this increasing? Is this something we can prevent? And what are those things that might be happening to athletes?

Harrington: Can we predict it?

Patel: Right. I think the idea of sudden cardiac death in athletes is really a critical one for us to think about because it does concern participation and what we think about that. There are many experts who’ve been studying this for years that I now get to work with.

Harrington: Tell us a little bit about the kind of things you’ve been doing in this area.

Patel: Even before these events in the COVID era, we were wondering about athletes getting myocarditis, just in general, what do we know about that? People like Aaron Baggish, Kim Harmon, Jonathan Drezner, and others have been studying this.

Harrington: You and I did a show on athletes and COVID-19.

Patel: With the American Heart Association (AHA), the Cornell Foundation, and others, we started the Outcomes Registry for Cardiac Conditions in Athletes (ORCCA). This registry is across the United States, and athletes can sign up.

Harrington: Is it voluntary? Do the schools sign them up?

Patel: The athletes sign up. Team trainers and doctors talk to the athletes. We don’t really know the risks of some of these conditions. There’s a lot of gray area – people with certain conditions that were really interesting; aortas that are dilated in tall people.

Harrington: Long QT.

Patel: Long QT. There are certainly things that we know we should be intervening on and others where participation is a question. All of these we are trying to longitudinally put into the registry and follow them over time.

The second thing is understanding from the last Bethesda Conference that we want shared decision-making. There are going to be conditions where you say, “Look, I think your risk is high. You’ve a family history of sudden cardiac death. You have arrhythmias while you’re exercising.”

Harrington: You have a big, thick heart.

Patel: If you have hypertrophic cardiomyopathy, whether you’re an athlete or a 40-year-old adult, we’re going to have the same conversation. I think that holds. There’s a variety or a spectrum where we don’t know. I think the registry is one big step.

Thinking back to when somebody has an event, I would say take the teachable moment with the AHA and others to make sure your communities and your areas have automated external defibrillators (AEDs) and CPR training, and that we get to 100%: 100% response, 100% CPR, 100% defibrillation. I think that’s the first step.
 

Chain of survival

Harrington: Let’s really focus on the chain of survival. It is a chain: If any link is broken, your chance of survival really drops. We’ve had some well-known cases within our AHA community, including somebody who talks about it regularly: Kevin Volpp, from the University of Pennsylvania, a health economist. He had almost the perfect chain of survival. He had sudden cardiac death in a restaurant that was immediately observed, CPR started, EMTs called, and AED on the scene. Impressive.

Patel: That was in Cincinnati, where there are communities that have really worked on these things. I think you’re right. The chain of survival with rapid CPR to build a nation of survivors is key. The people at the AHA are helping us do this; there is a national call to make sure CPR is something that people feel comfortable doing. That they do it in men and women. They do it for anyone that goes down. And realize that it’s CPR that is hands-only. I think that’s an important lesson from Damar’s work, Nancy Brown’s, and AHA’s. Actually, schools in many countries require that to get through primary school.

Harrington: CPR training is a requirement to graduate from high school in some states.

Patel: My son just graduated from high school, and we spent time at his school making sure that everybody had access to CPR training. I think the way to do this is to start with that. Now, getting more specific about teams and athletes, I think most have emergency action plans, but it’s having action plans that work because of where you are and where the AED locations might be, or what the sport is. Having a plan on how you’re going to get that athlete to a place where you can help them recover is an important piece.

From there, I think the conversation for us is about what can we do as a society and as a country to answer some critical questions, including some real-world questions that people are asking: We had COVID-19 and we’re hearing these cases. Is this going up or down, and are these related?

Soon, hopefully the same group I talked about and others will have a publication, working with the NCAA to look at all of the deaths that they observed in NCAA Division I athletes over 20 years, including the sudden cardiac deaths. I won’t share the results because the publication isn’t out, but I think that’s the kind of important information that will help us understand if these rates are going up or down.

Harrington: What’s associated with that risk? Then we can start getting at whether it is something that, when we’re doing assessment for suitability for sports, has risk factors that should warrant more investigation.

Patel: Much like the field of cardiology, we haven’t enough of an evidence base, the right technologies, or the studies to determine how we should do screening, or not screening, across the board. Again, there is variation. There are some countries where anyone participating is going to get an ECG and an echocardiogram. There are other countries, like the United States, where it’s going to be a bit dependent on athlete risk.

Harrington: And where you live.

Patel: And where you live. Unfortunately, again, that brings in the idea that it might not be equitable in how we’re evaluating these individuals. I do think the opportunity to start to standardize that evaluation exists, and it likely comes from the ability to look back and say, “Here are some higher-risk individuals or some higher-risk scenarios.”

Harrington: Isn’t this what we do all the time in clinical medicine?

Patel: It’s going to be applied to a population that maybe is not as studied. I said this to you before we came on. The other thing is to make sure that the shared decision-making allows athletes who feel like they have a chance or want to play. During COVID, we had many college athletes, high school athletes, and kids not able to participate in sports. There was significant depression, feeling of loneliness, and even physical loss. People were actually getting less conditioned quickly. There’s a great benefit to sports participation.

Harrington: We were extrapolating from older data. If I’ve just had this new infection, COVID, and I’ve maybe got some signs of it in my heart, why can’t I exercise? That’s extrapolating from old myocarditis data.

Patel: We’re having to learn and follow it. I think there’s value in following that and getting those data. The second thing I think is really valuable is that we’ve shown that these individuals, if you do have these conversations and follow them, can participate and can be part of understanding the risk just like anything else.

Harrington: Is it sport specific? Are there some sports where maybe the conversation should be a little more intense than in other sports?

Patel: I think what we’ll see is that the conversations may be sport specific, and some may concern the number of athletes tested. At times, it’s pretty complicated. It does look like there are, as you know, different weight-bearing performance athletes, endurance athletes, or what I’ll call burst sports. There will probably be data that will identify certain sports where we may need to pay a bit more attention.

Harrington: What about the contact issues? Damar had a very specific thing, we think, happen to him. Football is a violent, contact-oriented sport, but fortunately we don’t regularly see what happened to Damar.

Patel: We’re talking about sudden cardiac death, but obviously, contact issues and neurologic evaluation is a whole other topic. That’s another big issue that I know many are following, and the NCAA is carefully, too. For Damar, I think we know that it was commotio cordis. At least when that happens, when there’s a ball or a trauma to the chest, those things have to be timed just so to actually lead to this event. Thankfully, it’s not very frequent, but it can happen.

Harrington: Hockey pucks, baseballs, soccer balls, a helmet to the chest ...

Patel: You have to be in a specific cycle of the squeeze. We don’t see that very frequently. I do think the evaluation and treatment, hopefully, makes a difference. One thing that we’re evolving in the screening world is our imaging; it’s getting better. We are not just doing echocardiograms; we are able to do other studies. There’s a mix of imaging and other technologies.

Is screening the answer?

Harrington: Let’s talk about that because screening is the area, I would say, with the most controversy – and a large amount of emotional controversy. Some argue that the data are not good enough to screen, or doctors are saying, “Wait a minute, why are we screening all these kids?” You said you were at your son’s high school doing CPR training. How many athletes are at his high school? There are many, and that’s a pretty small high school. Big communities, big universities, and the professional sports can afford it. Should we be doing this at the community level?

Patel: There have been some data. The Italians have done standard screening for some time, and it’s shown us that if you did echocardiograms in many individuals, you do find some cases that are hypertrophic cardiomyopathy in pathology. The issue is just how much you have to do and the resource utilization. I think as we get to a world where screening studies can happen with smaller technology and AI, that can be democratizing in how we get to athletes.

Harrington: Give an example of that. We were talking outside, you and I, about some of the new stethoscope technology.

Patel: Yes, stethoscopes are going to be one of the examples. We have stethoscopes that have the ability to get sounds and ECG signals, or at least some lead signals.

Harrington: Yes.

Patel: Potentially you can imagine that sound and ECG tracing in an AI environment, at least getting you from “everyone gets a listen with one stethoscope in their gym from their coach,” and it goes to the cloud. When there are enough questions, these are the ones that have to go further. Now, that’s a big study that has to be carried out; I’m not in any way saying we should do that.

Harrington: The technology is coming.

Patel: We start to see that our ability to rapidly do something to meet our athletes or our patients where they are will happen soon. Remember that the performance curve can vary, but once you have a sound where you can start to say that this is a regular flow murmur vs. “I’m worried about this,” especially as you mark it with ECG – that’s one example.

Smaller imaging is another example. For many years, ECGs have been talked about. There are entire courses that we run looking at ECGs in athletes. Remembering that Aaron Baggish and others are publishing that these individuals are large. When we look at their hearts, we see that they’re large, but when you adjust for size, often you can identify that many of them are within what we think are normal. Structurally, there are still many cases where you look at hearts and you’re asking, “Is this a thick heart? Is this noncompaction? Is this some pathology?”

That’s where you need imaging expertise. I think you have to have those individuals. I’m not advocating screening. I’m advocating studying it and that we should be thinking about the population. I don’t see a world where we don’t eventually start to really look to prevent those.

Harrington: Right. Whether it’s understanding that there are certain risk factors associated with this and we have to dedicate screening resources to those individuals, or if we want to do it more broadly on the population level to understand this with deeper dives into certain individuals, we’ve got to study it.

Patel: Some of the experts in sports medicine and sports cardiology have been collecting these data for a while. It’s time that we are there, because with these events we have the opportunity to share more of these data and maybe raise awareness – not in the teachable moment only – to get others to contribute.

I do believe that long term there’s an opportunity. We’ve seen that. We see that the rates, unfortunately, for marathon runners, where people unfortunately have events, seem to be higher. And we’ve seen the studies on troponin leaks in these individuals or evidence that there’s some effect on the heart from these events. We want people to be able to be long-term healthy.
 

Early defibrillation

Harrington: A large amount of work needs to be done. We talked with regard to screening, we’ve talked about CPR. We really need to have a nation of people who can do hands-only CPR. Let’s talk about AEDs, another key part of the chain of survival.

Patel: We have another important study going on, but an important message first: AEDs are critical to survival. We know that CPR is critical, but so is getting people to a defibrillator.

Harrington: Early defibrillation.

Patel: Early defibrillation. Early CPR is one of the biggest markers of making sure we perfuse people to get to early defibrillation, but then you have to get early defibrillation. There’s been a huge push in many communities, again, along with AHA and others, to make sure that AEDs are available not only in the U.S. but around the world. We’re at ESC and we see the push around the world to get AEDs available. They’ve come down in size and come down in cost, and that’s made it much more accessible. That’s really good. They’re still not always there.

We’ve seen really interesting randomized studies with people in some European countries where they have certain areas, just because of the locations, where bystanders will help get an AED  vs. randomizing to the EMS truck. They seem better in some of those variations. Chris Granger, at our institution, with Monique Starks, Dan Mark, and others, is doing a study in North Carolina where we’re testing different ways to potentially get AEDs in communities. We’re randomizing counties to one or two ways of getting AEDs to those individuals.

Harrington: Can you have an app where you just click “Find me an AED”?

Patel: Is there a world where the AED is found or is something bringing you the AED? Are there drones? Are there people driving? Are there ways that an AED is brought to the scene? All of those are going to be critical. It starts with continuing to figure out ways to support the costs of getting AEDs in places. The technology is continuing to evolve.

Harrington: It really is the premedical system stuff that makes the difference. Once EMS arrives with trained individuals who can defibrillate, they can transport you to a medical facility where trained physicians are at. It’s that pre-EMS thing that is so critical.

Patel: We talk often about athletes, but cardiac arrest care in general, and the chain of survival with CPR and AEDs, is critical. I still see patients in the CICU at Duke where, unfortunately, the biggest driver, as you just highlighted in that chain of survival, is how rapid we were in that golden hour. In the first 15 minutes, are you getting CPR, are you getting AED? Are you getting to a system?

Harrington: Are you getting a rapid transport?

Patel: Are you getting a neurologic assessment? Are you getting cooled or not? Those are important things.

Harrington: All right. Let’s try to wrap this up. Teachable moments, we talked about. One of the things about cases in prominent athletes is that it makes it to the newspaper and then it raises awareness. There is a drawing inference from a small group of cases to the broader societal issues. That’s an important topic.

We’ve talked about possible screening options, identifying at-risk individuals and high-risk individuals. A large amount of data has already been accumulated, but there is more work to be done. We focused on how to use those teachable moments to really influence the chain of survival, not just for athletes but for society at large.

I love your point about the Bethesda Conference on shared decision-making. Like with everything else, we have to have that two-way conversation: What are the athlete’s goals, hopes, and aspirations?

Patel: That group of experts, in addition to shared decision-making, gave us a whole list of conditions that we should be aware of and the cutpoints of where we think normal and not normal live for athletes. I think that’s used by many.

Can we build our systems to make research happen faster for the individuals? These athletes are at colleges that are obviously doing so much to make sure they’re okay. The people who are helping with this registry, and others, are going to continue to work to ask whether we can engage them as citizen participants and scientists. I think athletes are going to become some of our best advocates for why you’d want to know about yourself and how to perform CPR.

Harrington: I love the concept of citizen scientists, that we all have an obligation to contribute to the evidence base because we all want to use that evidence.

This has been a terrific conversation. I’ve been joined by my good friend, Dr. Manesh Patel from Duke University. I hope you’ve enjoyed our discussion here at the ESC. We have been taking a little break from the science going on around us to talk about sudden cardiac death in athletes. It really does have implications for broader societal concepts.

Dr. Harrington is the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine and provost for medical affairs of Cornell University, New York, as well as a former president of the American Heart Association. He has disclosed the following relevant financial relationships: Research relationships with Baim Institute (DSMB); CSL (RCT executive committee); Janssen (RCT chair); National Heart, Lung, and Blood Institute (RCT executive committee, DSMB chair); Patient-Centered Outcomes Research Institute (RCT co-chair); Duke Clinical Research Institute. Consulting relationships with Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; Cytokinetics. Dr. Patel is professor of medicine, Duke University; chief, division of cardiology; director, Duke Heart Center, Duke University Medical Center, Durham, N.C. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bayer; Janssen; Novartis (consultant). Received research grant from Bayer; Janssen.

A version of this article appeared on Medscape.com.

Recorded Aug. 26, 2023. This transcript has been edited for clarity.

Robert A. Harrington, MD: I’m here with my good friend, Manesh Patel, from Duke University. We’re at the European Society of Cardiology (ESC) congress in Amsterdam, and I pulled Manesh into the studio for a conversation about something that’s really topical right now: sudden cardiac death in athletes.

What I hope to do [in this interview] is really pick Manesh’s brain on how we are thinking about this. Are we going to think about treatment issues? Are we going to think about prevention issues? Are we thinking about screening? We’ll try to make it practical.

Dr. Manesh Patel is chief of cardiovascular medicine at Duke University and also the director of the Duke Heart Center. Manesh, thanks for joining me here.
 

Bronny James and Damar Hamlin

Manesh R. Patel, MD: Excited to be here, Bob. Always.

Harrington: [Recently,] a news article comes out about the cause of Bronny James’ sudden cardiac death. Let me put this into a bigger societal context.

Last winter, Damar Hamlin, from the Buffalo Bills, suffered a traumatic injury on the field, and with that, had cardiac arrest. He’s back playing football – great to see. You and I are involved with the American Heart Association. He’s been very supportive of our efforts around things like CPR. He’s been terrific. It’s great to see him playing.

We know a little less about Bronny James. The news articles say the cause is both functional and anatomical, and it seems to be congenital, but we don’t have any details beyond this. Let’s not focus on the people; let’s focus on the topic.

Patel: I’m excited that we’re having the conversation. First and foremost, we’re excited that, with what we’ve seen on a national stage, these two individuals are doing well. They survived sudden cardiac death, which is a testament to all the things that we’ll talk about.

There are many important questions, like, is this increasing? Is this something we can prevent? And what are those things that might be happening to athletes?

Harrington: Can we predict it?

Patel: Right. I think the idea of sudden cardiac death in athletes is really a critical one for us to think about because it does concern participation and what we think about that. There are many experts who’ve been studying this for years that I now get to work with.

Harrington: Tell us a little bit about the kind of things you’ve been doing in this area.

Patel: Even before these events in the COVID era, we were wondering about athletes getting myocarditis, just in general, what do we know about that? People like Aaron Baggish, Kim Harmon, Jonathan Drezner, and others have been studying this.

Harrington: You and I did a show on athletes and COVID-19.

Patel: With the American Heart Association (AHA), the Cornell Foundation, and others, we started the Outcomes Registry for Cardiac Conditions in Athletes (ORCCA). This registry is across the United States, and athletes can sign up.

Harrington: Is it voluntary? Do the schools sign them up?

Patel: The athletes sign up. Team trainers and doctors talk to the athletes. We don’t really know the risks of some of these conditions. There’s a lot of gray area – people with certain conditions that were really interesting; aortas that are dilated in tall people.

Harrington: Long QT.

Patel: Long QT. There are certainly things that we know we should be intervening on and others where participation is a question. All of these we are trying to longitudinally put into the registry and follow them over time.

The second thing is understanding from the last Bethesda Conference that we want shared decision-making. There are going to be conditions where you say, “Look, I think your risk is high. You’ve a family history of sudden cardiac death. You have arrhythmias while you’re exercising.”

Harrington: You have a big, thick heart.

Patel: If you have hypertrophic cardiomyopathy, whether you’re an athlete or a 40-year-old adult, we’re going to have the same conversation. I think that holds. There’s a variety or a spectrum where we don’t know. I think the registry is one big step.

Thinking back to when somebody has an event, I would say take the teachable moment with the AHA and others to make sure your communities and your areas have automated external defibrillators (AEDs) and CPR training, and that we get to 100%: 100% response, 100% CPR, 100% defibrillation. I think that’s the first step.
 

Chain of survival

Harrington: Let’s really focus on the chain of survival. It is a chain: If any link is broken, your chance of survival really drops. We’ve had some well-known cases within our AHA community, including somebody who talks about it regularly: Kevin Volpp, from the University of Pennsylvania, a health economist. He had almost the perfect chain of survival. He had sudden cardiac death in a restaurant that was immediately observed, CPR started, EMTs called, and AED on the scene. Impressive.

Patel: That was in Cincinnati, where there are communities that have really worked on these things. I think you’re right. The chain of survival with rapid CPR to build a nation of survivors is key. The people at the AHA are helping us do this; there is a national call to make sure CPR is something that people feel comfortable doing. That they do it in men and women. They do it for anyone that goes down. And realize that it’s CPR that is hands-only. I think that’s an important lesson from Damar’s work, Nancy Brown’s, and AHA’s. Actually, schools in many countries require that to get through primary school.

Harrington: CPR training is a requirement to graduate from high school in some states.

Patel: My son just graduated from high school, and we spent time at his school making sure that everybody had access to CPR training. I think the way to do this is to start with that. Now, getting more specific about teams and athletes, I think most have emergency action plans, but it’s having action plans that work because of where you are and where the AED locations might be, or what the sport is. Having a plan on how you’re going to get that athlete to a place where you can help them recover is an important piece.

From there, I think the conversation for us is about what can we do as a society and as a country to answer some critical questions, including some real-world questions that people are asking: We had COVID-19 and we’re hearing these cases. Is this going up or down, and are these related?

Soon, hopefully the same group I talked about and others will have a publication, working with the NCAA to look at all of the deaths that they observed in NCAA Division I athletes over 20 years, including the sudden cardiac deaths. I won’t share the results because the publication isn’t out, but I think that’s the kind of important information that will help us understand if these rates are going up or down.

Harrington: What’s associated with that risk? Then we can start getting at whether it is something that, when we’re doing assessment for suitability for sports, has risk factors that should warrant more investigation.

Patel: Much like the field of cardiology, we haven’t enough of an evidence base, the right technologies, or the studies to determine how we should do screening, or not screening, across the board. Again, there is variation. There are some countries where anyone participating is going to get an ECG and an echocardiogram. There are other countries, like the United States, where it’s going to be a bit dependent on athlete risk.

Harrington: And where you live.

Patel: And where you live. Unfortunately, again, that brings in the idea that it might not be equitable in how we’re evaluating these individuals. I do think the opportunity to start to standardize that evaluation exists, and it likely comes from the ability to look back and say, “Here are some higher-risk individuals or some higher-risk scenarios.”

Harrington: Isn’t this what we do all the time in clinical medicine?

Patel: It’s going to be applied to a population that maybe is not as studied. I said this to you before we came on. The other thing is to make sure that the shared decision-making allows athletes who feel like they have a chance or want to play. During COVID, we had many college athletes, high school athletes, and kids not able to participate in sports. There was significant depression, feeling of loneliness, and even physical loss. People were actually getting less conditioned quickly. There’s a great benefit to sports participation.

Harrington: We were extrapolating from older data. If I’ve just had this new infection, COVID, and I’ve maybe got some signs of it in my heart, why can’t I exercise? That’s extrapolating from old myocarditis data.

Patel: We’re having to learn and follow it. I think there’s value in following that and getting those data. The second thing I think is really valuable is that we’ve shown that these individuals, if you do have these conversations and follow them, can participate and can be part of understanding the risk just like anything else.

Harrington: Is it sport specific? Are there some sports where maybe the conversation should be a little more intense than in other sports?

Patel: I think what we’ll see is that the conversations may be sport specific, and some may concern the number of athletes tested. At times, it’s pretty complicated. It does look like there are, as you know, different weight-bearing performance athletes, endurance athletes, or what I’ll call burst sports. There will probably be data that will identify certain sports where we may need to pay a bit more attention.

Harrington: What about the contact issues? Damar had a very specific thing, we think, happen to him. Football is a violent, contact-oriented sport, but fortunately we don’t regularly see what happened to Damar.

Patel: We’re talking about sudden cardiac death, but obviously, contact issues and neurologic evaluation is a whole other topic. That’s another big issue that I know many are following, and the NCAA is carefully, too. For Damar, I think we know that it was commotio cordis. At least when that happens, when there’s a ball or a trauma to the chest, those things have to be timed just so to actually lead to this event. Thankfully, it’s not very frequent, but it can happen.

Harrington: Hockey pucks, baseballs, soccer balls, a helmet to the chest ...

Patel: You have to be in a specific cycle of the squeeze. We don’t see that very frequently. I do think the evaluation and treatment, hopefully, makes a difference. One thing that we’re evolving in the screening world is our imaging; it’s getting better. We are not just doing echocardiograms; we are able to do other studies. There’s a mix of imaging and other technologies.

Is screening the answer?

Harrington: Let’s talk about that because screening is the area, I would say, with the most controversy – and a large amount of emotional controversy. Some argue that the data are not good enough to screen, or doctors are saying, “Wait a minute, why are we screening all these kids?” You said you were at your son’s high school doing CPR training. How many athletes are at his high school? There are many, and that’s a pretty small high school. Big communities, big universities, and the professional sports can afford it. Should we be doing this at the community level?

Patel: There have been some data. The Italians have done standard screening for some time, and it’s shown us that if you did echocardiograms in many individuals, you do find some cases that are hypertrophic cardiomyopathy in pathology. The issue is just how much you have to do and the resource utilization. I think as we get to a world where screening studies can happen with smaller technology and AI, that can be democratizing in how we get to athletes.

Harrington: Give an example of that. We were talking outside, you and I, about some of the new stethoscope technology.

Patel: Yes, stethoscopes are going to be one of the examples. We have stethoscopes that have the ability to get sounds and ECG signals, or at least some lead signals.

Harrington: Yes.

Patel: Potentially you can imagine that sound and ECG tracing in an AI environment, at least getting you from “everyone gets a listen with one stethoscope in their gym from their coach,” and it goes to the cloud. When there are enough questions, these are the ones that have to go further. Now, that’s a big study that has to be carried out; I’m not in any way saying we should do that.

Harrington: The technology is coming.

Patel: We start to see that our ability to rapidly do something to meet our athletes or our patients where they are will happen soon. Remember that the performance curve can vary, but once you have a sound where you can start to say that this is a regular flow murmur vs. “I’m worried about this,” especially as you mark it with ECG – that’s one example.

Smaller imaging is another example. For many years, ECGs have been talked about. There are entire courses that we run looking at ECGs in athletes. Remembering that Aaron Baggish and others are publishing that these individuals are large. When we look at their hearts, we see that they’re large, but when you adjust for size, often you can identify that many of them are within what we think are normal. Structurally, there are still many cases where you look at hearts and you’re asking, “Is this a thick heart? Is this noncompaction? Is this some pathology?”

That’s where you need imaging expertise. I think you have to have those individuals. I’m not advocating screening. I’m advocating studying it and that we should be thinking about the population. I don’t see a world where we don’t eventually start to really look to prevent those.

Harrington: Right. Whether it’s understanding that there are certain risk factors associated with this and we have to dedicate screening resources to those individuals, or if we want to do it more broadly on the population level to understand this with deeper dives into certain individuals, we’ve got to study it.

Patel: Some of the experts in sports medicine and sports cardiology have been collecting these data for a while. It’s time that we are there, because with these events we have the opportunity to share more of these data and maybe raise awareness – not in the teachable moment only – to get others to contribute.

I do believe that long term there’s an opportunity. We’ve seen that. We see that the rates, unfortunately, for marathon runners, where people unfortunately have events, seem to be higher. And we’ve seen the studies on troponin leaks in these individuals or evidence that there’s some effect on the heart from these events. We want people to be able to be long-term healthy.
 

Early defibrillation

Harrington: A large amount of work needs to be done. We talked with regard to screening, we’ve talked about CPR. We really need to have a nation of people who can do hands-only CPR. Let’s talk about AEDs, another key part of the chain of survival.

Patel: We have another important study going on, but an important message first: AEDs are critical to survival. We know that CPR is critical, but so is getting people to a defibrillator.

Harrington: Early defibrillation.

Patel: Early defibrillation. Early CPR is one of the biggest markers of making sure we perfuse people to get to early defibrillation, but then you have to get early defibrillation. There’s been a huge push in many communities, again, along with AHA and others, to make sure that AEDs are available not only in the U.S. but around the world. We’re at ESC and we see the push around the world to get AEDs available. They’ve come down in size and come down in cost, and that’s made it much more accessible. That’s really good. They’re still not always there.

We’ve seen really interesting randomized studies with people in some European countries where they have certain areas, just because of the locations, where bystanders will help get an AED  vs. randomizing to the EMS truck. They seem better in some of those variations. Chris Granger, at our institution, with Monique Starks, Dan Mark, and others, is doing a study in North Carolina where we’re testing different ways to potentially get AEDs in communities. We’re randomizing counties to one or two ways of getting AEDs to those individuals.

Harrington: Can you have an app where you just click “Find me an AED”?

Patel: Is there a world where the AED is found or is something bringing you the AED? Are there drones? Are there people driving? Are there ways that an AED is brought to the scene? All of those are going to be critical. It starts with continuing to figure out ways to support the costs of getting AEDs in places. The technology is continuing to evolve.

Harrington: It really is the premedical system stuff that makes the difference. Once EMS arrives with trained individuals who can defibrillate, they can transport you to a medical facility where trained physicians are at. It’s that pre-EMS thing that is so critical.

Patel: We talk often about athletes, but cardiac arrest care in general, and the chain of survival with CPR and AEDs, is critical. I still see patients in the CICU at Duke where, unfortunately, the biggest driver, as you just highlighted in that chain of survival, is how rapid we were in that golden hour. In the first 15 minutes, are you getting CPR, are you getting AED? Are you getting to a system?

Harrington: Are you getting a rapid transport?

Patel: Are you getting a neurologic assessment? Are you getting cooled or not? Those are important things.

Harrington: All right. Let’s try to wrap this up. Teachable moments, we talked about. One of the things about cases in prominent athletes is that it makes it to the newspaper and then it raises awareness. There is a drawing inference from a small group of cases to the broader societal issues. That’s an important topic.

We’ve talked about possible screening options, identifying at-risk individuals and high-risk individuals. A large amount of data has already been accumulated, but there is more work to be done. We focused on how to use those teachable moments to really influence the chain of survival, not just for athletes but for society at large.

I love your point about the Bethesda Conference on shared decision-making. Like with everything else, we have to have that two-way conversation: What are the athlete’s goals, hopes, and aspirations?

Patel: That group of experts, in addition to shared decision-making, gave us a whole list of conditions that we should be aware of and the cutpoints of where we think normal and not normal live for athletes. I think that’s used by many.

Can we build our systems to make research happen faster for the individuals? These athletes are at colleges that are obviously doing so much to make sure they’re okay. The people who are helping with this registry, and others, are going to continue to work to ask whether we can engage them as citizen participants and scientists. I think athletes are going to become some of our best advocates for why you’d want to know about yourself and how to perform CPR.

Harrington: I love the concept of citizen scientists, that we all have an obligation to contribute to the evidence base because we all want to use that evidence.

This has been a terrific conversation. I’ve been joined by my good friend, Dr. Manesh Patel from Duke University. I hope you’ve enjoyed our discussion here at the ESC. We have been taking a little break from the science going on around us to talk about sudden cardiac death in athletes. It really does have implications for broader societal concepts.

Dr. Harrington is the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine and provost for medical affairs of Cornell University, New York, as well as a former president of the American Heart Association. He has disclosed the following relevant financial relationships: Research relationships with Baim Institute (DSMB); CSL (RCT executive committee); Janssen (RCT chair); National Heart, Lung, and Blood Institute (RCT executive committee, DSMB chair); Patient-Centered Outcomes Research Institute (RCT co-chair); Duke Clinical Research Institute. Consulting relationships with Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; Cytokinetics. Dr. Patel is professor of medicine, Duke University; chief, division of cardiology; director, Duke Heart Center, Duke University Medical Center, Durham, N.C. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bayer; Janssen; Novartis (consultant). Received research grant from Bayer; Janssen.

A version of this article appeared on Medscape.com.

Recorded Aug. 26, 2023. This transcript has been edited for clarity.

Robert A. Harrington, MD: I’m here with my good friend, Manesh Patel, from Duke University. We’re at the European Society of Cardiology (ESC) congress in Amsterdam, and I pulled Manesh into the studio for a conversation about something that’s really topical right now: sudden cardiac death in athletes.

What I hope to do [in this interview] is really pick Manesh’s brain on how we are thinking about this. Are we going to think about treatment issues? Are we going to think about prevention issues? Are we thinking about screening? We’ll try to make it practical.

Dr. Manesh Patel is chief of cardiovascular medicine at Duke University and also the director of the Duke Heart Center. Manesh, thanks for joining me here.
 

Bronny James and Damar Hamlin

Manesh R. Patel, MD: Excited to be here, Bob. Always.

Harrington: [Recently,] a news article comes out about the cause of Bronny James’ sudden cardiac death. Let me put this into a bigger societal context.

Last winter, Damar Hamlin, from the Buffalo Bills, suffered a traumatic injury on the field, and with that, had cardiac arrest. He’s back playing football – great to see. You and I are involved with the American Heart Association. He’s been very supportive of our efforts around things like CPR. He’s been terrific. It’s great to see him playing.

We know a little less about Bronny James. The news articles say the cause is both functional and anatomical, and it seems to be congenital, but we don’t have any details beyond this. Let’s not focus on the people; let’s focus on the topic.

Patel: I’m excited that we’re having the conversation. First and foremost, we’re excited that, with what we’ve seen on a national stage, these two individuals are doing well. They survived sudden cardiac death, which is a testament to all the things that we’ll talk about.

There are many important questions, like, is this increasing? Is this something we can prevent? And what are those things that might be happening to athletes?

Harrington: Can we predict it?

Patel: Right. I think the idea of sudden cardiac death in athletes is really a critical one for us to think about because it does concern participation and what we think about that. There are many experts who’ve been studying this for years that I now get to work with.

Harrington: Tell us a little bit about the kind of things you’ve been doing in this area.

Patel: Even before these events in the COVID era, we were wondering about athletes getting myocarditis, just in general, what do we know about that? People like Aaron Baggish, Kim Harmon, Jonathan Drezner, and others have been studying this.

Harrington: You and I did a show on athletes and COVID-19.

Patel: With the American Heart Association (AHA), the Cornell Foundation, and others, we started the Outcomes Registry for Cardiac Conditions in Athletes (ORCCA). This registry is across the United States, and athletes can sign up.

Harrington: Is it voluntary? Do the schools sign them up?

Patel: The athletes sign up. Team trainers and doctors talk to the athletes. We don’t really know the risks of some of these conditions. There’s a lot of gray area – people with certain conditions that were really interesting; aortas that are dilated in tall people.

Harrington: Long QT.

Patel: Long QT. There are certainly things that we know we should be intervening on and others where participation is a question. All of these we are trying to longitudinally put into the registry and follow them over time.

The second thing is understanding from the last Bethesda Conference that we want shared decision-making. There are going to be conditions where you say, “Look, I think your risk is high. You’ve a family history of sudden cardiac death. You have arrhythmias while you’re exercising.”

Harrington: You have a big, thick heart.

Patel: If you have hypertrophic cardiomyopathy, whether you’re an athlete or a 40-year-old adult, we’re going to have the same conversation. I think that holds. There’s a variety or a spectrum where we don’t know. I think the registry is one big step.

Thinking back to when somebody has an event, I would say take the teachable moment with the AHA and others to make sure your communities and your areas have automated external defibrillators (AEDs) and CPR training, and that we get to 100%: 100% response, 100% CPR, 100% defibrillation. I think that’s the first step.
 

Chain of survival

Harrington: Let’s really focus on the chain of survival. It is a chain: If any link is broken, your chance of survival really drops. We’ve had some well-known cases within our AHA community, including somebody who talks about it regularly: Kevin Volpp, from the University of Pennsylvania, a health economist. He had almost the perfect chain of survival. He had sudden cardiac death in a restaurant that was immediately observed, CPR started, EMTs called, and AED on the scene. Impressive.

Patel: That was in Cincinnati, where there are communities that have really worked on these things. I think you’re right. The chain of survival with rapid CPR to build a nation of survivors is key. The people at the AHA are helping us do this; there is a national call to make sure CPR is something that people feel comfortable doing. That they do it in men and women. They do it for anyone that goes down. And realize that it’s CPR that is hands-only. I think that’s an important lesson from Damar’s work, Nancy Brown’s, and AHA’s. Actually, schools in many countries require that to get through primary school.

Harrington: CPR training is a requirement to graduate from high school in some states.

Patel: My son just graduated from high school, and we spent time at his school making sure that everybody had access to CPR training. I think the way to do this is to start with that. Now, getting more specific about teams and athletes, I think most have emergency action plans, but it’s having action plans that work because of where you are and where the AED locations might be, or what the sport is. Having a plan on how you’re going to get that athlete to a place where you can help them recover is an important piece.

From there, I think the conversation for us is about what can we do as a society and as a country to answer some critical questions, including some real-world questions that people are asking: We had COVID-19 and we’re hearing these cases. Is this going up or down, and are these related?

Soon, hopefully the same group I talked about and others will have a publication, working with the NCAA to look at all of the deaths that they observed in NCAA Division I athletes over 20 years, including the sudden cardiac deaths. I won’t share the results because the publication isn’t out, but I think that’s the kind of important information that will help us understand if these rates are going up or down.

Harrington: What’s associated with that risk? Then we can start getting at whether it is something that, when we’re doing assessment for suitability for sports, has risk factors that should warrant more investigation.

Patel: Much like the field of cardiology, we haven’t enough of an evidence base, the right technologies, or the studies to determine how we should do screening, or not screening, across the board. Again, there is variation. There are some countries where anyone participating is going to get an ECG and an echocardiogram. There are other countries, like the United States, where it’s going to be a bit dependent on athlete risk.

Harrington: And where you live.

Patel: And where you live. Unfortunately, again, that brings in the idea that it might not be equitable in how we’re evaluating these individuals. I do think the opportunity to start to standardize that evaluation exists, and it likely comes from the ability to look back and say, “Here are some higher-risk individuals or some higher-risk scenarios.”

Harrington: Isn’t this what we do all the time in clinical medicine?

Patel: It’s going to be applied to a population that maybe is not as studied. I said this to you before we came on. The other thing is to make sure that the shared decision-making allows athletes who feel like they have a chance or want to play. During COVID, we had many college athletes, high school athletes, and kids not able to participate in sports. There was significant depression, feeling of loneliness, and even physical loss. People were actually getting less conditioned quickly. There’s a great benefit to sports participation.

Harrington: We were extrapolating from older data. If I’ve just had this new infection, COVID, and I’ve maybe got some signs of it in my heart, why can’t I exercise? That’s extrapolating from old myocarditis data.

Patel: We’re having to learn and follow it. I think there’s value in following that and getting those data. The second thing I think is really valuable is that we’ve shown that these individuals, if you do have these conversations and follow them, can participate and can be part of understanding the risk just like anything else.

Harrington: Is it sport specific? Are there some sports where maybe the conversation should be a little more intense than in other sports?

Patel: I think what we’ll see is that the conversations may be sport specific, and some may concern the number of athletes tested. At times, it’s pretty complicated. It does look like there are, as you know, different weight-bearing performance athletes, endurance athletes, or what I’ll call burst sports. There will probably be data that will identify certain sports where we may need to pay a bit more attention.

Harrington: What about the contact issues? Damar had a very specific thing, we think, happen to him. Football is a violent, contact-oriented sport, but fortunately we don’t regularly see what happened to Damar.

Patel: We’re talking about sudden cardiac death, but obviously, contact issues and neurologic evaluation is a whole other topic. That’s another big issue that I know many are following, and the NCAA is carefully, too. For Damar, I think we know that it was commotio cordis. At least when that happens, when there’s a ball or a trauma to the chest, those things have to be timed just so to actually lead to this event. Thankfully, it’s not very frequent, but it can happen.

Harrington: Hockey pucks, baseballs, soccer balls, a helmet to the chest ...

Patel: You have to be in a specific cycle of the squeeze. We don’t see that very frequently. I do think the evaluation and treatment, hopefully, makes a difference. One thing that we’re evolving in the screening world is our imaging; it’s getting better. We are not just doing echocardiograms; we are able to do other studies. There’s a mix of imaging and other technologies.

Is screening the answer?

Harrington: Let’s talk about that because screening is the area, I would say, with the most controversy – and a large amount of emotional controversy. Some argue that the data are not good enough to screen, or doctors are saying, “Wait a minute, why are we screening all these kids?” You said you were at your son’s high school doing CPR training. How many athletes are at his high school? There are many, and that’s a pretty small high school. Big communities, big universities, and the professional sports can afford it. Should we be doing this at the community level?

Patel: There have been some data. The Italians have done standard screening for some time, and it’s shown us that if you did echocardiograms in many individuals, you do find some cases that are hypertrophic cardiomyopathy in pathology. The issue is just how much you have to do and the resource utilization. I think as we get to a world where screening studies can happen with smaller technology and AI, that can be democratizing in how we get to athletes.

Harrington: Give an example of that. We were talking outside, you and I, about some of the new stethoscope technology.

Patel: Yes, stethoscopes are going to be one of the examples. We have stethoscopes that have the ability to get sounds and ECG signals, or at least some lead signals.

Harrington: Yes.

Patel: Potentially you can imagine that sound and ECG tracing in an AI environment, at least getting you from “everyone gets a listen with one stethoscope in their gym from their coach,” and it goes to the cloud. When there are enough questions, these are the ones that have to go further. Now, that’s a big study that has to be carried out; I’m not in any way saying we should do that.

Harrington: The technology is coming.

Patel: We start to see that our ability to rapidly do something to meet our athletes or our patients where they are will happen soon. Remember that the performance curve can vary, but once you have a sound where you can start to say that this is a regular flow murmur vs. “I’m worried about this,” especially as you mark it with ECG – that’s one example.

Smaller imaging is another example. For many years, ECGs have been talked about. There are entire courses that we run looking at ECGs in athletes. Remembering that Aaron Baggish and others are publishing that these individuals are large. When we look at their hearts, we see that they’re large, but when you adjust for size, often you can identify that many of them are within what we think are normal. Structurally, there are still many cases where you look at hearts and you’re asking, “Is this a thick heart? Is this noncompaction? Is this some pathology?”

That’s where you need imaging expertise. I think you have to have those individuals. I’m not advocating screening. I’m advocating studying it and that we should be thinking about the population. I don’t see a world where we don’t eventually start to really look to prevent those.

Harrington: Right. Whether it’s understanding that there are certain risk factors associated with this and we have to dedicate screening resources to those individuals, or if we want to do it more broadly on the population level to understand this with deeper dives into certain individuals, we’ve got to study it.

Patel: Some of the experts in sports medicine and sports cardiology have been collecting these data for a while. It’s time that we are there, because with these events we have the opportunity to share more of these data and maybe raise awareness – not in the teachable moment only – to get others to contribute.

I do believe that long term there’s an opportunity. We’ve seen that. We see that the rates, unfortunately, for marathon runners, where people unfortunately have events, seem to be higher. And we’ve seen the studies on troponin leaks in these individuals or evidence that there’s some effect on the heart from these events. We want people to be able to be long-term healthy.
 

Early defibrillation

Harrington: A large amount of work needs to be done. We talked with regard to screening, we’ve talked about CPR. We really need to have a nation of people who can do hands-only CPR. Let’s talk about AEDs, another key part of the chain of survival.

Patel: We have another important study going on, but an important message first: AEDs are critical to survival. We know that CPR is critical, but so is getting people to a defibrillator.

Harrington: Early defibrillation.

Patel: Early defibrillation. Early CPR is one of the biggest markers of making sure we perfuse people to get to early defibrillation, but then you have to get early defibrillation. There’s been a huge push in many communities, again, along with AHA and others, to make sure that AEDs are available not only in the U.S. but around the world. We’re at ESC and we see the push around the world to get AEDs available. They’ve come down in size and come down in cost, and that’s made it much more accessible. That’s really good. They’re still not always there.

We’ve seen really interesting randomized studies with people in some European countries where they have certain areas, just because of the locations, where bystanders will help get an AED  vs. randomizing to the EMS truck. They seem better in some of those variations. Chris Granger, at our institution, with Monique Starks, Dan Mark, and others, is doing a study in North Carolina where we’re testing different ways to potentially get AEDs in communities. We’re randomizing counties to one or two ways of getting AEDs to those individuals.

Harrington: Can you have an app where you just click “Find me an AED”?

Patel: Is there a world where the AED is found or is something bringing you the AED? Are there drones? Are there people driving? Are there ways that an AED is brought to the scene? All of those are going to be critical. It starts with continuing to figure out ways to support the costs of getting AEDs in places. The technology is continuing to evolve.

Harrington: It really is the premedical system stuff that makes the difference. Once EMS arrives with trained individuals who can defibrillate, they can transport you to a medical facility where trained physicians are at. It’s that pre-EMS thing that is so critical.

Patel: We talk often about athletes, but cardiac arrest care in general, and the chain of survival with CPR and AEDs, is critical. I still see patients in the CICU at Duke where, unfortunately, the biggest driver, as you just highlighted in that chain of survival, is how rapid we were in that golden hour. In the first 15 minutes, are you getting CPR, are you getting AED? Are you getting to a system?

Harrington: Are you getting a rapid transport?

Patel: Are you getting a neurologic assessment? Are you getting cooled or not? Those are important things.

Harrington: All right. Let’s try to wrap this up. Teachable moments, we talked about. One of the things about cases in prominent athletes is that it makes it to the newspaper and then it raises awareness. There is a drawing inference from a small group of cases to the broader societal issues. That’s an important topic.

We’ve talked about possible screening options, identifying at-risk individuals and high-risk individuals. A large amount of data has already been accumulated, but there is more work to be done. We focused on how to use those teachable moments to really influence the chain of survival, not just for athletes but for society at large.

I love your point about the Bethesda Conference on shared decision-making. Like with everything else, we have to have that two-way conversation: What are the athlete’s goals, hopes, and aspirations?

Patel: That group of experts, in addition to shared decision-making, gave us a whole list of conditions that we should be aware of and the cutpoints of where we think normal and not normal live for athletes. I think that’s used by many.

Can we build our systems to make research happen faster for the individuals? These athletes are at colleges that are obviously doing so much to make sure they’re okay. The people who are helping with this registry, and others, are going to continue to work to ask whether we can engage them as citizen participants and scientists. I think athletes are going to become some of our best advocates for why you’d want to know about yourself and how to perform CPR.

Harrington: I love the concept of citizen scientists, that we all have an obligation to contribute to the evidence base because we all want to use that evidence.

This has been a terrific conversation. I’ve been joined by my good friend, Dr. Manesh Patel from Duke University. I hope you’ve enjoyed our discussion here at the ESC. We have been taking a little break from the science going on around us to talk about sudden cardiac death in athletes. It really does have implications for broader societal concepts.

Dr. Harrington is the Stephen and Suzanne Weiss Dean of Weill Cornell Medicine and provost for medical affairs of Cornell University, New York, as well as a former president of the American Heart Association. He has disclosed the following relevant financial relationships: Research relationships with Baim Institute (DSMB); CSL (RCT executive committee); Janssen (RCT chair); National Heart, Lung, and Blood Institute (RCT executive committee, DSMB chair); Patient-Centered Outcomes Research Institute (RCT co-chair); Duke Clinical Research Institute. Consulting relationships with Atropos Health; Bitterroot Bio; Bristol Myers Squibb; BridgeBio; Element Science; Edwards Lifesciences; Foresite Labs; Medscape/WebMD Board of Directors for: American Heart Association; College of the Holy Cross; Cytokinetics. Dr. Patel is professor of medicine, Duke University; chief, division of cardiology; director, Duke Heart Center, Duke University Medical Center, Durham, N.C. He has disclosed the following relevant financial relationships: Serve(d) as a director, officer, partner, employee, adviser, consultant, or trustee for Bayer; Janssen; Novartis (consultant). Received research grant from Bayer; Janssen.

A version of this article appeared on Medscape.com.

AMSTERDAM – New European Society of Cardiology guidelines on the management of acute coronary syndromes (ACS) have for the first time combined ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina into the same set of recommendations.

The new guideline was released at the annual congress of the European Society of Cardiology, and was published online in the European Heart Journal.

“We found that it was realized by the cardiology community that patients with STEMI, NSTEMI, or unstable angina represent a spectrum,” the chair of the guideline task force, Robert Byrne, MD, chair of cardiovascular research at the RCSI University of Medicine and Health Sciences, Dublin, explained to this news organization. “After the initial triage and management decisions, then most of the rest of the care follows a common pathway so it would make sense to consider everything in one guideline.”

Dr. Byrne noted that for all patients with a suspected ACS, the guideline recommendation is to administer an ECG within 10 minutes of presentation. The time is critical particularly for those with an occluded epicardial vessel. If there are features on the ECG that suggest an acutely occluded epicardial vessel, then the patient needs immediate angiography or primary angioplasty.

“The 10-minute guidance has been maintained from previous guidelines, but the nuance in the new guideline is that typically when we think of an occluded epicardial vessel we think of ST-elevation on the ECG,” Byrne said. “While this captures most occluded epicardial vessels, it doesn’t capture all of them. So, we have provided some guidance on alternative ECG patterns which might be indicative of an acute occlusion of the epicardial vessel and should be dealt with in the same way as an ST-elevation MI. This is a new concept.”

This situation could arise when a patient has an occluded circumflex artery and the regular ECG may not show ST elevation but the patient has ongoing pain, he noted. “There are additional ECG leads that can be looked at that might identify patients who need an immediate invasive strategy.

“This is one more reason why all ACS patients should be considered as part of one spectrum, and while the ECG gives us important information, it is not the only thing to consider. Dividing the conditions up as to whether a patient has ST elevation or not does not always make pathophysiological sense,” he added.

Dr. Byrne noted that the new guidelines have tried to reach a wider stakeholder group that includes emergency doctors, internal medicine physicians, general practitioners, and surgeons, as well as cardiologists. The document includes animations in an effort to increase the reach of the guidelines to noncardiology stakeholders, and for the first time, the task force included a patient representative.

“As part of this strategy, we have put more structure in to emphasize the importance that at first contact, we already want to be thinking of antithrombotic therapy and whether the patient needs urgent transfer to the nearest cath lab. We also want to be thinking straight away about preventing the next heart attack by implementing strong secondary prevention measures,” he commented.

Dr. Byrne highlighted a few changes to individual recommendations in the new guidelines.
 

Invasive management in NSTE-ACS

He pointed out that a small change has been made in the advice on invasive management for patients with non–ST-elevation ACS.

Dr. Byrne explained that patients with ST elevation should be sent immediately to a cath lab for PCI. If this is not possible within 120 minutes, then the patient should receive thrombolysis. This recommendation is the same as in previous guidelines.

He added, however, that there is some novelty in recommendations for patients who don’t have ST elevation but do have a positive troponin. For this group, previous guidelines gave a Class I recommendation that all such patients undergo an angiogram within the first 24 hours. However, an additional meta-analysis that was published in 2022 showed that the evidence for triaging all patients to the cath lab within 24 hours is somewhat limited, Dr. Byrne noted.

“At the end of the day, the task force felt that a Class I recommendation to get all patients to the cath lab within 24 hours was too strong and couldn’t be sustained, so it has been downgraded to a Class IIa recommendation, which we thought was more appropriate,” he said.

“So, while all patients should still have an angiogram during the hospital admission, if they are high-risk ACS, the imperative to get everyone to the cath lab within 24 hours – which many of our colleagues were finding difficult to achieve – does not seem to be backed up by the evidence,” he added.
 

Antithrombotic therapy

Addressing administration of antithrombotics, the guidelines emphasize that at the time of initial diagnosis, all patients should receive antithrombotic therapy, usually aspirin and a parenteral antithrombotic, such as heparin, enoxaparin, bivalirudin, or fondaparinux. Dr. Byrne noted that the guidelines have a new algorithm as to which of these antithrombotics to give, depending on the clinical presentation of the patient.

On the use of upfront P2Y12 inhibitors, Dr. Byrne said the new guidelines only give a weak recommendation for this.

“Giving a P2Y12 inhibitor up front does not have a strong evidence base, and it’s not unreasonable to wait, do the angiogram, see where you are, and then start the P2Y12 inhibitor. This is something that’s not widely done in clinical practice,” he commented.

“The last 2020 guideline gave a Class III recommendation for upfront P2Y12 inhibitor therapy for ACS patients who do not have STEMI. We’ve generally maintained that with the introduction of the exception that if you are in a health care system where there is a long wait to get to the cath lab – 5 ,6 or 7 days – then it’s reasonable to make an exception and give a P2Y12 inhibitor, but otherwise we’ve sustained the Class III recommendation,” he noted.

Also, for patients who have STEMI, there is a new Class IIb recommendation that upfront P2Y12 inhibitors may be considered.

“This is also rather a weak recommendation. There isn’t a strong rationale to give a P2Y12 inhibitor it in ST elevation either. It’s also reasonable to wait,” he added.
 

Don’t rush cardiac arrest patients to the cath lab

Another update in the guidelines involves the management of patients with cardiac arrest who have been resuscitated. Dr. Byrne explained that these patients would all receive an immediate ECG, and if it is found that they have ST elevation, they would be sent immediately to the cath lab. But a series of randomized trials has suggested that for patients who don’t have ST elevation, it is not necessary to rush these patients to the cath lab.

“We’ve given a Class III recommendation for this, saying it may be better to stabilize the patients first in the ICU. This is in recognition that a large proportion of these patients turn out not to have an MI. They have had a cardiac arrest for another reason,” Dr. Byrne noted. “Moving them to the cath lab when they are still unstable could be harming these patients rather than helping them.”
 

Revascularization for multivessel disease

Dr. Byrne notes that revascularization remains a critical element in the care for patients with STEMI, and there is a new recommendation in this area for patients with multivessel disease.

“Up to half of patients presenting with STEMI have multivessel disease, and we now have five randomized trials to say that these patients should have complete revascularization rather than just the culprit vessel. There is a new Class I recommendation for this,” he said.

However, the optimal timing of revascularization (immediate vs. staged) has still not been investigated in adequately sized randomized trials, and no recommendation has been made on this, the task force notes.

Dr. Byrne commented: “If you want to do everything in one go, that’s fine, but it’s also okay to do the culprit lesion first and then the other vessels at a later date within 45 days. This might depend on individual circumstances. For example, if there are complex lesions or the vessels are heavily calcified, then it may be best to get the culprit lesion fixed first and let the patient recover, then bring them back in for the rest.”

He pointed out that the results of the MULTISTARS trial, which were not available when the task force was formulating the guidelines, were reported at the ESC Congress and confirmed their recommendation.
 

DAPT after PCI

On the duration of dual antiplatelet therapy (DAPT) after PCI, the new guidelines have largely retained prior recommendations for a default strategy of 12 months for the combination of aspirin and a P2Y12 inhibitor.

“This was the subject of some discussion, as there have been several trials now looking at shorter durations of DAPT and deescalating after a few months to just one of these treatments. And while there is a rationale to do this, we think it’s best to be kept as an alternative strategy rather than the default strategy,” Dr. Byrne said.

He explained that the trials of DAPT deescalation tended to enroll lower-risk patients, which reduced the generalizability of the results.

Most of the trials only randomly assigned patients to shorter durations of DAPT when they were event-free for some period, she said.

“This is a dynamic decision-making process and reflects the real world to some extent. We think it is best to recommend the standard aspirin and a P2Y12 inhibitor for the 12-month duration, but at 3 months, if the patient is doing well but you may be worried about bleeding risk, then you could decide to deescalate to single antiplatelet therapy,” she noted. “So, there is Class IIa recommendation that this can be considered, but it is not recommended as the default position.”
 

Polypill for secondary prevention

Another innovation in the new guidelines is a new Class IIa recommendation for prescription of a polypill containing secondary prevention medications for patients on discharge from hospital.

This recommendation follows a trial that showed that the use of such a polypill helps patients be more adherent to the therapies prescribed.

Byrne explains that such a polypill may contain aspirin, an ACE inhibitor, and a statin. Several varieties are available in most European countries, but they are not widely used.

On secondary prevention, he stressed, “Prevention of the next heart attack starts before the patient leaves hospital. It is important to make sure the patient has the right medication on board, including a high-dose, high-intensity statin, and has been referred to a cardiac rehabilitation program. These are largely maintained recommendations from previous guidelines, but they are very important.”

A version of this article appeared on Medscape.com.

AMSTERDAM – New European Society of Cardiology guidelines on the management of acute coronary syndromes (ACS) have for the first time combined ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina into the same set of recommendations.

The new guideline was released at the annual congress of the European Society of Cardiology, and was published online in the European Heart Journal.

“We found that it was realized by the cardiology community that patients with STEMI, NSTEMI, or unstable angina represent a spectrum,” the chair of the guideline task force, Robert Byrne, MD, chair of cardiovascular research at the RCSI University of Medicine and Health Sciences, Dublin, explained to this news organization. “After the initial triage and management decisions, then most of the rest of the care follows a common pathway so it would make sense to consider everything in one guideline.”

Dr. Byrne noted that for all patients with a suspected ACS, the guideline recommendation is to administer an ECG within 10 minutes of presentation. The time is critical particularly for those with an occluded epicardial vessel. If there are features on the ECG that suggest an acutely occluded epicardial vessel, then the patient needs immediate angiography or primary angioplasty.

“The 10-minute guidance has been maintained from previous guidelines, but the nuance in the new guideline is that typically when we think of an occluded epicardial vessel we think of ST-elevation on the ECG,” Byrne said. “While this captures most occluded epicardial vessels, it doesn’t capture all of them. So, we have provided some guidance on alternative ECG patterns which might be indicative of an acute occlusion of the epicardial vessel and should be dealt with in the same way as an ST-elevation MI. This is a new concept.”

This situation could arise when a patient has an occluded circumflex artery and the regular ECG may not show ST elevation but the patient has ongoing pain, he noted. “There are additional ECG leads that can be looked at that might identify patients who need an immediate invasive strategy.

“This is one more reason why all ACS patients should be considered as part of one spectrum, and while the ECG gives us important information, it is not the only thing to consider. Dividing the conditions up as to whether a patient has ST elevation or not does not always make pathophysiological sense,” he added.

Dr. Byrne noted that the new guidelines have tried to reach a wider stakeholder group that includes emergency doctors, internal medicine physicians, general practitioners, and surgeons, as well as cardiologists. The document includes animations in an effort to increase the reach of the guidelines to noncardiology stakeholders, and for the first time, the task force included a patient representative.

“As part of this strategy, we have put more structure in to emphasize the importance that at first contact, we already want to be thinking of antithrombotic therapy and whether the patient needs urgent transfer to the nearest cath lab. We also want to be thinking straight away about preventing the next heart attack by implementing strong secondary prevention measures,” he commented.

Dr. Byrne highlighted a few changes to individual recommendations in the new guidelines.
 

Invasive management in NSTE-ACS

He pointed out that a small change has been made in the advice on invasive management for patients with non–ST-elevation ACS.

Dr. Byrne explained that patients with ST elevation should be sent immediately to a cath lab for PCI. If this is not possible within 120 minutes, then the patient should receive thrombolysis. This recommendation is the same as in previous guidelines.

He added, however, that there is some novelty in recommendations for patients who don’t have ST elevation but do have a positive troponin. For this group, previous guidelines gave a Class I recommendation that all such patients undergo an angiogram within the first 24 hours. However, an additional meta-analysis that was published in 2022 showed that the evidence for triaging all patients to the cath lab within 24 hours is somewhat limited, Dr. Byrne noted.

“At the end of the day, the task force felt that a Class I recommendation to get all patients to the cath lab within 24 hours was too strong and couldn’t be sustained, so it has been downgraded to a Class IIa recommendation, which we thought was more appropriate,” he said.

“So, while all patients should still have an angiogram during the hospital admission, if they are high-risk ACS, the imperative to get everyone to the cath lab within 24 hours – which many of our colleagues were finding difficult to achieve – does not seem to be backed up by the evidence,” he added.
 

Antithrombotic therapy

Addressing administration of antithrombotics, the guidelines emphasize that at the time of initial diagnosis, all patients should receive antithrombotic therapy, usually aspirin and a parenteral antithrombotic, such as heparin, enoxaparin, bivalirudin, or fondaparinux. Dr. Byrne noted that the guidelines have a new algorithm as to which of these antithrombotics to give, depending on the clinical presentation of the patient.

On the use of upfront P2Y12 inhibitors, Dr. Byrne said the new guidelines only give a weak recommendation for this.

“Giving a P2Y12 inhibitor up front does not have a strong evidence base, and it’s not unreasonable to wait, do the angiogram, see where you are, and then start the P2Y12 inhibitor. This is something that’s not widely done in clinical practice,” he commented.

“The last 2020 guideline gave a Class III recommendation for upfront P2Y12 inhibitor therapy for ACS patients who do not have STEMI. We’ve generally maintained that with the introduction of the exception that if you are in a health care system where there is a long wait to get to the cath lab – 5 ,6 or 7 days – then it’s reasonable to make an exception and give a P2Y12 inhibitor, but otherwise we’ve sustained the Class III recommendation,” he noted.

Also, for patients who have STEMI, there is a new Class IIb recommendation that upfront P2Y12 inhibitors may be considered.

“This is also rather a weak recommendation. There isn’t a strong rationale to give a P2Y12 inhibitor it in ST elevation either. It’s also reasonable to wait,” he added.
 

Don’t rush cardiac arrest patients to the cath lab

Another update in the guidelines involves the management of patients with cardiac arrest who have been resuscitated. Dr. Byrne explained that these patients would all receive an immediate ECG, and if it is found that they have ST elevation, they would be sent immediately to the cath lab. But a series of randomized trials has suggested that for patients who don’t have ST elevation, it is not necessary to rush these patients to the cath lab.

“We’ve given a Class III recommendation for this, saying it may be better to stabilize the patients first in the ICU. This is in recognition that a large proportion of these patients turn out not to have an MI. They have had a cardiac arrest for another reason,” Dr. Byrne noted. “Moving them to the cath lab when they are still unstable could be harming these patients rather than helping them.”
 

Revascularization for multivessel disease

Dr. Byrne notes that revascularization remains a critical element in the care for patients with STEMI, and there is a new recommendation in this area for patients with multivessel disease.

“Up to half of patients presenting with STEMI have multivessel disease, and we now have five randomized trials to say that these patients should have complete revascularization rather than just the culprit vessel. There is a new Class I recommendation for this,” he said.

However, the optimal timing of revascularization (immediate vs. staged) has still not been investigated in adequately sized randomized trials, and no recommendation has been made on this, the task force notes.

Dr. Byrne commented: “If you want to do everything in one go, that’s fine, but it’s also okay to do the culprit lesion first and then the other vessels at a later date within 45 days. This might depend on individual circumstances. For example, if there are complex lesions or the vessels are heavily calcified, then it may be best to get the culprit lesion fixed first and let the patient recover, then bring them back in for the rest.”

He pointed out that the results of the MULTISTARS trial, which were not available when the task force was formulating the guidelines, were reported at the ESC Congress and confirmed their recommendation.
 

DAPT after PCI

On the duration of dual antiplatelet therapy (DAPT) after PCI, the new guidelines have largely retained prior recommendations for a default strategy of 12 months for the combination of aspirin and a P2Y12 inhibitor.

“This was the subject of some discussion, as there have been several trials now looking at shorter durations of DAPT and deescalating after a few months to just one of these treatments. And while there is a rationale to do this, we think it’s best to be kept as an alternative strategy rather than the default strategy,” Dr. Byrne said.

He explained that the trials of DAPT deescalation tended to enroll lower-risk patients, which reduced the generalizability of the results.

Most of the trials only randomly assigned patients to shorter durations of DAPT when they were event-free for some period, she said.

“This is a dynamic decision-making process and reflects the real world to some extent. We think it is best to recommend the standard aspirin and a P2Y12 inhibitor for the 12-month duration, but at 3 months, if the patient is doing well but you may be worried about bleeding risk, then you could decide to deescalate to single antiplatelet therapy,” she noted. “So, there is Class IIa recommendation that this can be considered, but it is not recommended as the default position.”
 

Polypill for secondary prevention

Another innovation in the new guidelines is a new Class IIa recommendation for prescription of a polypill containing secondary prevention medications for patients on discharge from hospital.

This recommendation follows a trial that showed that the use of such a polypill helps patients be more adherent to the therapies prescribed.

Byrne explains that such a polypill may contain aspirin, an ACE inhibitor, and a statin. Several varieties are available in most European countries, but they are not widely used.

On secondary prevention, he stressed, “Prevention of the next heart attack starts before the patient leaves hospital. It is important to make sure the patient has the right medication on board, including a high-dose, high-intensity statin, and has been referred to a cardiac rehabilitation program. These are largely maintained recommendations from previous guidelines, but they are very important.”

A version of this article appeared on Medscape.com.

AMSTERDAM – New European Society of Cardiology guidelines on the management of acute coronary syndromes (ACS) have for the first time combined ST-elevation MI (STEMI), non–ST-elevation MI (NSTEMI), and unstable angina into the same set of recommendations.

The new guideline was released at the annual congress of the European Society of Cardiology, and was published online in the European Heart Journal.

“We found that it was realized by the cardiology community that patients with STEMI, NSTEMI, or unstable angina represent a spectrum,” the chair of the guideline task force, Robert Byrne, MD, chair of cardiovascular research at the RCSI University of Medicine and Health Sciences, Dublin, explained to this news organization. “After the initial triage and management decisions, then most of the rest of the care follows a common pathway so it would make sense to consider everything in one guideline.”

Dr. Byrne noted that for all patients with a suspected ACS, the guideline recommendation is to administer an ECG within 10 minutes of presentation. The time is critical particularly for those with an occluded epicardial vessel. If there are features on the ECG that suggest an acutely occluded epicardial vessel, then the patient needs immediate angiography or primary angioplasty.

“The 10-minute guidance has been maintained from previous guidelines, but the nuance in the new guideline is that typically when we think of an occluded epicardial vessel we think of ST-elevation on the ECG,” Byrne said. “While this captures most occluded epicardial vessels, it doesn’t capture all of them. So, we have provided some guidance on alternative ECG patterns which might be indicative of an acute occlusion of the epicardial vessel and should be dealt with in the same way as an ST-elevation MI. This is a new concept.”

This situation could arise when a patient has an occluded circumflex artery and the regular ECG may not show ST elevation but the patient has ongoing pain, he noted. “There are additional ECG leads that can be looked at that might identify patients who need an immediate invasive strategy.

“This is one more reason why all ACS patients should be considered as part of one spectrum, and while the ECG gives us important information, it is not the only thing to consider. Dividing the conditions up as to whether a patient has ST elevation or not does not always make pathophysiological sense,” he added.

Dr. Byrne noted that the new guidelines have tried to reach a wider stakeholder group that includes emergency doctors, internal medicine physicians, general practitioners, and surgeons, as well as cardiologists. The document includes animations in an effort to increase the reach of the guidelines to noncardiology stakeholders, and for the first time, the task force included a patient representative.

“As part of this strategy, we have put more structure in to emphasize the importance that at first contact, we already want to be thinking of antithrombotic therapy and whether the patient needs urgent transfer to the nearest cath lab. We also want to be thinking straight away about preventing the next heart attack by implementing strong secondary prevention measures,” he commented.

Dr. Byrne highlighted a few changes to individual recommendations in the new guidelines.
 

Invasive management in NSTE-ACS

He pointed out that a small change has been made in the advice on invasive management for patients with non–ST-elevation ACS.

Dr. Byrne explained that patients with ST elevation should be sent immediately to a cath lab for PCI. If this is not possible within 120 minutes, then the patient should receive thrombolysis. This recommendation is the same as in previous guidelines.

He added, however, that there is some novelty in recommendations for patients who don’t have ST elevation but do have a positive troponin. For this group, previous guidelines gave a Class I recommendation that all such patients undergo an angiogram within the first 24 hours. However, an additional meta-analysis that was published in 2022 showed that the evidence for triaging all patients to the cath lab within 24 hours is somewhat limited, Dr. Byrne noted.

“At the end of the day, the task force felt that a Class I recommendation to get all patients to the cath lab within 24 hours was too strong and couldn’t be sustained, so it has been downgraded to a Class IIa recommendation, which we thought was more appropriate,” he said.

“So, while all patients should still have an angiogram during the hospital admission, if they are high-risk ACS, the imperative to get everyone to the cath lab within 24 hours – which many of our colleagues were finding difficult to achieve – does not seem to be backed up by the evidence,” he added.
 

Antithrombotic therapy

Addressing administration of antithrombotics, the guidelines emphasize that at the time of initial diagnosis, all patients should receive antithrombotic therapy, usually aspirin and a parenteral antithrombotic, such as heparin, enoxaparin, bivalirudin, or fondaparinux. Dr. Byrne noted that the guidelines have a new algorithm as to which of these antithrombotics to give, depending on the clinical presentation of the patient.

On the use of upfront P2Y12 inhibitors, Dr. Byrne said the new guidelines only give a weak recommendation for this.

“Giving a P2Y12 inhibitor up front does not have a strong evidence base, and it’s not unreasonable to wait, do the angiogram, see where you are, and then start the P2Y12 inhibitor. This is something that’s not widely done in clinical practice,” he commented.

“The last 2020 guideline gave a Class III recommendation for upfront P2Y12 inhibitor therapy for ACS patients who do not have STEMI. We’ve generally maintained that with the introduction of the exception that if you are in a health care system where there is a long wait to get to the cath lab – 5 ,6 or 7 days – then it’s reasonable to make an exception and give a P2Y12 inhibitor, but otherwise we’ve sustained the Class III recommendation,” he noted.

Also, for patients who have STEMI, there is a new Class IIb recommendation that upfront P2Y12 inhibitors may be considered.

“This is also rather a weak recommendation. There isn’t a strong rationale to give a P2Y12 inhibitor it in ST elevation either. It’s also reasonable to wait,” he added.
 

Don’t rush cardiac arrest patients to the cath lab

Another update in the guidelines involves the management of patients with cardiac arrest who have been resuscitated. Dr. Byrne explained that these patients would all receive an immediate ECG, and if it is found that they have ST elevation, they would be sent immediately to the cath lab. But a series of randomized trials has suggested that for patients who don’t have ST elevation, it is not necessary to rush these patients to the cath lab.

“We’ve given a Class III recommendation for this, saying it may be better to stabilize the patients first in the ICU. This is in recognition that a large proportion of these patients turn out not to have an MI. They have had a cardiac arrest for another reason,” Dr. Byrne noted. “Moving them to the cath lab when they are still unstable could be harming these patients rather than helping them.”
 

Revascularization for multivessel disease

Dr. Byrne notes that revascularization remains a critical element in the care for patients with STEMI, and there is a new recommendation in this area for patients with multivessel disease.

“Up to half of patients presenting with STEMI have multivessel disease, and we now have five randomized trials to say that these patients should have complete revascularization rather than just the culprit vessel. There is a new Class I recommendation for this,” he said.

However, the optimal timing of revascularization (immediate vs. staged) has still not been investigated in adequately sized randomized trials, and no recommendation has been made on this, the task force notes.

Dr. Byrne commented: “If you want to do everything in one go, that’s fine, but it’s also okay to do the culprit lesion first and then the other vessels at a later date within 45 days. This might depend on individual circumstances. For example, if there are complex lesions or the vessels are heavily calcified, then it may be best to get the culprit lesion fixed first and let the patient recover, then bring them back in for the rest.”

He pointed out that the results of the MULTISTARS trial, which were not available when the task force was formulating the guidelines, were reported at the ESC Congress and confirmed their recommendation.
 

DAPT after PCI

On the duration of dual antiplatelet therapy (DAPT) after PCI, the new guidelines have largely retained prior recommendations for a default strategy of 12 months for the combination of aspirin and a P2Y12 inhibitor.

“This was the subject of some discussion, as there have been several trials now looking at shorter durations of DAPT and deescalating after a few months to just one of these treatments. And while there is a rationale to do this, we think it’s best to be kept as an alternative strategy rather than the default strategy,” Dr. Byrne said.

He explained that the trials of DAPT deescalation tended to enroll lower-risk patients, which reduced the generalizability of the results.

Most of the trials only randomly assigned patients to shorter durations of DAPT when they were event-free for some period, she said.

“This is a dynamic decision-making process and reflects the real world to some extent. We think it is best to recommend the standard aspirin and a P2Y12 inhibitor for the 12-month duration, but at 3 months, if the patient is doing well but you may be worried about bleeding risk, then you could decide to deescalate to single antiplatelet therapy,” she noted. “So, there is Class IIa recommendation that this can be considered, but it is not recommended as the default position.”
 

Polypill for secondary prevention

Another innovation in the new guidelines is a new Class IIa recommendation for prescription of a polypill containing secondary prevention medications for patients on discharge from hospital.

This recommendation follows a trial that showed that the use of such a polypill helps patients be more adherent to the therapies prescribed.

Byrne explains that such a polypill may contain aspirin, an ACE inhibitor, and a statin. Several varieties are available in most European countries, but they are not widely used.

On secondary prevention, he stressed, “Prevention of the next heart attack starts before the patient leaves hospital. It is important to make sure the patient has the right medication on board, including a high-dose, high-intensity statin, and has been referred to a cardiac rehabilitation program. These are largely maintained recommendations from previous guidelines, but they are very important.”

A version of this article appeared on Medscape.com.