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Gout and SGLT2 Inhibitors: Evidence Points to Reduced Need for ULT, Flare Drugs
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
WASHINGTON — Use of sodium-glucose cotransporter 2 inhibitors (SGLT2i) reduced the need for urate-lowering therapy (ULT) and gout flare therapies in people who had both type 2 diabetes (T2D) and gout, new research has found.
Data from a large US claims database showed that SGLT2i use was associated with a 31% lower rate of initiation of ULT. “This provides further support for the use of SLGT2i therapy in patients with gout, particularly those with high-risk multimorbidity and polypharmacy,” Greg Challener, MD, a postdoctoral fellow at the Rheumatology and Allergy Clinical Epidemiology Research Center, Massachusetts General Hospital, Boston, said in his presentation of the data at the annual meeting of the American College of Rheumatology.
The first agent of the SGLT2i class, dapagliflozin, was initially approved in the United States a decade ago for treating T2D. Since then, several other “flozins” have become available, and some have also received additional indications for heart failure and albuminuric chronic kidney disease. Several prior studies have linked SGLT2i use with lower rates of gout flares as well as lower likelihood of developing gout in the first place, although not all studies have found this benefit.
Asked about the clinical implications of the new data, Challener said in an interview that “I don’t think we’re quite at the point where this is changing gout management per se, but this just helps us understand that [SGT2is] may have a role at some point, maybe as a combination on top of another agent. Or, in some patients, it really may be enough if they’re already on an SGLT2i where we don’t need to jump to adding allopurinol. Maybe they have tophi, but they were just started on an SGLT2i and they’re not flaring. Typically, you would start those patients on allopurinol, but you could potentially just monitor them if they were just started on one of those [SGLT2i] agents.”
Asked to comment, session moderator J. Antonio Aviña-Zubieta, MD, PhD, head of the Division of Rheumatology at the University of British Columbia, Vancouver, Canada, and senior scientist at Arthritis Research Canada, said in an interview: “What I can see possibly happening when there’s more evidence is that SGLT2is may be used or even become standard of care as an adjuvant therapy to decrease flares, and by that, decrease the risk of complications.”
Reductions in ULT, Flares, and Healthcare Visits
The new study used administrative health data from the multicenter TriNetX Diamond network of electronic medical record and claims data from 92 healthcare sites with 212 million patients. Among those with both T2D and gout who were not taking ULT at baseline, a total of 16,104 initiated SGLT2is and 16,046 initiated glucagon-like peptide 1 receptor agonists (GLP-1 RA).
Propensity score matching was conducted for demographics including age, race, and sex; comorbidities; use of emergency, inpatient, and critical care services; medications; labs; and body mass index. That yielded 11,800 individuals each in the SGLT2i and GLP-1 RA groups.
Over 5 years, 9.9% of the SGLT2i group vs 13.4% of those using GLP-1 RA had initiated ULT, a significant difference with a hazard ratio (HR) of 0.69 (95% CI, 0.64-0.75). The risk for initiation of colchicine for gout flares was 4.7% with SGLT2i vs 6.0% for GLP-1 RA — also a significant difference with an HR of 0.74 (0.65-0.83).
Medical visits for gout occurred in 28.0% vs 28.4% of patients, which also reached statistical significance (HR, 0.94; 95% CI, 0.89-0.99).
Aviña-Zubieta, an author of one of the previous studies finding a reduction in gout flares with SGLT2i, said, “many patients do not want to start gout therapy until they start having more acute attacks. ... So, for a lot of people, it’s a burden taking another pill to prevent one attack. But, if you don’t treat it over time, the attacks come more often. So, can we still delay the initiation of therapy? If you’re not having that many flares, you’re decreasing the burden of the disease and polypharmacy, which I think is the potential benefit in the long run if you already have an indication for the therapy for diabetes. ... These data are supporting that.”
Indeed, Challener said these data can help in counseling patients. “Taking your SGLT2i for your heart failure and your diabetes is also providing some benefit for your gout, and we know that there is also cardiac benefit when gout is controlled.”
Challener and Aviña-Zubieta had no disclosures.
A version of this article first appeared on Medscape.com.
FROM ACR 2024
Angiotensin Receptor Blockers May Lead to Worse Outcomes in Celiac Disease
PHILADELPHIA — , according to a study presented at the American College of Gastroenterology (ACG) 2024 Annual Scientific Meeting.
The association may be related to the similar pathophysiology between ARB-associated enteropathy and celiac disease, though additional research is needed.
“Based on our findings, people should take caution when prescribing angiotensin receptor blockers to people with celiac disease,” said lead author Isabel Hujoel, MD, clinical assistant professor of gastroenterology and clinic director of the Celiac Disease Center at the University of Washington, Seattle.
“When we see someone with nonresponsive celiac disease, meaning persistent symptoms despite a gluten-free diet, I do think we should review their medication list, and if they’re on an ARB, we should consider a trial off those medications to see if they respond,” she said. “A primary care provider may choose other hypertensives as well.”
Hujoel and co-author Margaux Hujoel, PhD, a postdoctoral research fellow at Brigham and Women’s Hospital, Boston; Broad Institute, Cambridge; and Harvard Medical School, Boston, analyzed data from the National Institutes of Health’s All of Us, a large publicly available US longitudinal dataset.
The researchers conducted a survival analysis of time-to-first event after celiac disease diagnosis, allowing patients to have a time-dependent covariate of ARB use. They looked at outcomes such as iron deficiency, diarrhea, abdominal pain, vitamin deficiency, vitamin D deficiency, malabsorption, low hemoglobin, and weight loss.
The analysis included 1849 patients with celiac disease, including 1460 women and 389 men, with a median age of nearly 50 years at diagnosis. While the vast majority of patients (nearly 1600) didn’t take an ARB, 120 started one before celiac disease diagnosis and 142 started one after diagnosis.
Overall, taking an ARB was associated with increased hazard ratios [HRs] for low hemoglobin, iron deficiency, diarrhea, and abdominal pain. There weren’t increased risks for weight loss, malabsorption, or vitamin deficiencies.
When excluding those who had an ARB prescription before diagnosis, the HRs remained significantly higher for low hemoglobin (HR, 1.98) and iron deficiency (HR, 1.72) for those who started an ARB after diagnosis.
“The use of angiotensin receptor blockers may be associated with worse outcomes in the setting of celiac disease, specifically persistent symptoms and possibly poor small bowel healing as evidenced by malabsorption,” Hujoel said.
Future studies could look specifically at losartan, which was the most common ARB prescribed in this analysis, she said. Other studies could also analyze different patient outcomes, whether patients were on a gluten-free diet, medication adherence, and recurrence or persistence of symptoms rather than initial occurrence. The associations between ARB use and celiac disease could shift among patients who are in remission, for instance.
“ARBs are some of the most widely used medications, so studies like these can help people to understand that they may have symptoms but not know it’s related to their medication. Public awareness of this fact is key,” said Patricia Jones, MD, a hepatologist and associate professor of clinical medicine at the University of Miami Miller School of Medicine, Miami. Jones co-moderated the plenary session on small intestine, functional, and liver research.
“There are many types of antihypertensives, so while ARBs are used often, other options are available if people have symptoms, especially if they have worsening symptoms with celiac disease,” she said. “It’s important to make changes in your practice.”
The study was named an ACG Newsworthy Abstract. Isabel Hujoel and Patricia Jones reported no relevant disclosures.
A version of this article appeared on Medscape.com.
PHILADELPHIA — , according to a study presented at the American College of Gastroenterology (ACG) 2024 Annual Scientific Meeting.
The association may be related to the similar pathophysiology between ARB-associated enteropathy and celiac disease, though additional research is needed.
“Based on our findings, people should take caution when prescribing angiotensin receptor blockers to people with celiac disease,” said lead author Isabel Hujoel, MD, clinical assistant professor of gastroenterology and clinic director of the Celiac Disease Center at the University of Washington, Seattle.
“When we see someone with nonresponsive celiac disease, meaning persistent symptoms despite a gluten-free diet, I do think we should review their medication list, and if they’re on an ARB, we should consider a trial off those medications to see if they respond,” she said. “A primary care provider may choose other hypertensives as well.”
Hujoel and co-author Margaux Hujoel, PhD, a postdoctoral research fellow at Brigham and Women’s Hospital, Boston; Broad Institute, Cambridge; and Harvard Medical School, Boston, analyzed data from the National Institutes of Health’s All of Us, a large publicly available US longitudinal dataset.
The researchers conducted a survival analysis of time-to-first event after celiac disease diagnosis, allowing patients to have a time-dependent covariate of ARB use. They looked at outcomes such as iron deficiency, diarrhea, abdominal pain, vitamin deficiency, vitamin D deficiency, malabsorption, low hemoglobin, and weight loss.
The analysis included 1849 patients with celiac disease, including 1460 women and 389 men, with a median age of nearly 50 years at diagnosis. While the vast majority of patients (nearly 1600) didn’t take an ARB, 120 started one before celiac disease diagnosis and 142 started one after diagnosis.
Overall, taking an ARB was associated with increased hazard ratios [HRs] for low hemoglobin, iron deficiency, diarrhea, and abdominal pain. There weren’t increased risks for weight loss, malabsorption, or vitamin deficiencies.
When excluding those who had an ARB prescription before diagnosis, the HRs remained significantly higher for low hemoglobin (HR, 1.98) and iron deficiency (HR, 1.72) for those who started an ARB after diagnosis.
“The use of angiotensin receptor blockers may be associated with worse outcomes in the setting of celiac disease, specifically persistent symptoms and possibly poor small bowel healing as evidenced by malabsorption,” Hujoel said.
Future studies could look specifically at losartan, which was the most common ARB prescribed in this analysis, she said. Other studies could also analyze different patient outcomes, whether patients were on a gluten-free diet, medication adherence, and recurrence or persistence of symptoms rather than initial occurrence. The associations between ARB use and celiac disease could shift among patients who are in remission, for instance.
“ARBs are some of the most widely used medications, so studies like these can help people to understand that they may have symptoms but not know it’s related to their medication. Public awareness of this fact is key,” said Patricia Jones, MD, a hepatologist and associate professor of clinical medicine at the University of Miami Miller School of Medicine, Miami. Jones co-moderated the plenary session on small intestine, functional, and liver research.
“There are many types of antihypertensives, so while ARBs are used often, other options are available if people have symptoms, especially if they have worsening symptoms with celiac disease,” she said. “It’s important to make changes in your practice.”
The study was named an ACG Newsworthy Abstract. Isabel Hujoel and Patricia Jones reported no relevant disclosures.
A version of this article appeared on Medscape.com.
PHILADELPHIA — , according to a study presented at the American College of Gastroenterology (ACG) 2024 Annual Scientific Meeting.
The association may be related to the similar pathophysiology between ARB-associated enteropathy and celiac disease, though additional research is needed.
“Based on our findings, people should take caution when prescribing angiotensin receptor blockers to people with celiac disease,” said lead author Isabel Hujoel, MD, clinical assistant professor of gastroenterology and clinic director of the Celiac Disease Center at the University of Washington, Seattle.
“When we see someone with nonresponsive celiac disease, meaning persistent symptoms despite a gluten-free diet, I do think we should review their medication list, and if they’re on an ARB, we should consider a trial off those medications to see if they respond,” she said. “A primary care provider may choose other hypertensives as well.”
Hujoel and co-author Margaux Hujoel, PhD, a postdoctoral research fellow at Brigham and Women’s Hospital, Boston; Broad Institute, Cambridge; and Harvard Medical School, Boston, analyzed data from the National Institutes of Health’s All of Us, a large publicly available US longitudinal dataset.
The researchers conducted a survival analysis of time-to-first event after celiac disease diagnosis, allowing patients to have a time-dependent covariate of ARB use. They looked at outcomes such as iron deficiency, diarrhea, abdominal pain, vitamin deficiency, vitamin D deficiency, malabsorption, low hemoglobin, and weight loss.
The analysis included 1849 patients with celiac disease, including 1460 women and 389 men, with a median age of nearly 50 years at diagnosis. While the vast majority of patients (nearly 1600) didn’t take an ARB, 120 started one before celiac disease diagnosis and 142 started one after diagnosis.
Overall, taking an ARB was associated with increased hazard ratios [HRs] for low hemoglobin, iron deficiency, diarrhea, and abdominal pain. There weren’t increased risks for weight loss, malabsorption, or vitamin deficiencies.
When excluding those who had an ARB prescription before diagnosis, the HRs remained significantly higher for low hemoglobin (HR, 1.98) and iron deficiency (HR, 1.72) for those who started an ARB after diagnosis.
“The use of angiotensin receptor blockers may be associated with worse outcomes in the setting of celiac disease, specifically persistent symptoms and possibly poor small bowel healing as evidenced by malabsorption,” Hujoel said.
Future studies could look specifically at losartan, which was the most common ARB prescribed in this analysis, she said. Other studies could also analyze different patient outcomes, whether patients were on a gluten-free diet, medication adherence, and recurrence or persistence of symptoms rather than initial occurrence. The associations between ARB use and celiac disease could shift among patients who are in remission, for instance.
“ARBs are some of the most widely used medications, so studies like these can help people to understand that they may have symptoms but not know it’s related to their medication. Public awareness of this fact is key,” said Patricia Jones, MD, a hepatologist and associate professor of clinical medicine at the University of Miami Miller School of Medicine, Miami. Jones co-moderated the plenary session on small intestine, functional, and liver research.
“There are many types of antihypertensives, so while ARBs are used often, other options are available if people have symptoms, especially if they have worsening symptoms with celiac disease,” she said. “It’s important to make changes in your practice.”
The study was named an ACG Newsworthy Abstract. Isabel Hujoel and Patricia Jones reported no relevant disclosures.
A version of this article appeared on Medscape.com.
FROM ACG 2024
On Second Thought: Aspirin for Primary Prevention — What We Really Know
This transcript has been edited for clarity.
Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients.
That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).
Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy.
For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal.
People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day.
Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.
Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell.
More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.
We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does.
If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing.
The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead.
The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine.
That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.
But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?
Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients.
That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).
Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy.
For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal.
People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day.
Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.
Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell.
More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.
We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does.
If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing.
The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead.
The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine.
That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.
But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?
Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Our recommendations vis-à-vis aspirin have evolved at a dizzying pace. The young’uns watching us right now don’t know what things were like in the 1980s. The Reagan era was a wild, heady time where nuclear war was imminent and we didn’t prescribe aspirin to patients.
That only started in 1988, which was a banner year in human history. Not because a number of doves were incinerated by the lighting of the Olympic torch at the Seoul Olympics — look it up if you don’t know what I’m talking about — but because 1988 saw the publication of the ISIS-2 trial, which first showed a mortality benefit to prescribing aspirin post–myocardial infarction (MI).
Giving patients aspirin during or after a heart attack is not controversial. It’s one of the few things in this business that isn’t, but that’s secondary prevention — treating somebody after they develop a disease. Primary prevention, treating them before they have their incident event, is a very different ballgame. Here, things are messy.
For one thing, the doses used have been very inconsistent. We should point out that the reason for 81 mg of aspirin is very arbitrary and is rooted in the old apothecary system of weights and measurements. A standard dose of aspirin was 5 grains, where 20 grains made 1 scruple, 3 scruples made 1 dram, 8 drams made 1 oz, and 12 oz made 1 lb - because screw you, metric system. Therefore, 5 grains was 325 mg of aspirin, and 1 quarter of the standard dose became 81 mg if you rounded out the decimal.
People have tried all kinds of dosing structures with aspirin prophylaxis. The Physicians’ Health Study used a full-dose aspirin, 325 mg every 2 days, while the Hypertension Optimal Treatment (HOT) trial tested 75 mg daily and the Women’s Health Study tested 100 mg, but every other day.
Ironically, almost no one has studied 81 mg every day, which is weird if you think about it. The bigger problem here is not the variability of doses used, but the discrepancy when you look at older vs newer studies.
Older studies, like the Physicians’ Health Study, did show a benefit, at least in the subgroup of patients over age 50 years, which is probably where the “everybody over 50 should be taking an aspirin” idea comes from, at least as near as I can tell.
More recent studies, like the Women’s Health Study, ASPREE, or ASPIRE, didn’t show a benefit. I know what you’re thinking: Newer stuff is always better. That’s why you should never trust anybody over age 40 years. The context of primary prevention studies has changed. In the ‘80s and ‘90s, people smoked more and we didn’t have the same medications that we have today. We talked about all this in the beta-blocker video to explain why beta-blockers don’t seem to have a benefit post MI.
We have a similar issue here. The magnitude of the benefit with aspirin primary prevention has decreased because we’re all just healthier overall. So, yay! Progress! Here’s where the numbers matter. No one is saying that aspirin doesn’t help. It does.
If we look at the 2019 meta-analysis published in JAMA, there is a cardiovascular benefit. The numbers bear that out. I know you’re all here for the math, so here we go. Aspirin reduced the composite cardiovascular endpoint from 65.2 to 60.2 events per 10,000 patient-years; or to put it more meaningfully in absolute risk reduction terms, because that’s my jam, an absolute risk reduction of 0.41%, which means a number needed to treat of 241, which is okay-ish. It’s not super-great, but it may be justifiable for something that costs next to nothing.
The tradeoff is bleeding. Major bleeding increased from 16.4 to 23.1 bleeds per 10,000 patient-years, or an absolute risk increase of 0.47%, which is a number needed to harm of 210. That’s the problem. Aspirin does prevent heart disease. The benefit is small, for sure, but the real problem is that it’s outweighed by the risk of bleeding, so you’re not really coming out ahead.
The real tragedy here is that the public is locked into this idea of everyone over age 50 years should be taking an aspirin. Even today, even though guidelines have recommended against aspirin for primary prevention for some time, data from the National Health Interview Survey sample found that nearly one in three older adults take aspirin for primary prevention when they shouldn’t be. That’s a large number of people. That’s millions of Americans — and Canadians, but nobody cares about us. It’s fine.
That’s the point. We’re not debunking aspirin. It does work. The benefits are just really small in a primary prevention population and offset by the admittedly also really small risks of bleeding. It’s a tradeoff that doesn’t really work in your favor.
But that’s aspirin for cardiovascular disease. When it comes to cancer or DVT prophylaxis, that’s another really interesting story. We might have to save that for another time. Do I know how to tease a sequel or what?
Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Social Adversity Increases Mortality Risk in Patients With Pulmonary Hypertension
BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population.
A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.
“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.
“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.
Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.
The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).
Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028).
The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.
Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.
The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.
That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.
Dr. Biavati and Dr. Jain reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population.
A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.
“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.
“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.
Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.
The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).
Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028).
The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.
Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.
The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.
That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.
Dr. Biavati and Dr. Jain reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
BOSTON — Social adversity is associated with worse survival among patients with pulmonary hypertension (PH), according to a new retrospective study of a New York City population.
A sub-analysis of both HIV+ and HIV– patients showed worse mortality outcomes with social adversity in both groups.
“Almost the majority of patients that we treat have either some social adversity or no insurance or are undocumented, so as a group of residents, we decided to study the impact of these factors on their health and the care that can be provided. We started using the two cohorts and now we keep it going with every new resident,” said Luca Biavati, MD, who presented the study at the CHEST Annual Meeting.
“The presence of any form of socioeconomic disadvantage is negatively impacting care and for a large part of the population, there are some factors that could probably be addressed by either an institutional or hospital policy,” said Dr. Biavati, who is an internal medicine resident at Jacobi Medical Center, New York.
Other factors are more difficult to address, such as lack of education. “[Some patients] don’t understand the gravity of their issue and medical condition until it’s too late, and then they’re not fit enough for the treatment, or just because of the social situation, they cannot qualify for advanced therapies,” said Dr. Biavati.
The researchers established two cohorts: One consisting of patients with HIV and heart failure who may or may not have had PH and one comprising patients with PH with or without HIV and heart failure. In the HIV/heart failure group, PH without social adversity was associated with a nearly threefold increase in all-cause mortality (hazard ratio [HR], 2.83; P = .004), whereas PH with social adversity was linked to a more than sevenfold increase in all-cause mortality (HR, 7.14; P < .001). Social adversity without PA was associated with a more than fourfold increase (HR, 4.47; P < .001).
Within the PH cohort, social adversity was associated with lower survival (P < .001). When the researchers broke down the results by types of social adversity, they found statistically significant relationships between greater mortality risk and economic instability within the HIV+ population (HR, 2.59; P = .040), transportation issues within the HIV– population (HR, 12.8; P < .001), and lack of social or family support within both the HIV– (HR, 5.49; P < .001) and the HIV+ population (HR, 2.03; P = .028).
The research has prompted interventions, which are now being studied at the institution, according to Dr. Biavati. “We have a policy of giving medications in bags when we discharge a patient with a social adversity. We literally go to the pharmacy, bring up the bag of medication, and we [put it] in their hands before they leave the hospital. They get a 1- or 3-month supply, depending on the medication, and then we usually discharge them with a clinical appointment already scheduled with either a pulmonary or primary care provider, and we usually call them before every appointment to confirm that they’re coming. That increases the chances of some success, but there’s still a very long way to go,” said Dr. Biavati.
Dr. Biavati was blinded to the results of the intervention, so he could not report on whether it was working. “But I can tell you that I’ve had busier clinics, so hopefully that means that they’re showing up more,” he said.
The problem is complex, according to Sandeep Jain, MD, who moderated the session. “Social adversity means lack of education. Lack of education means lack of compliance. Lack of compliance means what can you do if people are not taking medications? So it’s all matched together. It’s all lack of education and lack of money, lack of family support. And these drugs they have to take every single day. It’s not that easy. It’s very easy for us to say I had antiretroviral treatment for 6 months. It is almost impossible to continue regular treatment for that long [for a patient with social adversity]. You can’t blame them if they aren’t taking treatments. It’s very difficult for them,” said Dr. Jain.
That underscores the need for interventions that can address the needs of patients with social adversity. “We have to [practice] medicine considering the social situation of the patient and not just the medicine that we study in books. That’s kind of what we are faced with every day. We have therapies, and then life happens. It’s much harder to care for those patients,” said Dr. Biavati.
Dr. Biavati and Dr. Jain reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM CHEST 2024
AHA Scientific Statement Links Three Common Cardiovascular Diseases to Cognitive Decline, Dementia
The statement includes an extensive research review and offers compelling evidence of the inextricable link between heart health and brain health, which investigators said underscores the benefit of early intervention.
The cumulative evidence “confirms that the trajectories of cardiac health and brain health are inextricably intertwined through modifiable and nonmodifiable factors,” the authors wrote.
Investigators say the findings reinforce the message that addressing cardiovascular health early in life may deter the onset or progression of cognitive impairment later on.
And the earlier this is done, the better, said lead author Fernando D. Testai, MD, PhD, a professor of neurology and the vascular neurology section head, Department of Neurology and Rehabilitation, University of Illinois, Chicago.
The statement was published online in Stroke.
Bridging the Research Gap
It’s well known that there’s a bidirectional relationship between heart and brain function. For example, heart failure can lead to decreased blood flow that can damage the brain, and stroke in some areas of the brain can affect the heart.
However, that’s only part of the puzzle and doesn’t address all the gaps in the understanding of how cardiovascular disease contributes to cognition, said Testai.
“What we’re trying to do here is to go one step further and describe other connections between the heart and the brain,” he said.
Investigators carried out an extensive PubMed search for heart failure, atrial fibrillation, and coronary heart disease. Researchers detailed the frequency of each condition, mechanisms by which they might cause cognitive impairment, and prospects for prevention and treatment to maintain brain health.
A recurring theme in the paper is the role of inflammation. Evidence shows there are “remarkable similarities in the inflammatory response that takes place,” with both cardiac disease and cognitive decline, said Testai.
Another potential shared mechanism relates to biomarkers, particularly amyloid, which is strongly linked to Alzheimer’s disease.
“But some studies show amyloid can also be present in the heart, especially in patients who have decreased ejection fraction,” said Testai.
Robust Heart-Brain Connection
The statement’s authors collected a substantial amount of evidence showing vascular risk factors such as hypertension and diabetes “can change how the brain processes and clears up amyloid,” Testai added.
The paper also provides a compilation of evidence of shared genetic predispositions when it comes to heart and brain disorders.
“We noticed that some genetic signatures that have historically been associated with heart disease seem to also correlate with structural changes in the brain. That means that at the end of the day, some patients may be born with a genetic predisposition to developing both conditions,” said Testai.
This indicates that the link between the two organs “begins as early as conception” and underscores the importance of adopting healthy lifestyle habits as early as possible, he added.
“That means you can avoid bad habits that eventually lead to hypertension, diabetes, and cholesterol, that eventually will lead to cardiac disease, which eventually will lead to stroke, which eventually will lead to cognitive decline,” Testai noted.
However, cardiovascular health is more complicated than having good genes and adhering to a healthy lifestyle. It’s not clear, for example, why some people who should be predisposed to developing heart disease do not develop it, something Testai refers to as enhanced “resilience.”
For example, Hispanic or Latino patients, who have relatively poor cardiovascular risk factor profiles, seem to be less susceptible to developing cardiac disease.
More Research Needed
While genetics may partly explain the paradox, Testai believes other protective factors are at play, including strong social support networks.
Testai referred to the AHA’s “Life’s Essential 8” — the eight components of cardiovascular health. These include a healthy diet, participation in physical activity, nicotine avoidance, healthy sleep, healthy weight, and healthy levels of blood lipids, blood glucose, and blood pressure.
More evidence is needed to show that effective management of cardiac disease positively affects cognition. Currently, cognitive measures are rarely included in studies examining various heart disease treatments, said Testai.
“There should probably be an effort to include brain health outcomes in some of the cardiac literature to make sure we can also measure whether the intervention in the heart leads to an advantage for the brain,” he said.
More research is also needed to determine whether immunomodulation has a beneficial effect on the cognitive trajectory, the statement’s authors noted.
They point out that the interpretation and generalizability of the studies described in the statement are confounded by disparate methodologies, including small sample sizes, cross-sectional designs, and underrepresentation of Black and Hispanic individuals.
‘An Important Step’
Reached for a comment, Natalia S. Rost, MD, Chief of the Stroke Division at Massachusetts General Hospital and professor of neurology at Harvard Medical School, both in Boston, said this paper “is an important step” in terms of pulling together pertinent information on the topic of heart-brain health.
She praised the authors for gathering evidence on risk factors related to atrial fibrillation, heart failure, and coronary heart disease, which is “the part of the puzzle that is controllable.”
This helps reinforce the message that controlling vascular risk factors helps with brain health, said Rost.
But brain health is “much more complex than just vascular health,” she said. It includes other elements such as freedom from epilepsy, migraine, traumatic brain injury, and adult learning disabilities.
No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
The statement includes an extensive research review and offers compelling evidence of the inextricable link between heart health and brain health, which investigators said underscores the benefit of early intervention.
The cumulative evidence “confirms that the trajectories of cardiac health and brain health are inextricably intertwined through modifiable and nonmodifiable factors,” the authors wrote.
Investigators say the findings reinforce the message that addressing cardiovascular health early in life may deter the onset or progression of cognitive impairment later on.
And the earlier this is done, the better, said lead author Fernando D. Testai, MD, PhD, a professor of neurology and the vascular neurology section head, Department of Neurology and Rehabilitation, University of Illinois, Chicago.
The statement was published online in Stroke.
Bridging the Research Gap
It’s well known that there’s a bidirectional relationship between heart and brain function. For example, heart failure can lead to decreased blood flow that can damage the brain, and stroke in some areas of the brain can affect the heart.
However, that’s only part of the puzzle and doesn’t address all the gaps in the understanding of how cardiovascular disease contributes to cognition, said Testai.
“What we’re trying to do here is to go one step further and describe other connections between the heart and the brain,” he said.
Investigators carried out an extensive PubMed search for heart failure, atrial fibrillation, and coronary heart disease. Researchers detailed the frequency of each condition, mechanisms by which they might cause cognitive impairment, and prospects for prevention and treatment to maintain brain health.
A recurring theme in the paper is the role of inflammation. Evidence shows there are “remarkable similarities in the inflammatory response that takes place,” with both cardiac disease and cognitive decline, said Testai.
Another potential shared mechanism relates to biomarkers, particularly amyloid, which is strongly linked to Alzheimer’s disease.
“But some studies show amyloid can also be present in the heart, especially in patients who have decreased ejection fraction,” said Testai.
Robust Heart-Brain Connection
The statement’s authors collected a substantial amount of evidence showing vascular risk factors such as hypertension and diabetes “can change how the brain processes and clears up amyloid,” Testai added.
The paper also provides a compilation of evidence of shared genetic predispositions when it comes to heart and brain disorders.
“We noticed that some genetic signatures that have historically been associated with heart disease seem to also correlate with structural changes in the brain. That means that at the end of the day, some patients may be born with a genetic predisposition to developing both conditions,” said Testai.
This indicates that the link between the two organs “begins as early as conception” and underscores the importance of adopting healthy lifestyle habits as early as possible, he added.
“That means you can avoid bad habits that eventually lead to hypertension, diabetes, and cholesterol, that eventually will lead to cardiac disease, which eventually will lead to stroke, which eventually will lead to cognitive decline,” Testai noted.
However, cardiovascular health is more complicated than having good genes and adhering to a healthy lifestyle. It’s not clear, for example, why some people who should be predisposed to developing heart disease do not develop it, something Testai refers to as enhanced “resilience.”
For example, Hispanic or Latino patients, who have relatively poor cardiovascular risk factor profiles, seem to be less susceptible to developing cardiac disease.
More Research Needed
While genetics may partly explain the paradox, Testai believes other protective factors are at play, including strong social support networks.
Testai referred to the AHA’s “Life’s Essential 8” — the eight components of cardiovascular health. These include a healthy diet, participation in physical activity, nicotine avoidance, healthy sleep, healthy weight, and healthy levels of blood lipids, blood glucose, and blood pressure.
More evidence is needed to show that effective management of cardiac disease positively affects cognition. Currently, cognitive measures are rarely included in studies examining various heart disease treatments, said Testai.
“There should probably be an effort to include brain health outcomes in some of the cardiac literature to make sure we can also measure whether the intervention in the heart leads to an advantage for the brain,” he said.
More research is also needed to determine whether immunomodulation has a beneficial effect on the cognitive trajectory, the statement’s authors noted.
They point out that the interpretation and generalizability of the studies described in the statement are confounded by disparate methodologies, including small sample sizes, cross-sectional designs, and underrepresentation of Black and Hispanic individuals.
‘An Important Step’
Reached for a comment, Natalia S. Rost, MD, Chief of the Stroke Division at Massachusetts General Hospital and professor of neurology at Harvard Medical School, both in Boston, said this paper “is an important step” in terms of pulling together pertinent information on the topic of heart-brain health.
She praised the authors for gathering evidence on risk factors related to atrial fibrillation, heart failure, and coronary heart disease, which is “the part of the puzzle that is controllable.”
This helps reinforce the message that controlling vascular risk factors helps with brain health, said Rost.
But brain health is “much more complex than just vascular health,” she said. It includes other elements such as freedom from epilepsy, migraine, traumatic brain injury, and adult learning disabilities.
No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
The statement includes an extensive research review and offers compelling evidence of the inextricable link between heart health and brain health, which investigators said underscores the benefit of early intervention.
The cumulative evidence “confirms that the trajectories of cardiac health and brain health are inextricably intertwined through modifiable and nonmodifiable factors,” the authors wrote.
Investigators say the findings reinforce the message that addressing cardiovascular health early in life may deter the onset or progression of cognitive impairment later on.
And the earlier this is done, the better, said lead author Fernando D. Testai, MD, PhD, a professor of neurology and the vascular neurology section head, Department of Neurology and Rehabilitation, University of Illinois, Chicago.
The statement was published online in Stroke.
Bridging the Research Gap
It’s well known that there’s a bidirectional relationship between heart and brain function. For example, heart failure can lead to decreased blood flow that can damage the brain, and stroke in some areas of the brain can affect the heart.
However, that’s only part of the puzzle and doesn’t address all the gaps in the understanding of how cardiovascular disease contributes to cognition, said Testai.
“What we’re trying to do here is to go one step further and describe other connections between the heart and the brain,” he said.
Investigators carried out an extensive PubMed search for heart failure, atrial fibrillation, and coronary heart disease. Researchers detailed the frequency of each condition, mechanisms by which they might cause cognitive impairment, and prospects for prevention and treatment to maintain brain health.
A recurring theme in the paper is the role of inflammation. Evidence shows there are “remarkable similarities in the inflammatory response that takes place,” with both cardiac disease and cognitive decline, said Testai.
Another potential shared mechanism relates to biomarkers, particularly amyloid, which is strongly linked to Alzheimer’s disease.
“But some studies show amyloid can also be present in the heart, especially in patients who have decreased ejection fraction,” said Testai.
Robust Heart-Brain Connection
The statement’s authors collected a substantial amount of evidence showing vascular risk factors such as hypertension and diabetes “can change how the brain processes and clears up amyloid,” Testai added.
The paper also provides a compilation of evidence of shared genetic predispositions when it comes to heart and brain disorders.
“We noticed that some genetic signatures that have historically been associated with heart disease seem to also correlate with structural changes in the brain. That means that at the end of the day, some patients may be born with a genetic predisposition to developing both conditions,” said Testai.
This indicates that the link between the two organs “begins as early as conception” and underscores the importance of adopting healthy lifestyle habits as early as possible, he added.
“That means you can avoid bad habits that eventually lead to hypertension, diabetes, and cholesterol, that eventually will lead to cardiac disease, which eventually will lead to stroke, which eventually will lead to cognitive decline,” Testai noted.
However, cardiovascular health is more complicated than having good genes and adhering to a healthy lifestyle. It’s not clear, for example, why some people who should be predisposed to developing heart disease do not develop it, something Testai refers to as enhanced “resilience.”
For example, Hispanic or Latino patients, who have relatively poor cardiovascular risk factor profiles, seem to be less susceptible to developing cardiac disease.
More Research Needed
While genetics may partly explain the paradox, Testai believes other protective factors are at play, including strong social support networks.
Testai referred to the AHA’s “Life’s Essential 8” — the eight components of cardiovascular health. These include a healthy diet, participation in physical activity, nicotine avoidance, healthy sleep, healthy weight, and healthy levels of blood lipids, blood glucose, and blood pressure.
More evidence is needed to show that effective management of cardiac disease positively affects cognition. Currently, cognitive measures are rarely included in studies examining various heart disease treatments, said Testai.
“There should probably be an effort to include brain health outcomes in some of the cardiac literature to make sure we can also measure whether the intervention in the heart leads to an advantage for the brain,” he said.
More research is also needed to determine whether immunomodulation has a beneficial effect on the cognitive trajectory, the statement’s authors noted.
They point out that the interpretation and generalizability of the studies described in the statement are confounded by disparate methodologies, including small sample sizes, cross-sectional designs, and underrepresentation of Black and Hispanic individuals.
‘An Important Step’
Reached for a comment, Natalia S. Rost, MD, Chief of the Stroke Division at Massachusetts General Hospital and professor of neurology at Harvard Medical School, both in Boston, said this paper “is an important step” in terms of pulling together pertinent information on the topic of heart-brain health.
She praised the authors for gathering evidence on risk factors related to atrial fibrillation, heart failure, and coronary heart disease, which is “the part of the puzzle that is controllable.”
This helps reinforce the message that controlling vascular risk factors helps with brain health, said Rost.
But brain health is “much more complex than just vascular health,” she said. It includes other elements such as freedom from epilepsy, migraine, traumatic brain injury, and adult learning disabilities.
No relevant conflicts of interest were disclosed.
A version of this article first appeared on Medscape.com.
FROM STROKE
Can AI Improve Cardiomyopathy Detection in Pregnant Women?
TOPLINE:
Artificial intelligence (AI)–guided screening using digital stethoscopes doubled the detection of left ventricular systolic dysfunction (LVSD) in pregnant and postpartum women in Nigeria. Cardiomyopathy during pregnancy and post partum is challenging to diagnose because of symptom overlap with normal pregnancy changes. AI-guided screening showed a significant improvement in diagnosis rates, compared with usual care.
METHODOLOGY:
- Researchers conducted an open-label, randomized clinical trial involving 1232 pregnant and postpartum women in Nigeria.
- Participants were randomized to either AI-guided screening using digital stethoscopes and 12-lead ECGs or usual care.
- The primary outcome was the identification of LVSD confirmed by echocardiography.
- Secondary outcomes were AI model performance across subgroups and the effectiveness of AI in identifying various levels of LVSD.
TAKEAWAY:
- AI-guided screening using digital stethoscopes detected LVSD in 4.1% of participants, compared with 2.0% of controls (P = .032).
- The 12-lead AI-ECG model detected LVSD in 3.4% of participants in the intervention arm, compared with 2.0% of those in the control arm (P = .125).
- No serious adverse events related to study participation were reported.
- The study highlighted the potential of AI-guided screening to improve the diagnosis of pregnancy-related cardiomyopathy.
IN PRACTICE:
“Delays in the diagnosis of cardiomyopathy during the peripartum period is associated with poorer outcomes as such, it is imperative that we are able to identify cardiac dysfunction early so that appropriate care can be initiated to reduce associated adverse maternal and infant outcomes,” wrote the authors of the study.
SOURCE:
This study was led by Demilade A. Adedinsewo, MBchB, Mayo Clinic in Jacksonville, Florida. It was published online in Nature Medicine.
LIMITATIONS:
The study’s pragmatic design and enrollment at teaching hospitals with echocardiography capabilities limited generalizability. Two thirds of participants were in the third trimester or postpartum at study entry, which limited follow-up visits. The study did not require completion of all seven visits, which led to potential attrition bias. The selected cutoff for LVSD (left ventricular ejection fraction < 50%) did not match the original model specifications, which potentially affected results.
DISCLOSURES:
Dr. Adedinsewo disclosed receiving grants from the Mayo Clinic BIRCWH program funded by the National Institutes of Health. Two coauthors reported holding patents for AI algorithms licensed to Anumana, AliveCor, and Eko Health. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Artificial intelligence (AI)–guided screening using digital stethoscopes doubled the detection of left ventricular systolic dysfunction (LVSD) in pregnant and postpartum women in Nigeria. Cardiomyopathy during pregnancy and post partum is challenging to diagnose because of symptom overlap with normal pregnancy changes. AI-guided screening showed a significant improvement in diagnosis rates, compared with usual care.
METHODOLOGY:
- Researchers conducted an open-label, randomized clinical trial involving 1232 pregnant and postpartum women in Nigeria.
- Participants were randomized to either AI-guided screening using digital stethoscopes and 12-lead ECGs or usual care.
- The primary outcome was the identification of LVSD confirmed by echocardiography.
- Secondary outcomes were AI model performance across subgroups and the effectiveness of AI in identifying various levels of LVSD.
TAKEAWAY:
- AI-guided screening using digital stethoscopes detected LVSD in 4.1% of participants, compared with 2.0% of controls (P = .032).
- The 12-lead AI-ECG model detected LVSD in 3.4% of participants in the intervention arm, compared with 2.0% of those in the control arm (P = .125).
- No serious adverse events related to study participation were reported.
- The study highlighted the potential of AI-guided screening to improve the diagnosis of pregnancy-related cardiomyopathy.
IN PRACTICE:
“Delays in the diagnosis of cardiomyopathy during the peripartum period is associated with poorer outcomes as such, it is imperative that we are able to identify cardiac dysfunction early so that appropriate care can be initiated to reduce associated adverse maternal and infant outcomes,” wrote the authors of the study.
SOURCE:
This study was led by Demilade A. Adedinsewo, MBchB, Mayo Clinic in Jacksonville, Florida. It was published online in Nature Medicine.
LIMITATIONS:
The study’s pragmatic design and enrollment at teaching hospitals with echocardiography capabilities limited generalizability. Two thirds of participants were in the third trimester or postpartum at study entry, which limited follow-up visits. The study did not require completion of all seven visits, which led to potential attrition bias. The selected cutoff for LVSD (left ventricular ejection fraction < 50%) did not match the original model specifications, which potentially affected results.
DISCLOSURES:
Dr. Adedinsewo disclosed receiving grants from the Mayo Clinic BIRCWH program funded by the National Institutes of Health. Two coauthors reported holding patents for AI algorithms licensed to Anumana, AliveCor, and Eko Health. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
TOPLINE:
Artificial intelligence (AI)–guided screening using digital stethoscopes doubled the detection of left ventricular systolic dysfunction (LVSD) in pregnant and postpartum women in Nigeria. Cardiomyopathy during pregnancy and post partum is challenging to diagnose because of symptom overlap with normal pregnancy changes. AI-guided screening showed a significant improvement in diagnosis rates, compared with usual care.
METHODOLOGY:
- Researchers conducted an open-label, randomized clinical trial involving 1232 pregnant and postpartum women in Nigeria.
- Participants were randomized to either AI-guided screening using digital stethoscopes and 12-lead ECGs or usual care.
- The primary outcome was the identification of LVSD confirmed by echocardiography.
- Secondary outcomes were AI model performance across subgroups and the effectiveness of AI in identifying various levels of LVSD.
TAKEAWAY:
- AI-guided screening using digital stethoscopes detected LVSD in 4.1% of participants, compared with 2.0% of controls (P = .032).
- The 12-lead AI-ECG model detected LVSD in 3.4% of participants in the intervention arm, compared with 2.0% of those in the control arm (P = .125).
- No serious adverse events related to study participation were reported.
- The study highlighted the potential of AI-guided screening to improve the diagnosis of pregnancy-related cardiomyopathy.
IN PRACTICE:
“Delays in the diagnosis of cardiomyopathy during the peripartum period is associated with poorer outcomes as such, it is imperative that we are able to identify cardiac dysfunction early so that appropriate care can be initiated to reduce associated adverse maternal and infant outcomes,” wrote the authors of the study.
SOURCE:
This study was led by Demilade A. Adedinsewo, MBchB, Mayo Clinic in Jacksonville, Florida. It was published online in Nature Medicine.
LIMITATIONS:
The study’s pragmatic design and enrollment at teaching hospitals with echocardiography capabilities limited generalizability. Two thirds of participants were in the third trimester or postpartum at study entry, which limited follow-up visits. The study did not require completion of all seven visits, which led to potential attrition bias. The selected cutoff for LVSD (left ventricular ejection fraction < 50%) did not match the original model specifications, which potentially affected results.
DISCLOSURES:
Dr. Adedinsewo disclosed receiving grants from the Mayo Clinic BIRCWH program funded by the National Institutes of Health. Two coauthors reported holding patents for AI algorithms licensed to Anumana, AliveCor, and Eko Health. Additional disclosures are noted in the original article.
This article was created using several editorial tools, including AI, as part of the process. Human editors reviewed this content before publication. A version of this article first appeared on Medscape.com.
New AFib Guidelines Address Underlying Illness, Comorbidities
LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.
, Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.
It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.
Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
Class I Recommendation
In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.
Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.
Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.
Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.
However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care.
These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.
Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1.
The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.
In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.
For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.
The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF.
The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
Pathways Are Appropriate for All Patients
A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.
The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.
“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.
This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
A version of this article first appeared on Medscape.com.
LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.
, Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.
It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.
Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
Class I Recommendation
In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.
Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.
Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.
Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.
However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care.
These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.
Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1.
The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.
In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.
For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.
The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF.
The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
Pathways Are Appropriate for All Patients
A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.
The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.
“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.
This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
A version of this article first appeared on Medscape.com.
LONDON — Updated guidelines for the management of atrial fibrillation released by the European Society of Cardiology are revamping the approach to care for this complex, multifactorial disease.
, Isabelle Van Gelder, MD, PhD, professor of cardiology at the University Medical Center in Groningen, the Netherlands, explained at the European Society of Cardiology (ESC) Congress.
It is not just appropriate to place the same emphasis on the control of comorbidities as on the rhythm disturbance, it is critical, said Dr. Van Gelder, who served as chair of the ESC-AF guidelines task force.
Comorbidities are the drivers of both the onset and recurrence of atrial fibrillation, and a dynamic approach to comorbidities is “central for the success of AF management.”
Class I Recommendation
In fact, on the basis of overwhelming evidence, a class I recommendation has been issued for a large number of goals in the comorbidity and risk factor management step of atrial fibrillation management, including those for hypertension, components of heart failure, obesity, diabetes, alcohol consumption, and exercise.
Sodium-glucose cotransporter-2 (SGLT2) inhibitors “should be offered to all patients with AF,” according to Dr. Van Gelder, who identified this as a new class I recommendation.
Patients who are not managed aggressively for the listed comorbidities ultimately face “treatment failure, poor patient outcomes, and a waste of healthcare resources,” she said.
Control of sleep apnea is also noted as a key target, although Van Gelder acknowledged that the supporting evidence only allows for a class IIb recommendation.
Control of comorbidities is not a new idea. In the 2023 joint guideline, led by a consortium of professional groups, including the American Heart Association (AHA) and the American College of Cardiology (ACC), the control of comorbidities, including most of those identified in the new ESC guidelines, was second in a list of 10 key take-home messages.
However, the new ESC guidelines have prioritized comorbidity management by listing it first in each of the specific patient-care pathways developed to define optimized care.
These pathways, defined in algorithms for newly diagnosed AF, paroxysmal AF, and persistent AF, always start with the assessment of comorbidities, followed by step A — avoiding stroke — largely with anticoagulation.
Direct oral anticoagulants should be used, “except in those with a mechanical valve or mitral stenosis,” Dr. Van Gelder said. This includes, essentially, all patients with a CHA2DS2-VASc score of 2 or greater, and it should be “considered” in those with a score of 1.
The ESC framework has been identified with the acronym AF-CARE, in which the C stands for comorbidities.
In the A step of the framework, identifying and treating all modifiable bleeding risk factors in AF patients is a class I recommendation. On the basis of a class III recommendation, she cautioned against withholding anticoagulants because of CHA2DS2-VASc risk factors alone. Rather, Dr. Van Gelder called the decision to administer or withhold anticoagulation — like all decisions — one that should be individualized in consultation with the patient.
For reducing AF symptoms and rhythm control, the specific pathways diverge for newly diagnosed AF, paroxysmal AF, and persistent AF. Like all of the guidelines, the specific options for symptom management and AF ablation are color coded, with green signifying level 1 evidence.
The evaluation and dynamic reassessment step refers to the need to periodically assess patients for new modifiable risk factors related to comorbidities, risk for stroke, risk for bleeding, and risk for AF.
The management of risk factors for AF has long been emphasized in guidelines, but a previous focus on AF with attention to comorbidities has been replaced by a focus on comorbidities with an expectation of more durable AF control. The success of this pivot is based on multidisciplinary care, chosen in collaboration with the patient, to reduce or eliminate the triggers of AF and the risks of its complications.
Pathways Are Appropriate for All Patients
A very important recommendation — and this is new — is “to treat all our patients with atrial fibrillation, whether they are young or old, men or women, Black or White, or at high or low risk, according to our patient-centered integrated AF-CARE approach,” Dr. Van Gelder said.
The changes reflect a shared appreciation for the tight relation between the control of comorbidities and the control of AF, according to José A. Joglar, MD, professor of cardiac electrophysiologic research at the University of Texas Southwestern Medical Center in Dallas. Dr. Joglar was chair of the writing committee for the joint 2023 AF guidelines released by the AHA, ACC, the American College of Clinical Pharmacy, and the Heart Rhythm Society.
“It is increasingly clear that AF in many cases is the consequence of underlying risk factors and comorbidities, which cannot be separated from AF alone,” Dr. Joglar explained in an interview.
This was placed first “to emphasize the importance of viewing AFib as a complex disease that requires a holistic, multidisciplinary approach to care, as opposed to being viewed just as a rhythm abnormality,” he said.
A version of this article first appeared on Medscape.com.
FROM ESC 2024
On Second Thought: The Truth About Beta-Blockers
This transcript has been edited for clarity.
Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck.
They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!
The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy.
It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices.
The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes.
In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81.
What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects.
Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics.
By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for.
Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care.
Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct.
We don’t use IV beta-blockers that much anymore because of the risk for shock.
Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker.
Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure?
The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.)
For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant.
In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t.
Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video.
Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era.
That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen.
Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck.
They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!
The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy.
It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices.
The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes.
In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81.
What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects.
Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics.
By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for.
Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care.
Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct.
We don’t use IV beta-blockers that much anymore because of the risk for shock.
Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker.
Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure?
The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.)
For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant.
In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t.
Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video.
Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era.
That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen.
Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
This transcript has been edited for clarity.
Giving patients a beta-blocker after a myocardial infarction is standard of care. It’s in the guidelines. It’s one of the performance measures used by the American College of Cardiology (ACC) and the American Heart Association (AHA). If you aren’t putting your post–acute coronary syndrome (ACS) patients on a beta-blocker, the ACC and the AHA both think you suck.
They are very disappointed in you, just like your mother was when you told her you didn’t want to become a surgeon because you don’t like waking up early, your hands shake when you get nervous, it’s not your fault, there’s nothing you can do about it, so just leave me alone!
The data on beta-blockers are decades old. In the time before stents, statins, angiotensin-converting enzyme inhibitors, and dual antiplatelet therapy, when patients either died or got better on their own, beta-blockers showed major benefits. Studies like the Norwegian Multicenter Study Group, the BHAT trial, and the ISIS-1 trial proved the benefits of beta blockade. These studies date back to the 1980s, when you could call a study ISIS without controversy.
It was a simpler time, when all you had to worry about was the Cold War, apartheid, and the global AIDS pandemic. It was a time when doctors smoked in their offices, and patients had bigger infarcts that caused large scars and systolic dysfunction. That world is no longer our world, except for the war, the global pandemic, and the out-of-control gas prices.
The reality is that, before troponins, we probably missed most small heart attacks. Now, most infarcts are small, and most patients walk away from their heart attacks with essentially normal hearts. Do beta-blockers still matter? If you’re a fan of Cochrane reviews, the answer is yes.
In 2021, Cochrane published a review of beta-blockers in patients without heart failure after myocardial infarction (MI). The authors of that analysis concluded, after the usual caveats about heterogeneity, potential bias, and the whims of a random universe, that, yes, beta-blockers do reduce mortality. The risk ratio for max all-cause mortality was 0.81.
What does that mean practically? The absolute risk was reduced from 10.9% to 8.7%, a 2.2–percentage point absolute decrease and about a 20% relative drop. A little math gives us a third number: 46. That’s the number needed to treat. If you think about how many patients you admit during a typical week of critical care unit with an MI, a number needed to treat of 46 is a pretty good trade-off for a fairly inexpensive medication with fairly minimal side effects.
Of course, these are the same people who claim that masks don’t stop the spread of COVID-19. Sure, were they the only people who thought that handwashing was the best way to stop a respiratory virus? No. We all believed that fantasy for far longer than we should have. Not everybody can bat a thousand, if by batting a thousand, you mean reflecting on how your words will impact on a broader population primed to believe misinformation because of the increasingly toxic social media environment and worsening politicization and radicalization of our politics.
By the way, if any of you want to come to Canada, you can stay with me. Things are incrementally better here. In this day and age, incrementally better is the best we can hope for.
Here’s the wrinkle with the Cochrane beta-blocker review: Many of the studies took place before early revascularization became the norm and before our current armamentarium of drugs became standard of care.
Back in the day, bed rest and the power of positive thinking were the mainstays of cardiac treatment. Also, many of these studies mixed together ST-segment MI (STEMI) and non-STEMI patients, so you’re obviously going to see more benefits in STEMI patients who are at higher risk. Some of them used intravenous (IV) beta-blockers right away, whereas some were looking only at oral beta-blockers started days after the infarct.
We don’t use IV beta-blockers that much anymore because of the risk for shock.
Also, some studies had short-term follow-up where the benefits were less pronounced, and some studies used doses and types of beta-blockers rarely used today. Some of the studies had a mix of coronary and heart failure patients, which muddies the water because the heart failure patients would clearly benefit from being on a beta-blocker.
Basically, the data are not definitive because they are old and don’t reflect our current standard of care. The data contain a heterogeneous mix of patients that aren’t really relevant to the question that we’re asking. The question we’re asking is, should you put all your post-MI patients on a beta-blocker routinely, even if they don’t have heart failure?
The REDUCE-AMI trial is the first of a few trials testing, or to be more accurate, retesting, whether beta-blockers are useful after an MI. BETAMI, REBOOT, DANBLOCK— you’ll be hearing these names in the next few years, either because the studies get published or because they’re the Twitter handles of people harassing you online. Either/or. (By the way, I’ll be cold in my grave before I call it X.)
For now, REDUCE-AMI is the first across the finish line, and at least in cardiology, finishing first is a good thing. This study enrolled patients with ACS, both STEMI and non-STEMI, with a post-MI ejection fraction ≥ 50%, and the result was nothing. The risk ratio for all-cause mortality was 0.94 and was not statistically significant.
In absolute terms, that’s a reduction from 4.1% to 3.9%, or a 0.2–percentage point decrease; this translates into a number needed to treat of 500, which is 10 times higher than what the Cochrane review found. That’s if you assume that there is, in fact, a small benefit amidst all the statistical noise, which there probably isn’t.
Now, studies like this can never rule out small effects, either positive or negative, so maybe there is a small benefit from using beta-blockers. If it’s there, it’s really small. Do beta-blockers work? Well, yes, obviously, for heart failure and atrial fibrillation — which, let’s face it, are not exactly rare and often coexist in patients with heart disease. They probably aren’t that great as blood pressure pills, but that’s a story for another day and another video.
Yes, beta-blockers are useful pills, and they are standard of care, just maybe not for post-MI patients with normal ejection fractions because they probably don’t really need them. They worked in the pre-stent, pre-aspirin, pre-anything era.
That’s not our world anymore. Things change. It’s not the 1980s. That’s why I don’t have a mullet, and that’s why you need to update your kitchen.
Dr. Labos, a cardiologist at Kirkland Medical Center, Montreal, Quebec, Canada, has disclosed no relevant financial relationships.
A version of this article appeared on Medscape.com.
Will Hospital-at-Home Go Mainstream?
Jordan Stohler, a 42-year-old nurse in Knoxville, Tennessee, was readmitted to Fort Sanders Medical Center in June 2023 with sepsis after a double mastectomy.
She spent 5 days in the hospital after surgery to clear up the infection. Then she was offered a choice: She could either stay in the hospital while she received IV antibiotics, or she could go home and have the antibiotics given to her there under the Advanced Care at Home program of Covenant Health, the nine-hospital system to which Fort Sanders belongs.
She opted to go home, where she knew she’d be more comfortable and would be close to her beloved dog. In the end, she was very glad she did.
“I received great care in the hospital, but to be allowed to be in the comfort of your own home, to be around my dog, who I think is therapeutic, to be able to cook my own meals, and to have the same one-on-one nursing care that I would have gotten in the hospital was great,” Ms. Stohler said. “
Being cared for at home helped her heal, she said. “I probably would have gotten a little stir crazy if I’d stayed in the hospital any longer. I received excellent care at home.”
Currently, 322 hospitals in 37 states have Medicare waivers for these kinds of programs, although not all of them are currently functioning.
A recent survey published in JAMA found that nearly half of consumers would accept hospital-at-home, and more than a third were neutral on it. Only 17% said they’d rather be cared for in a brick-and-mortar hospital.
The findings of the JAMA survey confirm those of earlier studies, said Bruce Leff, MD, a professor at Johns Hopkins Medical School in Baltimore, who has researched hospital-at-home since the 1990s. Like the new study, those trials found that the results had no relationship to individual traits, such as socioeconomic status, medical conditions, age, gender, or race.
Whether a person felt comfortable with the idea of hospital-at-home boiled down “to a preference for receiving care at home or in the hospital,” he said. Some people distrust hospitals, and others feel insecure about receiving care at home, even if it is provided by qualified health care professionals.
How Patients Are Selected
While the details of hospital-at-home vary from program to program, the basic scenario is that patients who need certain kinds of acute care can be sent home from hospitals, emergency departments, or clinics to receive that care at home. Among the kinds of conditions that make stable patients eligible are heart failure, COPD, pneumonia, cellulitis, and COVID-19, said John Busigin, MD, a hospitalist and medical director of Covenant Advanced Care at Home.
When a patient is admitted to hospital-at-home, the hospital will send along whatever equipment and medications that person needs. In some cases, this may include a hospital bed, although Ms. Stohler used her own. An IV line was put into her arm, and the IV stand was placed next to the bed.
Ms. Stohler received a computer tablet that she used to communicate with doctors and nurses in Covenant’s “command center” in Knoxville. She also wore a watch with a button she could push in case of an emergency. And she had a telephone line that went directly to her medical team, in case she had an issue and the tablet didn’t work.
Twice a day, or as needed, specially trained paramedics came to Ms. Stohler’s home. They checked on the IV line, changed the IV bag, performed tests, and uploaded vital signs from monitoring equipment to Ms. Stohler’s tablet so it could be transmitted to the command center. A physician assistant came in on the second and fourth days of her weeklong stay in the program, and she saw a hospitalist remotely every day.
While some hospital-at-home programs have registered nurses visit patients at home, RNs are in short supply. To fill this gap, Covenant’s program uses community paramedics who have been in the field for at least 5 years, doing everything from intubating patients and placing them on ventilators to providing advanced cardiac life support, Dr. Busigin said. To get certified as community paramedics, they go through a 3-month training program.
Shortly after Ms. Stohler went into hospital-at-home, she had another crisis. Excess fluid had built up in her body because of all the IV fluids she’d received in the hospital while fighting the sepsis. As a result, she became short of breath. If she had been discharged to home rather than hospital-at-home, she said, she would have had to go to the emergency room. Instead, she sent out a distress call. One of the paramedics rushed to her house and gave her an IV diuretic medication, which helped her urinate to get rid of the excess fluid.
A small number of the estimated 300 people who have gone through the program had to be admitted to the hospital, Dr. Busigin said. Nationally, he said, about 5%-10% are admitted. But readmissions among the patients in the Covenant program have been 25% lower than for patients who received conventional hospital care and had the same conditions as those in hospital-at-home.
Studies have shown that these programs not only reduce readmissions, but also cost less, on average, and create a better patient experience than traditional hospital care does. And, according to the JAMA survey, most consumers like the idea. Fifty-six percent of people who took the survey agreed with the statement that people recover faster at home than in the hospital. Fifty-nine percent agreed they’d feel safe being treated at home, and 49% said they’d be more comfortable if treated at home.
The 1134 people who took the survey were also asked about their comfort level with providing various kinds of care to their loved ones during a hospital-at-home episode. The results varied with the type of task: For example, 82% of the respondents agreed or strongly agreed they could manage a patient’s medications, while just 41% said they’d be willing to change a feeding tube. Smaller percentages were willing to change an IV bag or a catheter or do wound care.
However, hospital-at-home programs don’t allow caregivers to take part in clinical care, which is prohibited by Medicare waivers and state licensing regulations. None of the 22 health systems that use the hospital-at-home services of Medically Home, including Covenant, ask caregivers to do anything along this line, said Pippa Shulman, DO, medical director of the company, which provides equipment, technology, and protocols for hospital programs
The only exception at Covenant, Dr. Busigin said, is that the hospital may train family members to do wound care when a patient is discharged from the hospital to Advanced Care at Home. They may also prepare meals for their loved ones, although the program provides balanced meals to patients if they want them. Ms. Stohler had some of these meals, which just had to be heated up, for the first few days of hospital-at-home, and later her relatives brought meals to her house.
Challenges for the Future
The number of Medicare hospital-at-home waivers has nearly doubled since 2021. A year earlier, when Medicare began reimbursing hospitals for acute care at home to help them cope with the overflow of COVID patients, there were only about 15-20 programs in the United States, said Dr. Leff of Johns Hopkins.
A big reason for the lack of use before the pandemic, Dr. Leff said, is that there was no payment system for hospitals that offered hospital-at-home. Now, they can get paid by Medicare and 10 state Medicaid programs, and a number of private payers are also coming on board. Ms. Stohler’s private insurer covered her hospital-at-home stay, and Dr. Busigin said several plans that contract with Covenant will pay for it.
Dr. Leff said he’s cautiously optimistic Congress will extend the Medicare waiver program, which is scheduled to end in December, for another 5 years. A couple of key House committees have signed off on a bill to do that, he said, and a Congressional Budget Office report found that the program did not cost Medicare more money.
But even if the waiver is renewed, some health systems may find it tough to deliver the service. The current version of this model depends a lot on technology, because telemedicine is used and reliable communication is needed for patients in hospital-at-home. That’s why many of the hospitals hire outside vendors like Medically Home to provide the infrastructure they need.
Medically Home manages the tablets given to patients and all connection and networking services, including internet and cellphone connections. It also provides technical services in the command centers that hospitals set up for the doctors and nurses who provide care remotely.
And the firm figures out how to deliver the standard care for each condition in each hospital-at-home. “We need to make sure that the patient is going to get what they need in the time frame it needs to be delivered in, and that it’s safe and effective for the patient,” Dr. Shulman said. “So we’ve developed logistical protocols for a multitude of disease states that allow us to provide high-acuity care in the home to a variety of complex patients.”
The health care workers use the hospital electronic health record for hospital-at-home patients, and vital signs uploaded from patient tablets flow directly into the electronic health record, she said.
Rural Areas Need Help
The use of hospital-at-home in rural areas holds a lot of promise, Dr. Leff said.
“A lot of rural hospitals have been closing, and hospital-at-home could be a mechanism to create hospital-level care where facilities have closed down. It’s easier to do this in urban areas, but it can be done in rural environments as well.”
Rami Karjian, CEO of Medically Home, agreed. The firm services hospital-at-home programs in rural areas of Oklahoma and California, using cellphones and paramedics in areas that lack broadband connections and nurses, he pointed out.
“Hospital-at-home can’t just be available to people who live in big cities,” he said. “The access problems in health care are pervasive, and this is part of how we solve access problems in rural areas.”
A version of this article first appeared on WebMD.com.
Jordan Stohler, a 42-year-old nurse in Knoxville, Tennessee, was readmitted to Fort Sanders Medical Center in June 2023 with sepsis after a double mastectomy.
She spent 5 days in the hospital after surgery to clear up the infection. Then she was offered a choice: She could either stay in the hospital while she received IV antibiotics, or she could go home and have the antibiotics given to her there under the Advanced Care at Home program of Covenant Health, the nine-hospital system to which Fort Sanders belongs.
She opted to go home, where she knew she’d be more comfortable and would be close to her beloved dog. In the end, she was very glad she did.
“I received great care in the hospital, but to be allowed to be in the comfort of your own home, to be around my dog, who I think is therapeutic, to be able to cook my own meals, and to have the same one-on-one nursing care that I would have gotten in the hospital was great,” Ms. Stohler said. “
Being cared for at home helped her heal, she said. “I probably would have gotten a little stir crazy if I’d stayed in the hospital any longer. I received excellent care at home.”
Currently, 322 hospitals in 37 states have Medicare waivers for these kinds of programs, although not all of them are currently functioning.
A recent survey published in JAMA found that nearly half of consumers would accept hospital-at-home, and more than a third were neutral on it. Only 17% said they’d rather be cared for in a brick-and-mortar hospital.
The findings of the JAMA survey confirm those of earlier studies, said Bruce Leff, MD, a professor at Johns Hopkins Medical School in Baltimore, who has researched hospital-at-home since the 1990s. Like the new study, those trials found that the results had no relationship to individual traits, such as socioeconomic status, medical conditions, age, gender, or race.
Whether a person felt comfortable with the idea of hospital-at-home boiled down “to a preference for receiving care at home or in the hospital,” he said. Some people distrust hospitals, and others feel insecure about receiving care at home, even if it is provided by qualified health care professionals.
How Patients Are Selected
While the details of hospital-at-home vary from program to program, the basic scenario is that patients who need certain kinds of acute care can be sent home from hospitals, emergency departments, or clinics to receive that care at home. Among the kinds of conditions that make stable patients eligible are heart failure, COPD, pneumonia, cellulitis, and COVID-19, said John Busigin, MD, a hospitalist and medical director of Covenant Advanced Care at Home.
When a patient is admitted to hospital-at-home, the hospital will send along whatever equipment and medications that person needs. In some cases, this may include a hospital bed, although Ms. Stohler used her own. An IV line was put into her arm, and the IV stand was placed next to the bed.
Ms. Stohler received a computer tablet that she used to communicate with doctors and nurses in Covenant’s “command center” in Knoxville. She also wore a watch with a button she could push in case of an emergency. And she had a telephone line that went directly to her medical team, in case she had an issue and the tablet didn’t work.
Twice a day, or as needed, specially trained paramedics came to Ms. Stohler’s home. They checked on the IV line, changed the IV bag, performed tests, and uploaded vital signs from monitoring equipment to Ms. Stohler’s tablet so it could be transmitted to the command center. A physician assistant came in on the second and fourth days of her weeklong stay in the program, and she saw a hospitalist remotely every day.
While some hospital-at-home programs have registered nurses visit patients at home, RNs are in short supply. To fill this gap, Covenant’s program uses community paramedics who have been in the field for at least 5 years, doing everything from intubating patients and placing them on ventilators to providing advanced cardiac life support, Dr. Busigin said. To get certified as community paramedics, they go through a 3-month training program.
Shortly after Ms. Stohler went into hospital-at-home, she had another crisis. Excess fluid had built up in her body because of all the IV fluids she’d received in the hospital while fighting the sepsis. As a result, she became short of breath. If she had been discharged to home rather than hospital-at-home, she said, she would have had to go to the emergency room. Instead, she sent out a distress call. One of the paramedics rushed to her house and gave her an IV diuretic medication, which helped her urinate to get rid of the excess fluid.
A small number of the estimated 300 people who have gone through the program had to be admitted to the hospital, Dr. Busigin said. Nationally, he said, about 5%-10% are admitted. But readmissions among the patients in the Covenant program have been 25% lower than for patients who received conventional hospital care and had the same conditions as those in hospital-at-home.
Studies have shown that these programs not only reduce readmissions, but also cost less, on average, and create a better patient experience than traditional hospital care does. And, according to the JAMA survey, most consumers like the idea. Fifty-six percent of people who took the survey agreed with the statement that people recover faster at home than in the hospital. Fifty-nine percent agreed they’d feel safe being treated at home, and 49% said they’d be more comfortable if treated at home.
The 1134 people who took the survey were also asked about their comfort level with providing various kinds of care to their loved ones during a hospital-at-home episode. The results varied with the type of task: For example, 82% of the respondents agreed or strongly agreed they could manage a patient’s medications, while just 41% said they’d be willing to change a feeding tube. Smaller percentages were willing to change an IV bag or a catheter or do wound care.
However, hospital-at-home programs don’t allow caregivers to take part in clinical care, which is prohibited by Medicare waivers and state licensing regulations. None of the 22 health systems that use the hospital-at-home services of Medically Home, including Covenant, ask caregivers to do anything along this line, said Pippa Shulman, DO, medical director of the company, which provides equipment, technology, and protocols for hospital programs
The only exception at Covenant, Dr. Busigin said, is that the hospital may train family members to do wound care when a patient is discharged from the hospital to Advanced Care at Home. They may also prepare meals for their loved ones, although the program provides balanced meals to patients if they want them. Ms. Stohler had some of these meals, which just had to be heated up, for the first few days of hospital-at-home, and later her relatives brought meals to her house.
Challenges for the Future
The number of Medicare hospital-at-home waivers has nearly doubled since 2021. A year earlier, when Medicare began reimbursing hospitals for acute care at home to help them cope with the overflow of COVID patients, there were only about 15-20 programs in the United States, said Dr. Leff of Johns Hopkins.
A big reason for the lack of use before the pandemic, Dr. Leff said, is that there was no payment system for hospitals that offered hospital-at-home. Now, they can get paid by Medicare and 10 state Medicaid programs, and a number of private payers are also coming on board. Ms. Stohler’s private insurer covered her hospital-at-home stay, and Dr. Busigin said several plans that contract with Covenant will pay for it.
Dr. Leff said he’s cautiously optimistic Congress will extend the Medicare waiver program, which is scheduled to end in December, for another 5 years. A couple of key House committees have signed off on a bill to do that, he said, and a Congressional Budget Office report found that the program did not cost Medicare more money.
But even if the waiver is renewed, some health systems may find it tough to deliver the service. The current version of this model depends a lot on technology, because telemedicine is used and reliable communication is needed for patients in hospital-at-home. That’s why many of the hospitals hire outside vendors like Medically Home to provide the infrastructure they need.
Medically Home manages the tablets given to patients and all connection and networking services, including internet and cellphone connections. It also provides technical services in the command centers that hospitals set up for the doctors and nurses who provide care remotely.
And the firm figures out how to deliver the standard care for each condition in each hospital-at-home. “We need to make sure that the patient is going to get what they need in the time frame it needs to be delivered in, and that it’s safe and effective for the patient,” Dr. Shulman said. “So we’ve developed logistical protocols for a multitude of disease states that allow us to provide high-acuity care in the home to a variety of complex patients.”
The health care workers use the hospital electronic health record for hospital-at-home patients, and vital signs uploaded from patient tablets flow directly into the electronic health record, she said.
Rural Areas Need Help
The use of hospital-at-home in rural areas holds a lot of promise, Dr. Leff said.
“A lot of rural hospitals have been closing, and hospital-at-home could be a mechanism to create hospital-level care where facilities have closed down. It’s easier to do this in urban areas, but it can be done in rural environments as well.”
Rami Karjian, CEO of Medically Home, agreed. The firm services hospital-at-home programs in rural areas of Oklahoma and California, using cellphones and paramedics in areas that lack broadband connections and nurses, he pointed out.
“Hospital-at-home can’t just be available to people who live in big cities,” he said. “The access problems in health care are pervasive, and this is part of how we solve access problems in rural areas.”
A version of this article first appeared on WebMD.com.
Jordan Stohler, a 42-year-old nurse in Knoxville, Tennessee, was readmitted to Fort Sanders Medical Center in June 2023 with sepsis after a double mastectomy.
She spent 5 days in the hospital after surgery to clear up the infection. Then she was offered a choice: She could either stay in the hospital while she received IV antibiotics, or she could go home and have the antibiotics given to her there under the Advanced Care at Home program of Covenant Health, the nine-hospital system to which Fort Sanders belongs.
She opted to go home, where she knew she’d be more comfortable and would be close to her beloved dog. In the end, she was very glad she did.
“I received great care in the hospital, but to be allowed to be in the comfort of your own home, to be around my dog, who I think is therapeutic, to be able to cook my own meals, and to have the same one-on-one nursing care that I would have gotten in the hospital was great,” Ms. Stohler said. “
Being cared for at home helped her heal, she said. “I probably would have gotten a little stir crazy if I’d stayed in the hospital any longer. I received excellent care at home.”
Currently, 322 hospitals in 37 states have Medicare waivers for these kinds of programs, although not all of them are currently functioning.
A recent survey published in JAMA found that nearly half of consumers would accept hospital-at-home, and more than a third were neutral on it. Only 17% said they’d rather be cared for in a brick-and-mortar hospital.
The findings of the JAMA survey confirm those of earlier studies, said Bruce Leff, MD, a professor at Johns Hopkins Medical School in Baltimore, who has researched hospital-at-home since the 1990s. Like the new study, those trials found that the results had no relationship to individual traits, such as socioeconomic status, medical conditions, age, gender, or race.
Whether a person felt comfortable with the idea of hospital-at-home boiled down “to a preference for receiving care at home or in the hospital,” he said. Some people distrust hospitals, and others feel insecure about receiving care at home, even if it is provided by qualified health care professionals.
How Patients Are Selected
While the details of hospital-at-home vary from program to program, the basic scenario is that patients who need certain kinds of acute care can be sent home from hospitals, emergency departments, or clinics to receive that care at home. Among the kinds of conditions that make stable patients eligible are heart failure, COPD, pneumonia, cellulitis, and COVID-19, said John Busigin, MD, a hospitalist and medical director of Covenant Advanced Care at Home.
When a patient is admitted to hospital-at-home, the hospital will send along whatever equipment and medications that person needs. In some cases, this may include a hospital bed, although Ms. Stohler used her own. An IV line was put into her arm, and the IV stand was placed next to the bed.
Ms. Stohler received a computer tablet that she used to communicate with doctors and nurses in Covenant’s “command center” in Knoxville. She also wore a watch with a button she could push in case of an emergency. And she had a telephone line that went directly to her medical team, in case she had an issue and the tablet didn’t work.
Twice a day, or as needed, specially trained paramedics came to Ms. Stohler’s home. They checked on the IV line, changed the IV bag, performed tests, and uploaded vital signs from monitoring equipment to Ms. Stohler’s tablet so it could be transmitted to the command center. A physician assistant came in on the second and fourth days of her weeklong stay in the program, and she saw a hospitalist remotely every day.
While some hospital-at-home programs have registered nurses visit patients at home, RNs are in short supply. To fill this gap, Covenant’s program uses community paramedics who have been in the field for at least 5 years, doing everything from intubating patients and placing them on ventilators to providing advanced cardiac life support, Dr. Busigin said. To get certified as community paramedics, they go through a 3-month training program.
Shortly after Ms. Stohler went into hospital-at-home, she had another crisis. Excess fluid had built up in her body because of all the IV fluids she’d received in the hospital while fighting the sepsis. As a result, she became short of breath. If she had been discharged to home rather than hospital-at-home, she said, she would have had to go to the emergency room. Instead, she sent out a distress call. One of the paramedics rushed to her house and gave her an IV diuretic medication, which helped her urinate to get rid of the excess fluid.
A small number of the estimated 300 people who have gone through the program had to be admitted to the hospital, Dr. Busigin said. Nationally, he said, about 5%-10% are admitted. But readmissions among the patients in the Covenant program have been 25% lower than for patients who received conventional hospital care and had the same conditions as those in hospital-at-home.
Studies have shown that these programs not only reduce readmissions, but also cost less, on average, and create a better patient experience than traditional hospital care does. And, according to the JAMA survey, most consumers like the idea. Fifty-six percent of people who took the survey agreed with the statement that people recover faster at home than in the hospital. Fifty-nine percent agreed they’d feel safe being treated at home, and 49% said they’d be more comfortable if treated at home.
The 1134 people who took the survey were also asked about their comfort level with providing various kinds of care to their loved ones during a hospital-at-home episode. The results varied with the type of task: For example, 82% of the respondents agreed or strongly agreed they could manage a patient’s medications, while just 41% said they’d be willing to change a feeding tube. Smaller percentages were willing to change an IV bag or a catheter or do wound care.
However, hospital-at-home programs don’t allow caregivers to take part in clinical care, which is prohibited by Medicare waivers and state licensing regulations. None of the 22 health systems that use the hospital-at-home services of Medically Home, including Covenant, ask caregivers to do anything along this line, said Pippa Shulman, DO, medical director of the company, which provides equipment, technology, and protocols for hospital programs
The only exception at Covenant, Dr. Busigin said, is that the hospital may train family members to do wound care when a patient is discharged from the hospital to Advanced Care at Home. They may also prepare meals for their loved ones, although the program provides balanced meals to patients if they want them. Ms. Stohler had some of these meals, which just had to be heated up, for the first few days of hospital-at-home, and later her relatives brought meals to her house.
Challenges for the Future
The number of Medicare hospital-at-home waivers has nearly doubled since 2021. A year earlier, when Medicare began reimbursing hospitals for acute care at home to help them cope with the overflow of COVID patients, there were only about 15-20 programs in the United States, said Dr. Leff of Johns Hopkins.
A big reason for the lack of use before the pandemic, Dr. Leff said, is that there was no payment system for hospitals that offered hospital-at-home. Now, they can get paid by Medicare and 10 state Medicaid programs, and a number of private payers are also coming on board. Ms. Stohler’s private insurer covered her hospital-at-home stay, and Dr. Busigin said several plans that contract with Covenant will pay for it.
Dr. Leff said he’s cautiously optimistic Congress will extend the Medicare waiver program, which is scheduled to end in December, for another 5 years. A couple of key House committees have signed off on a bill to do that, he said, and a Congressional Budget Office report found that the program did not cost Medicare more money.
But even if the waiver is renewed, some health systems may find it tough to deliver the service. The current version of this model depends a lot on technology, because telemedicine is used and reliable communication is needed for patients in hospital-at-home. That’s why many of the hospitals hire outside vendors like Medically Home to provide the infrastructure they need.
Medically Home manages the tablets given to patients and all connection and networking services, including internet and cellphone connections. It also provides technical services in the command centers that hospitals set up for the doctors and nurses who provide care remotely.
And the firm figures out how to deliver the standard care for each condition in each hospital-at-home. “We need to make sure that the patient is going to get what they need in the time frame it needs to be delivered in, and that it’s safe and effective for the patient,” Dr. Shulman said. “So we’ve developed logistical protocols for a multitude of disease states that allow us to provide high-acuity care in the home to a variety of complex patients.”
The health care workers use the hospital electronic health record for hospital-at-home patients, and vital signs uploaded from patient tablets flow directly into the electronic health record, she said.
Rural Areas Need Help
The use of hospital-at-home in rural areas holds a lot of promise, Dr. Leff said.
“A lot of rural hospitals have been closing, and hospital-at-home could be a mechanism to create hospital-level care where facilities have closed down. It’s easier to do this in urban areas, but it can be done in rural environments as well.”
Rami Karjian, CEO of Medically Home, agreed. The firm services hospital-at-home programs in rural areas of Oklahoma and California, using cellphones and paramedics in areas that lack broadband connections and nurses, he pointed out.
“Hospital-at-home can’t just be available to people who live in big cities,” he said. “The access problems in health care are pervasive, and this is part of how we solve access problems in rural areas.”
A version of this article first appeared on WebMD.com.
Risk of MACE Comparable Among Biologic Classes for Psoriasis, PsA
TOPLINE:
a database analysis finds.
METHODOLOGY:
- Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
- The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
- Subset analyses compared MACE in patients with and without existing cardiovascular disease.
TAKEAWAY:
- Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
- There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.
IN PRACTICE:
Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.
SOURCE:
Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.
LIMITATIONS:
The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.
DISCLOSURES:
Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.
A version of this article first appeared on Medscape.com.
TOPLINE:
a database analysis finds.
METHODOLOGY:
- Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
- The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
- Subset analyses compared MACE in patients with and without existing cardiovascular disease.
TAKEAWAY:
- Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
- There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.
IN PRACTICE:
Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.
SOURCE:
Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.
LIMITATIONS:
The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.
DISCLOSURES:
Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.
A version of this article first appeared on Medscape.com.
TOPLINE:
a database analysis finds.
METHODOLOGY:
- Data from the TriNetX health records database included 32,758 patients treated with TNF inhibitors (TNFi, 62.9%), interleukin-17 inhibitors (IL-17i, 15.4%), IL-23i (10.7%), and IL-12i/IL-23i (10.7%).
- The researchers calculated time-dependent risk for MACE using multinomial Cox proportional hazard ratios. The reference was TNFi exposure.
- Subset analyses compared MACE in patients with and without existing cardiovascular disease.
TAKEAWAY:
- Compared with TNFi use, there was no difference in the incidence of MACE events in the IL-17i, IL-23i, or IL-12i/IL-23i group.
- There were also no significant differences between biologic groups in the incidence of congestive heart failure, myocardial infarction, or cerebral vascular accident/stroke.
IN PRACTICE:
Despite some concern about increased risk for MACE with TNFi use, this study suggests no special risk for patients with psoriasis or PsA associated with TNFi vs other biologics. “Given our results, as it pertains to MACE, prescribers shouldn’t favor any one biologic class over another,” said lead investigator Shikha Singla, MD, medical director of the Psoriatic Arthritis Program at Medical College of Wisconsin in Milwaukee, Wisconsin.
SOURCE:
Bonit Gill, MD, a second-year fellow at Medical College of Wisconsin, presented the study as a poster at the annual meeting of the Group for Research and Assessment of Psoriasis and Psoriatic Arthritis.
LIMITATIONS:
The study’s retrospective nature makes it impossible to prove causation and the patients included in the study were from Wisconsin, which may limit generalizability.
DISCLOSURES:
Dr. Gill had no relevant financial disclosures. Other study authors participated in trials or consulted for AbbVie, AstraZeneca, Novartis, Eli Lilly, Janssen, and UCB.
A version of this article first appeared on Medscape.com.