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MDedge Daily News: Why most heart failure may be preventable
Why most heart failure may be preventable. Statins miss the mark in familial high cholesterol. Why mumps outbreaks are on the rise. And how using epileptic drugs in pregnancy affects school test scores.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
Why most heart failure may be preventable. Statins miss the mark in familial high cholesterol. Why mumps outbreaks are on the rise. And how using epileptic drugs in pregnancy affects school test scores.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
Why most heart failure may be preventable. Statins miss the mark in familial high cholesterol. Why mumps outbreaks are on the rise. And how using epileptic drugs in pregnancy affects school test scores.
Listen to the MDedge Daily News podcast for all the details on today’s top news.
Major message: Most heart failure is preventable
SNOWMASS, COLO. – More than 960,000 new cases of heart failure will occur in the United States this year – and most of them could have been prevented, Gregg C. Fonarow, MD, asserted at the Annual Cardiovascular Conference at Snowmass.
Preventing heart failure doesn’t require heroic measures. It entails identifying high-risk individuals while they are still asymptomatic and free of structural heart disease – that is, patients who are stage A, pre–heart failure, in the American College of Cardiology/American Heart Association classification system for heart failure – and then addressing their modifiable risk factors via evidence-based, guideline-directed medical therapy, said Dr. Fonarow, professor of cardiovascular medicine and cochief of cardiology at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.
A special word about obesity: A Framingham Heart Study analysis concluded that, after controlling for other cardiovascular risk factors, obese individuals had double the risk of new-onset heart failure, compared with normal weight subjects, during a mean follow-up of 14 years. For each one-unit increase in body mass index, the adjusted risk of heart failure climbed by 5% in men and 7% in women (N Engl J Med. 2002 Aug 1;347[5]:305-13). And that spells trouble down the line.
“You can imagine, with the marked increase in overweight and obesity status now affecting over half of U.S. adults, what this will mean for a potential rise in heart failure prevalence and incidence unless we do something further to modify this,” the cardiologist observed.
Dr. Fonarow is a member of the writing group for the ACC/AHA guidelines on management of heart failure. They recommend as a risk reduction strategy identification of patients with stage A pre–heart failure and addressing their risk factors: treating their hypertension and lipid disorders, gaining control over metabolic syndrome, discouraging heavy alcohol intake, and encouraging smoking cessation and regular exercise (J Am Coll Cardiol. 2013 Oct 15;62[16]:e147-239).
What kind of reduction in heart failure risk can be expected via these measures?
Antihypertensive therapy
More than a quarter century ago, the landmark SHEP trial (Systolic Hypertension in the Elderly Program) in more than 4,700 hypertensive seniors showed that treatment with diuretics and beta-blockers resulted in a 49% reduction in heart failure events, compared with placebo. And this has been a consistent finding in other studies: A meta-analysis of all 12 major randomized trials of antihypertensive therapy conducted over a 20-year period showed that treatment resulted in a whopping 52% reduction in the risk of heart failure (J Am Coll Cardiol. 1995 Apr; 27[5]:1214-8).
“If you ask most people why they’re on antihypertensive medication, they say, ‘Oh, to prevent heart attacks and stroke.’ But in fact the greatest relative risk reduction that we see is this remarkable reduction in the risk of developing heart failure with blood pressure treatment,” Dr. Fonarow said.
There has been some argument within medicine as to whether aggressive blood pressure lowering is appropriate in individuals over age 80. But in the HYVET trial (Hypertension in the Very Elderly Trial) conducted in that age group, the use of diuretics and/or ACE inhibitors to lower systolic blood pressure from roughly 155 mm Hg to 145 mm Hg resulted in a dramatic 64% reduction in the rate of new-onset heart failure (N Engl J Med. 2008 May 1;358[18]:1887-98).
How low to go with blood pressure reduction in order to maximize the heart failure risk reduction benefit? In the SPRINT trial (Systolic Blood Pressure Intervention Trial) of 9,361 hypertensive patients with a history of cardiovascular disease or multiple risk factors, participants randomized to a goal of less than 120 mm Hg enjoyed a 38% lower risk of heart failure events, compared with those whose target was less than 140 mm Hg (N Engl J Med. 2015 Nov 26;373[22]:2103-16).
A secondary analysis from SPRINT showed that the risk of acute decompensated heart failure was 37% lower in patients treated to the target of less than 120 mm Hg. That finding takes on particular importance because SPRINT participants who developed acute decompensated heart failure had a 27-fold increase in cardiovascular death (Circ Heart Fail. 2017 Apr; doi: 10.1161/CIRCHEARTFAILURE.116.003613).
Lipid lowering
A meta-analysis of four major, randomized clinical trials of intensive versus moderate statin therapy in 27,546 patients with stable coronary artery disease or acute coronary syndrome concluded that intensive therapy resulted in a 27% reduction in the risk of hospitalization for heart failure (J Am Coll Cardiol. 2006 Jun 6;47[11]:2326-31).
SGLT-2 inhibition
Until the randomized EMPA-REG OUTCOME trial of the sodium-glucose transporter 2 (SGLT-2) inhibitor empagliflozin(Jardiance), no glucose-lowering drug available for treatment of type 2 diabetes had shown any benefit in terms of reducing diabetic patients’ elevated risk of heart failure. Neither had weight loss. Abundant evidence showed that glycemic control had no impact on the risk of heart failure events. So EMPA-REG OUTCOME was cause for celebration among heart failure specialists, with its demonstration of a 35% reduction in the risk of hospitalization for heart failure, compared with placebo in more than 7,000 randomized patients. The risk of death because of heart failure was chopped by 68%. Sharp reductions in other cardiovascular events were also seen with empagliflozin (N Engl J Med. 2015 Nov 26;373[22]:2117-28).
Similar benefits were subsequently documented with another SGLT-2 inhibitor, canagliflozin(Invokana), in the CANVAS study program (N Engl J Med. 2017 Aug 17;377:644-57).
The reduction in cardiovascular mortality achieved with empagliflozin in EMPA-REG OUTCOME was actually bigger than seen with ACE inhibitors and angiotensin-receptor blockers (ARBs) in earlier landmark heart failure trials (Eur J Heart Fail. 2017 Jan;19[1]:43-53).
Dr. Fonarow views these data as “compelling.” These trials mark a huge step forward in the prevention of heart failure.
“We now for the first time in patients with diabetes have the ability to markedly prevent heart failure as well as cardiovascular death,” the cardiologist commented. “It is critical for cardiologists and heart failure specialists to play an active role in this [pharmacologic diabetes] management, as choice of therapy is a key determinant of outcomes, including survival.”
ACE inhibitors and ARBs
The ACC/AHA heart failure guidelines give a Class I recommendation to the routine use of ACE inhibitors or ARBs in patients at high risk for developing heart failure because of a history of diabetes, hypertension with associated cardiovascular risk factors, or any form of atherosclerotic vascular disease.
Lifestyle modification
Heavy drinking is known to raise the risk of heart failure. However, moderate alcohol consumption may be protective. In a classic prospective cohort study, individuals who reported consuming 1.5-4 drinks per day in the previous month had a 47% reduction in subsequent new-onset heart failure, compared with teetotalers in a multivariate analysis adjusted for conventional cardiovascular risk factors. Those who drank less than 1.5 drinks per day had a 21% reduction in heart failure risk, compared with the nondrinkers (JAMA. 2001 Apr 18;285[15]:1971-7).
In the prospective observational Physicians’ Health Study of nearly 21,000 men, adherence to six modifiable healthy lifestyle factors was associated with an incremental stepwise reduction in lifetime risk of developing heart failure. The six lifestyle factors – a forerunner of the AHA’s Life’s Simple 7 – were maintaining a normal body weight, stopping smoking, getting exercise, drinking alcohol in moderation, consuming breakfast cereals, and eating fruits and vegetables. Male physicians who shunned all six had a 21.2% lifetime risk of heart failure; those who followed at least four of the healthy lifestyle factors had a 10.1% risk (JAMA 2009 Jul 22;302[4]:394-400).
In a separate analysis from the Physicians’ Health Study, men who engaged in vigorous exercise to the point of breaking a sweat as little as one to three times per month had an 18% lower risk of developing heart failure during follow-up, compared with inactive men (Circulation 2009 Jan 6;119[1]:44-52).
What’s next in prevention of heart failure
Heart failure is one of the most expensive health care problems in the United States, and one of the deadliest. Today an estimated 6.5 million Americans have symptomatic heart failure. But that’s just the tip of the iceberg.
“Countless millions more are likely to manifest heart failure in the future,” Dr. Fonarow warned, noting the vast prevalence of identifiable risk factors.
It’s time for a high-visibility public health campaign designed to foster community education and engagement regarding heart failure prevention, he added.
“We have a lot of action and events around preventing atherosclerotic cardiovascular disease. But can you think of any campaign you’ve seen focusing specifically on heart failure? Heart failure isn’t one of the endpoints in the ACC/AHA Atherosclerotic Cardiovascular Disease Risk Calculator or even the new hypertension risk calculator, so we need to take this a whole lot more seriously,” the cardiologist said.
The 2017 focused update of the ACC/AHA heart failure guidelines endorsed a novel strategy of primary care–centered, biomarker-based screening of patients with cardiovascular risk factors as a means of triggering early intervention to prevent heart failure (J Am Coll Cardiol. 2017 Aug 8;70[6]:776-803). This strategy, which received a Class IIa recommendation, involves screening measurement of a natriuretic peptide biomarker.
The recommendation was based on evidence including the STOP-HF randomized trial (St. Vincent’s Screening to Prevent Heart Failure Study), in which 1,374 asymptomatic Irish patients with cardiovascular risk factors were randomized to routine primary care or primary care plus screening with brain-type natriuretic peptide testing. Patients with a brain-type natriuretic peptide level of 50 pg/mL or more were directed to team-based care involving a collaboration between their primary care physician and a specialist cardiovascular service focused on optimizing guideline-directed medical therapy. During a mean follow-up of 4.2 years, the primary endpoint of new-onset left ventricular dysfunction occurred in 5.3% of the intervention group and 8.7% of controls, for a 45% relative risk reduction (JAMA 2013 Jul 3;310[1]:66-74).
Dr. Fonarow reported receiving research grants from and serving as a consultant to the National Heart, Lung, and Blood Institute and a handful of medical companies.
SNOWMASS, COLO. – More than 960,000 new cases of heart failure will occur in the United States this year – and most of them could have been prevented, Gregg C. Fonarow, MD, asserted at the Annual Cardiovascular Conference at Snowmass.
Preventing heart failure doesn’t require heroic measures. It entails identifying high-risk individuals while they are still asymptomatic and free of structural heart disease – that is, patients who are stage A, pre–heart failure, in the American College of Cardiology/American Heart Association classification system for heart failure – and then addressing their modifiable risk factors via evidence-based, guideline-directed medical therapy, said Dr. Fonarow, professor of cardiovascular medicine and cochief of cardiology at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.
A special word about obesity: A Framingham Heart Study analysis concluded that, after controlling for other cardiovascular risk factors, obese individuals had double the risk of new-onset heart failure, compared with normal weight subjects, during a mean follow-up of 14 years. For each one-unit increase in body mass index, the adjusted risk of heart failure climbed by 5% in men and 7% in women (N Engl J Med. 2002 Aug 1;347[5]:305-13). And that spells trouble down the line.
“You can imagine, with the marked increase in overweight and obesity status now affecting over half of U.S. adults, what this will mean for a potential rise in heart failure prevalence and incidence unless we do something further to modify this,” the cardiologist observed.
Dr. Fonarow is a member of the writing group for the ACC/AHA guidelines on management of heart failure. They recommend as a risk reduction strategy identification of patients with stage A pre–heart failure and addressing their risk factors: treating their hypertension and lipid disorders, gaining control over metabolic syndrome, discouraging heavy alcohol intake, and encouraging smoking cessation and regular exercise (J Am Coll Cardiol. 2013 Oct 15;62[16]:e147-239).
What kind of reduction in heart failure risk can be expected via these measures?
Antihypertensive therapy
More than a quarter century ago, the landmark SHEP trial (Systolic Hypertension in the Elderly Program) in more than 4,700 hypertensive seniors showed that treatment with diuretics and beta-blockers resulted in a 49% reduction in heart failure events, compared with placebo. And this has been a consistent finding in other studies: A meta-analysis of all 12 major randomized trials of antihypertensive therapy conducted over a 20-year period showed that treatment resulted in a whopping 52% reduction in the risk of heart failure (J Am Coll Cardiol. 1995 Apr; 27[5]:1214-8).
“If you ask most people why they’re on antihypertensive medication, they say, ‘Oh, to prevent heart attacks and stroke.’ But in fact the greatest relative risk reduction that we see is this remarkable reduction in the risk of developing heart failure with blood pressure treatment,” Dr. Fonarow said.
There has been some argument within medicine as to whether aggressive blood pressure lowering is appropriate in individuals over age 80. But in the HYVET trial (Hypertension in the Very Elderly Trial) conducted in that age group, the use of diuretics and/or ACE inhibitors to lower systolic blood pressure from roughly 155 mm Hg to 145 mm Hg resulted in a dramatic 64% reduction in the rate of new-onset heart failure (N Engl J Med. 2008 May 1;358[18]:1887-98).
How low to go with blood pressure reduction in order to maximize the heart failure risk reduction benefit? In the SPRINT trial (Systolic Blood Pressure Intervention Trial) of 9,361 hypertensive patients with a history of cardiovascular disease or multiple risk factors, participants randomized to a goal of less than 120 mm Hg enjoyed a 38% lower risk of heart failure events, compared with those whose target was less than 140 mm Hg (N Engl J Med. 2015 Nov 26;373[22]:2103-16).
A secondary analysis from SPRINT showed that the risk of acute decompensated heart failure was 37% lower in patients treated to the target of less than 120 mm Hg. That finding takes on particular importance because SPRINT participants who developed acute decompensated heart failure had a 27-fold increase in cardiovascular death (Circ Heart Fail. 2017 Apr; doi: 10.1161/CIRCHEARTFAILURE.116.003613).
Lipid lowering
A meta-analysis of four major, randomized clinical trials of intensive versus moderate statin therapy in 27,546 patients with stable coronary artery disease or acute coronary syndrome concluded that intensive therapy resulted in a 27% reduction in the risk of hospitalization for heart failure (J Am Coll Cardiol. 2006 Jun 6;47[11]:2326-31).
SGLT-2 inhibition
Until the randomized EMPA-REG OUTCOME trial of the sodium-glucose transporter 2 (SGLT-2) inhibitor empagliflozin(Jardiance), no glucose-lowering drug available for treatment of type 2 diabetes had shown any benefit in terms of reducing diabetic patients’ elevated risk of heart failure. Neither had weight loss. Abundant evidence showed that glycemic control had no impact on the risk of heart failure events. So EMPA-REG OUTCOME was cause for celebration among heart failure specialists, with its demonstration of a 35% reduction in the risk of hospitalization for heart failure, compared with placebo in more than 7,000 randomized patients. The risk of death because of heart failure was chopped by 68%. Sharp reductions in other cardiovascular events were also seen with empagliflozin (N Engl J Med. 2015 Nov 26;373[22]:2117-28).
Similar benefits were subsequently documented with another SGLT-2 inhibitor, canagliflozin(Invokana), in the CANVAS study program (N Engl J Med. 2017 Aug 17;377:644-57).
The reduction in cardiovascular mortality achieved with empagliflozin in EMPA-REG OUTCOME was actually bigger than seen with ACE inhibitors and angiotensin-receptor blockers (ARBs) in earlier landmark heart failure trials (Eur J Heart Fail. 2017 Jan;19[1]:43-53).
Dr. Fonarow views these data as “compelling.” These trials mark a huge step forward in the prevention of heart failure.
“We now for the first time in patients with diabetes have the ability to markedly prevent heart failure as well as cardiovascular death,” the cardiologist commented. “It is critical for cardiologists and heart failure specialists to play an active role in this [pharmacologic diabetes] management, as choice of therapy is a key determinant of outcomes, including survival.”
ACE inhibitors and ARBs
The ACC/AHA heart failure guidelines give a Class I recommendation to the routine use of ACE inhibitors or ARBs in patients at high risk for developing heart failure because of a history of diabetes, hypertension with associated cardiovascular risk factors, or any form of atherosclerotic vascular disease.
Lifestyle modification
Heavy drinking is known to raise the risk of heart failure. However, moderate alcohol consumption may be protective. In a classic prospective cohort study, individuals who reported consuming 1.5-4 drinks per day in the previous month had a 47% reduction in subsequent new-onset heart failure, compared with teetotalers in a multivariate analysis adjusted for conventional cardiovascular risk factors. Those who drank less than 1.5 drinks per day had a 21% reduction in heart failure risk, compared with the nondrinkers (JAMA. 2001 Apr 18;285[15]:1971-7).
In the prospective observational Physicians’ Health Study of nearly 21,000 men, adherence to six modifiable healthy lifestyle factors was associated with an incremental stepwise reduction in lifetime risk of developing heart failure. The six lifestyle factors – a forerunner of the AHA’s Life’s Simple 7 – were maintaining a normal body weight, stopping smoking, getting exercise, drinking alcohol in moderation, consuming breakfast cereals, and eating fruits and vegetables. Male physicians who shunned all six had a 21.2% lifetime risk of heart failure; those who followed at least four of the healthy lifestyle factors had a 10.1% risk (JAMA 2009 Jul 22;302[4]:394-400).
In a separate analysis from the Physicians’ Health Study, men who engaged in vigorous exercise to the point of breaking a sweat as little as one to three times per month had an 18% lower risk of developing heart failure during follow-up, compared with inactive men (Circulation 2009 Jan 6;119[1]:44-52).
What’s next in prevention of heart failure
Heart failure is one of the most expensive health care problems in the United States, and one of the deadliest. Today an estimated 6.5 million Americans have symptomatic heart failure. But that’s just the tip of the iceberg.
“Countless millions more are likely to manifest heart failure in the future,” Dr. Fonarow warned, noting the vast prevalence of identifiable risk factors.
It’s time for a high-visibility public health campaign designed to foster community education and engagement regarding heart failure prevention, he added.
“We have a lot of action and events around preventing atherosclerotic cardiovascular disease. But can you think of any campaign you’ve seen focusing specifically on heart failure? Heart failure isn’t one of the endpoints in the ACC/AHA Atherosclerotic Cardiovascular Disease Risk Calculator or even the new hypertension risk calculator, so we need to take this a whole lot more seriously,” the cardiologist said.
The 2017 focused update of the ACC/AHA heart failure guidelines endorsed a novel strategy of primary care–centered, biomarker-based screening of patients with cardiovascular risk factors as a means of triggering early intervention to prevent heart failure (J Am Coll Cardiol. 2017 Aug 8;70[6]:776-803). This strategy, which received a Class IIa recommendation, involves screening measurement of a natriuretic peptide biomarker.
The recommendation was based on evidence including the STOP-HF randomized trial (St. Vincent’s Screening to Prevent Heart Failure Study), in which 1,374 asymptomatic Irish patients with cardiovascular risk factors were randomized to routine primary care or primary care plus screening with brain-type natriuretic peptide testing. Patients with a brain-type natriuretic peptide level of 50 pg/mL or more were directed to team-based care involving a collaboration between their primary care physician and a specialist cardiovascular service focused on optimizing guideline-directed medical therapy. During a mean follow-up of 4.2 years, the primary endpoint of new-onset left ventricular dysfunction occurred in 5.3% of the intervention group and 8.7% of controls, for a 45% relative risk reduction (JAMA 2013 Jul 3;310[1]:66-74).
Dr. Fonarow reported receiving research grants from and serving as a consultant to the National Heart, Lung, and Blood Institute and a handful of medical companies.
SNOWMASS, COLO. – More than 960,000 new cases of heart failure will occur in the United States this year – and most of them could have been prevented, Gregg C. Fonarow, MD, asserted at the Annual Cardiovascular Conference at Snowmass.
Preventing heart failure doesn’t require heroic measures. It entails identifying high-risk individuals while they are still asymptomatic and free of structural heart disease – that is, patients who are stage A, pre–heart failure, in the American College of Cardiology/American Heart Association classification system for heart failure – and then addressing their modifiable risk factors via evidence-based, guideline-directed medical therapy, said Dr. Fonarow, professor of cardiovascular medicine and cochief of cardiology at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.
A special word about obesity: A Framingham Heart Study analysis concluded that, after controlling for other cardiovascular risk factors, obese individuals had double the risk of new-onset heart failure, compared with normal weight subjects, during a mean follow-up of 14 years. For each one-unit increase in body mass index, the adjusted risk of heart failure climbed by 5% in men and 7% in women (N Engl J Med. 2002 Aug 1;347[5]:305-13). And that spells trouble down the line.
“You can imagine, with the marked increase in overweight and obesity status now affecting over half of U.S. adults, what this will mean for a potential rise in heart failure prevalence and incidence unless we do something further to modify this,” the cardiologist observed.
Dr. Fonarow is a member of the writing group for the ACC/AHA guidelines on management of heart failure. They recommend as a risk reduction strategy identification of patients with stage A pre–heart failure and addressing their risk factors: treating their hypertension and lipid disorders, gaining control over metabolic syndrome, discouraging heavy alcohol intake, and encouraging smoking cessation and regular exercise (J Am Coll Cardiol. 2013 Oct 15;62[16]:e147-239).
What kind of reduction in heart failure risk can be expected via these measures?
Antihypertensive therapy
More than a quarter century ago, the landmark SHEP trial (Systolic Hypertension in the Elderly Program) in more than 4,700 hypertensive seniors showed that treatment with diuretics and beta-blockers resulted in a 49% reduction in heart failure events, compared with placebo. And this has been a consistent finding in other studies: A meta-analysis of all 12 major randomized trials of antihypertensive therapy conducted over a 20-year period showed that treatment resulted in a whopping 52% reduction in the risk of heart failure (J Am Coll Cardiol. 1995 Apr; 27[5]:1214-8).
“If you ask most people why they’re on antihypertensive medication, they say, ‘Oh, to prevent heart attacks and stroke.’ But in fact the greatest relative risk reduction that we see is this remarkable reduction in the risk of developing heart failure with blood pressure treatment,” Dr. Fonarow said.
There has been some argument within medicine as to whether aggressive blood pressure lowering is appropriate in individuals over age 80. But in the HYVET trial (Hypertension in the Very Elderly Trial) conducted in that age group, the use of diuretics and/or ACE inhibitors to lower systolic blood pressure from roughly 155 mm Hg to 145 mm Hg resulted in a dramatic 64% reduction in the rate of new-onset heart failure (N Engl J Med. 2008 May 1;358[18]:1887-98).
How low to go with blood pressure reduction in order to maximize the heart failure risk reduction benefit? In the SPRINT trial (Systolic Blood Pressure Intervention Trial) of 9,361 hypertensive patients with a history of cardiovascular disease or multiple risk factors, participants randomized to a goal of less than 120 mm Hg enjoyed a 38% lower risk of heart failure events, compared with those whose target was less than 140 mm Hg (N Engl J Med. 2015 Nov 26;373[22]:2103-16).
A secondary analysis from SPRINT showed that the risk of acute decompensated heart failure was 37% lower in patients treated to the target of less than 120 mm Hg. That finding takes on particular importance because SPRINT participants who developed acute decompensated heart failure had a 27-fold increase in cardiovascular death (Circ Heart Fail. 2017 Apr; doi: 10.1161/CIRCHEARTFAILURE.116.003613).
Lipid lowering
A meta-analysis of four major, randomized clinical trials of intensive versus moderate statin therapy in 27,546 patients with stable coronary artery disease or acute coronary syndrome concluded that intensive therapy resulted in a 27% reduction in the risk of hospitalization for heart failure (J Am Coll Cardiol. 2006 Jun 6;47[11]:2326-31).
SGLT-2 inhibition
Until the randomized EMPA-REG OUTCOME trial of the sodium-glucose transporter 2 (SGLT-2) inhibitor empagliflozin(Jardiance), no glucose-lowering drug available for treatment of type 2 diabetes had shown any benefit in terms of reducing diabetic patients’ elevated risk of heart failure. Neither had weight loss. Abundant evidence showed that glycemic control had no impact on the risk of heart failure events. So EMPA-REG OUTCOME was cause for celebration among heart failure specialists, with its demonstration of a 35% reduction in the risk of hospitalization for heart failure, compared with placebo in more than 7,000 randomized patients. The risk of death because of heart failure was chopped by 68%. Sharp reductions in other cardiovascular events were also seen with empagliflozin (N Engl J Med. 2015 Nov 26;373[22]:2117-28).
Similar benefits were subsequently documented with another SGLT-2 inhibitor, canagliflozin(Invokana), in the CANVAS study program (N Engl J Med. 2017 Aug 17;377:644-57).
The reduction in cardiovascular mortality achieved with empagliflozin in EMPA-REG OUTCOME was actually bigger than seen with ACE inhibitors and angiotensin-receptor blockers (ARBs) in earlier landmark heart failure trials (Eur J Heart Fail. 2017 Jan;19[1]:43-53).
Dr. Fonarow views these data as “compelling.” These trials mark a huge step forward in the prevention of heart failure.
“We now for the first time in patients with diabetes have the ability to markedly prevent heart failure as well as cardiovascular death,” the cardiologist commented. “It is critical for cardiologists and heart failure specialists to play an active role in this [pharmacologic diabetes] management, as choice of therapy is a key determinant of outcomes, including survival.”
ACE inhibitors and ARBs
The ACC/AHA heart failure guidelines give a Class I recommendation to the routine use of ACE inhibitors or ARBs in patients at high risk for developing heart failure because of a history of diabetes, hypertension with associated cardiovascular risk factors, or any form of atherosclerotic vascular disease.
Lifestyle modification
Heavy drinking is known to raise the risk of heart failure. However, moderate alcohol consumption may be protective. In a classic prospective cohort study, individuals who reported consuming 1.5-4 drinks per day in the previous month had a 47% reduction in subsequent new-onset heart failure, compared with teetotalers in a multivariate analysis adjusted for conventional cardiovascular risk factors. Those who drank less than 1.5 drinks per day had a 21% reduction in heart failure risk, compared with the nondrinkers (JAMA. 2001 Apr 18;285[15]:1971-7).
In the prospective observational Physicians’ Health Study of nearly 21,000 men, adherence to six modifiable healthy lifestyle factors was associated with an incremental stepwise reduction in lifetime risk of developing heart failure. The six lifestyle factors – a forerunner of the AHA’s Life’s Simple 7 – were maintaining a normal body weight, stopping smoking, getting exercise, drinking alcohol in moderation, consuming breakfast cereals, and eating fruits and vegetables. Male physicians who shunned all six had a 21.2% lifetime risk of heart failure; those who followed at least four of the healthy lifestyle factors had a 10.1% risk (JAMA 2009 Jul 22;302[4]:394-400).
In a separate analysis from the Physicians’ Health Study, men who engaged in vigorous exercise to the point of breaking a sweat as little as one to three times per month had an 18% lower risk of developing heart failure during follow-up, compared with inactive men (Circulation 2009 Jan 6;119[1]:44-52).
What’s next in prevention of heart failure
Heart failure is one of the most expensive health care problems in the United States, and one of the deadliest. Today an estimated 6.5 million Americans have symptomatic heart failure. But that’s just the tip of the iceberg.
“Countless millions more are likely to manifest heart failure in the future,” Dr. Fonarow warned, noting the vast prevalence of identifiable risk factors.
It’s time for a high-visibility public health campaign designed to foster community education and engagement regarding heart failure prevention, he added.
“We have a lot of action and events around preventing atherosclerotic cardiovascular disease. But can you think of any campaign you’ve seen focusing specifically on heart failure? Heart failure isn’t one of the endpoints in the ACC/AHA Atherosclerotic Cardiovascular Disease Risk Calculator or even the new hypertension risk calculator, so we need to take this a whole lot more seriously,” the cardiologist said.
The 2017 focused update of the ACC/AHA heart failure guidelines endorsed a novel strategy of primary care–centered, biomarker-based screening of patients with cardiovascular risk factors as a means of triggering early intervention to prevent heart failure (J Am Coll Cardiol. 2017 Aug 8;70[6]:776-803). This strategy, which received a Class IIa recommendation, involves screening measurement of a natriuretic peptide biomarker.
The recommendation was based on evidence including the STOP-HF randomized trial (St. Vincent’s Screening to Prevent Heart Failure Study), in which 1,374 asymptomatic Irish patients with cardiovascular risk factors were randomized to routine primary care or primary care plus screening with brain-type natriuretic peptide testing. Patients with a brain-type natriuretic peptide level of 50 pg/mL or more were directed to team-based care involving a collaboration between their primary care physician and a specialist cardiovascular service focused on optimizing guideline-directed medical therapy. During a mean follow-up of 4.2 years, the primary endpoint of new-onset left ventricular dysfunction occurred in 5.3% of the intervention group and 8.7% of controls, for a 45% relative risk reduction (JAMA 2013 Jul 3;310[1]:66-74).
Dr. Fonarow reported receiving research grants from and serving as a consultant to the National Heart, Lung, and Blood Institute and a handful of medical companies.
EXPERT ANALYSIS FROM THE ANNUAL CARDIOVASCULAR CONFERENCE AT SNOWMASS
‘If this is an emergency, call 911’
This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.
To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.
Enter the current situation. Many patients still perceive the need to call their doctor for everything from a mild cough or headache or an actual fever to just not feeling well. This perceived patient need to seek expert medical help short of an ambulance ride to the emergency room leads the patient into the frustrating downward spiral associated with this bizarre need to communicate with their doctor.
I presume many patients assume that they may be able to actually talk to their doctor by telephone. They learn, as I have, that presumption is an arcane curiosity. First of all, most of my young colleagues, like most of their generation, do not own a land line and therefore are not listed in any known telephone directory. They work in an environment driven by the pressure to see more and more patients, and at the end of the day they are pretty much ready to “hang it up.” But many in my generation worked hard, and we still answered the telephone, and many of us actually made house calls.
But, should you have your doctor’s telephone number and make the call, you are immediately put in touch with a triage nurse who demands to know the intimate details of your problem in order to assist you in speaking to the doctor. Having divulged your symptoms in their gory details and achieved an appropriate threshold, you will be placed on hold while being connected to the clinic nurse. Once again you will be asked to divulge your intimate symptoms and again will be passed on to the doctor’s physician assistant who is familiar with the innermost knowledge of your doctor. But, again, if you persist you may again be put on hold to talk to your doctor or asked to leave a message with the physician assistant, since the doctor is seeing a patient or does not take calls during office hours. “Perhaps you would like to leave an email, and the doctor will contact you.”
Now, I have to admit that many of my friends find this process acceptable and use a variety of digital devices like “My Chart” to communicate with their doctor. But having grown up in the shadow of the horse and buggy era, and having adapted to the contemporary world, I give my patients my cell phone number. I will give it to you, too.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.
To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.
Enter the current situation. Many patients still perceive the need to call their doctor for everything from a mild cough or headache or an actual fever to just not feeling well. This perceived patient need to seek expert medical help short of an ambulance ride to the emergency room leads the patient into the frustrating downward spiral associated with this bizarre need to communicate with their doctor.
I presume many patients assume that they may be able to actually talk to their doctor by telephone. They learn, as I have, that presumption is an arcane curiosity. First of all, most of my young colleagues, like most of their generation, do not own a land line and therefore are not listed in any known telephone directory. They work in an environment driven by the pressure to see more and more patients, and at the end of the day they are pretty much ready to “hang it up.” But many in my generation worked hard, and we still answered the telephone, and many of us actually made house calls.
But, should you have your doctor’s telephone number and make the call, you are immediately put in touch with a triage nurse who demands to know the intimate details of your problem in order to assist you in speaking to the doctor. Having divulged your symptoms in their gory details and achieved an appropriate threshold, you will be placed on hold while being connected to the clinic nurse. Once again you will be asked to divulge your intimate symptoms and again will be passed on to the doctor’s physician assistant who is familiar with the innermost knowledge of your doctor. But, again, if you persist you may again be put on hold to talk to your doctor or asked to leave a message with the physician assistant, since the doctor is seeing a patient or does not take calls during office hours. “Perhaps you would like to leave an email, and the doctor will contact you.”
Now, I have to admit that many of my friends find this process acceptable and use a variety of digital devices like “My Chart” to communicate with their doctor. But having grown up in the shadow of the horse and buggy era, and having adapted to the contemporary world, I give my patients my cell phone number. I will give it to you, too.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
This is the mantra that the world hears when they call most, if not all, hospitals and medical clinics for the symptomatic relief of a myriad of health care complaints. Exactly what is the definition of an emergency is uncertain. We all could include severe chest pain, shortness of breath or sudden collapse or loss of consciousness.
To a patient, an emergency might just include the pressing need to speak to their doctor about the occurrence of symptoms and or anxieties that suddenly have occurred. In the past, before the telephone was invented, a friend or family member was sent by horseback or a Ford V8 to find the local doctor. With the advent of the telephone, doctors actually listed their number in a phone directory to facilitate contact with their patient.
Enter the current situation. Many patients still perceive the need to call their doctor for everything from a mild cough or headache or an actual fever to just not feeling well. This perceived patient need to seek expert medical help short of an ambulance ride to the emergency room leads the patient into the frustrating downward spiral associated with this bizarre need to communicate with their doctor.
I presume many patients assume that they may be able to actually talk to their doctor by telephone. They learn, as I have, that presumption is an arcane curiosity. First of all, most of my young colleagues, like most of their generation, do not own a land line and therefore are not listed in any known telephone directory. They work in an environment driven by the pressure to see more and more patients, and at the end of the day they are pretty much ready to “hang it up.” But many in my generation worked hard, and we still answered the telephone, and many of us actually made house calls.
But, should you have your doctor’s telephone number and make the call, you are immediately put in touch with a triage nurse who demands to know the intimate details of your problem in order to assist you in speaking to the doctor. Having divulged your symptoms in their gory details and achieved an appropriate threshold, you will be placed on hold while being connected to the clinic nurse. Once again you will be asked to divulge your intimate symptoms and again will be passed on to the doctor’s physician assistant who is familiar with the innermost knowledge of your doctor. But, again, if you persist you may again be put on hold to talk to your doctor or asked to leave a message with the physician assistant, since the doctor is seeing a patient or does not take calls during office hours. “Perhaps you would like to leave an email, and the doctor will contact you.”
Now, I have to admit that many of my friends find this process acceptable and use a variety of digital devices like “My Chart” to communicate with their doctor. But having grown up in the shadow of the horse and buggy era, and having adapted to the contemporary world, I give my patients my cell phone number. I will give it to you, too.
Dr. Goldstein, medical editor of Cardiology News, is professor of medicine at Wayne State University and division head emeritus of cardiovascular medicine at Henry Ford Hospital, both in Detroit. He is on data safety monitoring committees for the National Institutes of Health and several pharmaceutical companies.
Top hospital heart failure performance translates to longer survival
ORLANDO – Hospitals in the first quartile of short-term performance in treating heart failure patients had higher long-term survival rates for those patients, based on data from 317 hospitals that participated in a voluntary quality improvement program.
The burden of heart failure remains substantial in the United States, and health policies are increasingly focused on improving care for heart failure patients, said Ambarish Pandey, MD, of the University of Texas, Dallas, in a presentation at the annual meeting of the American College of Cardiology.
The researchers assessed hospital performance based on 30-day risk-standardized mortality rates (RSMR) in hospitals participating in the Get With the Guidelines–Heart Failure (GWTG-HF) registry, using a hierarchical, logistic regression model to calculate hospital-specific 30-day RSMRs.
Get With the Guidelines is a voluntary, observational quality improvement program that has been linked with CMS to capture long-term follow-up data, Dr. Pandey explained.
The study included 106,304 heart failure patients older than 65 years at 317 GWTG hospitals across the United States during 2005-2013. The hospitals were divided into performance quartiles based on 30-day RSMR. The 30-day RSMRs were 8.6%, 9.4%, 9.9%, and 10.7% in the first, second, third, and fourth quartiles, respectively.
There was a strong association between the top-performing hospitals and long-term survival rates for the patients that persisted beyond 30 days, said Dr. Pandey. The mortality rates after 5 years were 75.6%, 76.2%, 76.9%, and 79.6%, in the first, second, third, and fourth quartiles, respectively.
The hospitals in the first quartile were more likely than those in the fourth quartile to have primary percutaneous coronary intervention capabilities (80% vs. 73%), in-house cardiac surgery (66% vs. 57%), and a heart transplant center (13% vs. 2%).
In addition, the hospitals in the highest quartile had higher rates of adherence than those in the lowest quartile to guideline-directed heart failure therapies, including evidence-based beta-blocker use, ACE inhibitor and angiotensin receptor blocker use, postdischarge heart failure follow-up, implantable cardioverter defibrillator placement prior to discharge, and cardiac resynchronization therapy prior to discharge.The study was limited by a possible lack of generalizability to hospitals not participating in the GWTG program, Dr. Pandey said. In addition, “we cannot establish causation between hospital performance based on 30-day RSMR and long-term survival.”
However, the long-term survival advantage for heart failure patients treated at hospitals with the highest measures of short-term performance suggests that the 30-day RSMR could be used as an incentive for quality care and the improvement of long-term outcomes, he said.
Dr. Pandey had no financial conflicts to disclose. The Get With the Guidelines–Heart Failure program is supported by the American Heart Association, and has been previously funded by Medtronic, GlaxoSmithKline, Ortho-McNeil, and the AHA Pharmaceutical Roundtable. The findings were published simultaneously in JAMA Cardiology (2018 Mar 12. doi:10.1001/jamacardio.2018.0579).
SOURCE: Pandy A. ACC 2018.
ORLANDO – Hospitals in the first quartile of short-term performance in treating heart failure patients had higher long-term survival rates for those patients, based on data from 317 hospitals that participated in a voluntary quality improvement program.
The burden of heart failure remains substantial in the United States, and health policies are increasingly focused on improving care for heart failure patients, said Ambarish Pandey, MD, of the University of Texas, Dallas, in a presentation at the annual meeting of the American College of Cardiology.
The researchers assessed hospital performance based on 30-day risk-standardized mortality rates (RSMR) in hospitals participating in the Get With the Guidelines–Heart Failure (GWTG-HF) registry, using a hierarchical, logistic regression model to calculate hospital-specific 30-day RSMRs.
Get With the Guidelines is a voluntary, observational quality improvement program that has been linked with CMS to capture long-term follow-up data, Dr. Pandey explained.
The study included 106,304 heart failure patients older than 65 years at 317 GWTG hospitals across the United States during 2005-2013. The hospitals were divided into performance quartiles based on 30-day RSMR. The 30-day RSMRs were 8.6%, 9.4%, 9.9%, and 10.7% in the first, second, third, and fourth quartiles, respectively.
There was a strong association between the top-performing hospitals and long-term survival rates for the patients that persisted beyond 30 days, said Dr. Pandey. The mortality rates after 5 years were 75.6%, 76.2%, 76.9%, and 79.6%, in the first, second, third, and fourth quartiles, respectively.
The hospitals in the first quartile were more likely than those in the fourth quartile to have primary percutaneous coronary intervention capabilities (80% vs. 73%), in-house cardiac surgery (66% vs. 57%), and a heart transplant center (13% vs. 2%).
In addition, the hospitals in the highest quartile had higher rates of adherence than those in the lowest quartile to guideline-directed heart failure therapies, including evidence-based beta-blocker use, ACE inhibitor and angiotensin receptor blocker use, postdischarge heart failure follow-up, implantable cardioverter defibrillator placement prior to discharge, and cardiac resynchronization therapy prior to discharge.The study was limited by a possible lack of generalizability to hospitals not participating in the GWTG program, Dr. Pandey said. In addition, “we cannot establish causation between hospital performance based on 30-day RSMR and long-term survival.”
However, the long-term survival advantage for heart failure patients treated at hospitals with the highest measures of short-term performance suggests that the 30-day RSMR could be used as an incentive for quality care and the improvement of long-term outcomes, he said.
Dr. Pandey had no financial conflicts to disclose. The Get With the Guidelines–Heart Failure program is supported by the American Heart Association, and has been previously funded by Medtronic, GlaxoSmithKline, Ortho-McNeil, and the AHA Pharmaceutical Roundtable. The findings were published simultaneously in JAMA Cardiology (2018 Mar 12. doi:10.1001/jamacardio.2018.0579).
SOURCE: Pandy A. ACC 2018.
ORLANDO – Hospitals in the first quartile of short-term performance in treating heart failure patients had higher long-term survival rates for those patients, based on data from 317 hospitals that participated in a voluntary quality improvement program.
The burden of heart failure remains substantial in the United States, and health policies are increasingly focused on improving care for heart failure patients, said Ambarish Pandey, MD, of the University of Texas, Dallas, in a presentation at the annual meeting of the American College of Cardiology.
The researchers assessed hospital performance based on 30-day risk-standardized mortality rates (RSMR) in hospitals participating in the Get With the Guidelines–Heart Failure (GWTG-HF) registry, using a hierarchical, logistic regression model to calculate hospital-specific 30-day RSMRs.
Get With the Guidelines is a voluntary, observational quality improvement program that has been linked with CMS to capture long-term follow-up data, Dr. Pandey explained.
The study included 106,304 heart failure patients older than 65 years at 317 GWTG hospitals across the United States during 2005-2013. The hospitals were divided into performance quartiles based on 30-day RSMR. The 30-day RSMRs were 8.6%, 9.4%, 9.9%, and 10.7% in the first, second, third, and fourth quartiles, respectively.
There was a strong association between the top-performing hospitals and long-term survival rates for the patients that persisted beyond 30 days, said Dr. Pandey. The mortality rates after 5 years were 75.6%, 76.2%, 76.9%, and 79.6%, in the first, second, third, and fourth quartiles, respectively.
The hospitals in the first quartile were more likely than those in the fourth quartile to have primary percutaneous coronary intervention capabilities (80% vs. 73%), in-house cardiac surgery (66% vs. 57%), and a heart transplant center (13% vs. 2%).
In addition, the hospitals in the highest quartile had higher rates of adherence than those in the lowest quartile to guideline-directed heart failure therapies, including evidence-based beta-blocker use, ACE inhibitor and angiotensin receptor blocker use, postdischarge heart failure follow-up, implantable cardioverter defibrillator placement prior to discharge, and cardiac resynchronization therapy prior to discharge.The study was limited by a possible lack of generalizability to hospitals not participating in the GWTG program, Dr. Pandey said. In addition, “we cannot establish causation between hospital performance based on 30-day RSMR and long-term survival.”
However, the long-term survival advantage for heart failure patients treated at hospitals with the highest measures of short-term performance suggests that the 30-day RSMR could be used as an incentive for quality care and the improvement of long-term outcomes, he said.
Dr. Pandey had no financial conflicts to disclose. The Get With the Guidelines–Heart Failure program is supported by the American Heart Association, and has been previously funded by Medtronic, GlaxoSmithKline, Ortho-McNeil, and the AHA Pharmaceutical Roundtable. The findings were published simultaneously in JAMA Cardiology (2018 Mar 12. doi:10.1001/jamacardio.2018.0579).
SOURCE: Pandy A. ACC 2018.
REPORTING FROM ACC 2018
Key clinical point:
Major finding: Hospitals in the lowest quartile had a 22% higher 5-year mortality rate for heart failure patients compared with the highest quartile hospitals.
Study details: The data come from 106,304 heart failure patients admitted to 317 hospitals participating in a voluntary quality improvement program.
Disclosures: Dr. Pandey had no financial conflicts to disclose. The Get With the Guidelines–Heart Failure program is supported by the American Heart Association, and has been previously funded by Medtronic, GlaxoSmithKline, Ortho-McNeil, and the AHA Pharmaceutical Roundtable.
Source: Pandey A. ACC 2018.
Takotsubo cardiomyopathy incidence, mortality on the rise
WASHINGTON – Hospitalizations for Takotsubo cardiomyopathy (TCM), a condition that primarily affects postmenopausal women, have been rising steadily, along with rates of in-hospital mortality due to this condition, according to a study conducted with outcomes from the National Inpatient Sample (NIS) database.
The study was presented at CRT 2018, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.
Importantly, a multivariate analysis of predictors of in-hospital mortality based on this database revealed that there were “several potentially reversible causes,” reported Konstantinos V. Voudris, MD, PhD, who is completing a residency in internal medicine at the University of Illinois at Chicago.
TCM, which is characterized by left ventricular apical akinesis and chest pain that mimics the features of acute coronary syndromes (ACS), was first described in 1990 in Japan. The first U.S. case was reported in 1998, but the condition is now well recognized and an ICD code was created for Takotsubo cardiomyopathy in 2007.
There were 72,559 TCM admissions during the study period. When stratified by year, the annual rate of TCM cases rose significantly, from 11.1 to 43.8 per 100,000 hospitalizations from 2007 to 2013.
Although overall in-hospital mortality was 2.5%, it climbed from 1.4% in 2007 to 3.2% in 2013. When compared to patients who did not die during hospitalizations, those who did die were on average older (69.9 vs. 66.4 years; P less than .0001) and had more comorbidities. When a multivariate adjustment was made for baseline clinical risk, the presence of acute kidney injury (AKI), chronic obstructive pulmonary disease (COPD), peripheral artery disease (PAD), pulmonary hypertension, and arrhythmias remained significant predictors of mortality in patients with TCM.
“We found a number of modifiable and nonmodifiable factors that are associated with a significantly increased mortality, and we think clinicians should be aware of these factors when managing this condition,” Dr. Voudris reported.
Of these risk factors, AKI was associated with the greatest increased odds ratio (OR) with a more than fourfold increased risk of death (OR, 4.18; P less than .001). The presence of PAD (OR, 1.87; P less than .0001) and arrhythmia (OR, 1.88; P less than .0001) almost doubled the risk of in-hospital mortality.
Although females represented 89% of the TCM cases collected during the study period, males with comorbid diseases were at particularly high risk of death, an observation that is consistent with previous reports, according to Dr. Voudris. Relative to women, men were more likely to present with unstable hemodynamics and to develop cardiogenic shock.
Although Dr. Voudris acknowledged that the rising number of hospitalizations for TCM is likely due largely to increasing recognition of this condition, he suggested that there may be other contributing factors to the growing incidence, such as the aging of the U.S. population. He noted that the rise in cases persisted throughout the study period when awareness of TCM might be expected to have improved.
“This is still an uncommon disease, but it is important to recognize,” agreed Sachin Kumar, MD, an interventional cardiologist at the University of Texas Health Science Center at Houston. Moderator of the session in which these data were presented, Dr. Kumar indicated that it is important to increase awareness of the condition to accelerate the time to diagnosis and treatment.
Dr. Voudris reported no financial relationships relevant to this study.
SOURCE: Voudris, KV. CRT 2018.
WASHINGTON – Hospitalizations for Takotsubo cardiomyopathy (TCM), a condition that primarily affects postmenopausal women, have been rising steadily, along with rates of in-hospital mortality due to this condition, according to a study conducted with outcomes from the National Inpatient Sample (NIS) database.
The study was presented at CRT 2018, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.
Importantly, a multivariate analysis of predictors of in-hospital mortality based on this database revealed that there were “several potentially reversible causes,” reported Konstantinos V. Voudris, MD, PhD, who is completing a residency in internal medicine at the University of Illinois at Chicago.
TCM, which is characterized by left ventricular apical akinesis and chest pain that mimics the features of acute coronary syndromes (ACS), was first described in 1990 in Japan. The first U.S. case was reported in 1998, but the condition is now well recognized and an ICD code was created for Takotsubo cardiomyopathy in 2007.
There were 72,559 TCM admissions during the study period. When stratified by year, the annual rate of TCM cases rose significantly, from 11.1 to 43.8 per 100,000 hospitalizations from 2007 to 2013.
Although overall in-hospital mortality was 2.5%, it climbed from 1.4% in 2007 to 3.2% in 2013. When compared to patients who did not die during hospitalizations, those who did die were on average older (69.9 vs. 66.4 years; P less than .0001) and had more comorbidities. When a multivariate adjustment was made for baseline clinical risk, the presence of acute kidney injury (AKI), chronic obstructive pulmonary disease (COPD), peripheral artery disease (PAD), pulmonary hypertension, and arrhythmias remained significant predictors of mortality in patients with TCM.
“We found a number of modifiable and nonmodifiable factors that are associated with a significantly increased mortality, and we think clinicians should be aware of these factors when managing this condition,” Dr. Voudris reported.
Of these risk factors, AKI was associated with the greatest increased odds ratio (OR) with a more than fourfold increased risk of death (OR, 4.18; P less than .001). The presence of PAD (OR, 1.87; P less than .0001) and arrhythmia (OR, 1.88; P less than .0001) almost doubled the risk of in-hospital mortality.
Although females represented 89% of the TCM cases collected during the study period, males with comorbid diseases were at particularly high risk of death, an observation that is consistent with previous reports, according to Dr. Voudris. Relative to women, men were more likely to present with unstable hemodynamics and to develop cardiogenic shock.
Although Dr. Voudris acknowledged that the rising number of hospitalizations for TCM is likely due largely to increasing recognition of this condition, he suggested that there may be other contributing factors to the growing incidence, such as the aging of the U.S. population. He noted that the rise in cases persisted throughout the study period when awareness of TCM might be expected to have improved.
“This is still an uncommon disease, but it is important to recognize,” agreed Sachin Kumar, MD, an interventional cardiologist at the University of Texas Health Science Center at Houston. Moderator of the session in which these data were presented, Dr. Kumar indicated that it is important to increase awareness of the condition to accelerate the time to diagnosis and treatment.
Dr. Voudris reported no financial relationships relevant to this study.
SOURCE: Voudris, KV. CRT 2018.
WASHINGTON – Hospitalizations for Takotsubo cardiomyopathy (TCM), a condition that primarily affects postmenopausal women, have been rising steadily, along with rates of in-hospital mortality due to this condition, according to a study conducted with outcomes from the National Inpatient Sample (NIS) database.
The study was presented at CRT 2018, sponsored by the Cardiovascular Research Institute at Washington Hospital Center.
Importantly, a multivariate analysis of predictors of in-hospital mortality based on this database revealed that there were “several potentially reversible causes,” reported Konstantinos V. Voudris, MD, PhD, who is completing a residency in internal medicine at the University of Illinois at Chicago.
TCM, which is characterized by left ventricular apical akinesis and chest pain that mimics the features of acute coronary syndromes (ACS), was first described in 1990 in Japan. The first U.S. case was reported in 1998, but the condition is now well recognized and an ICD code was created for Takotsubo cardiomyopathy in 2007.
There were 72,559 TCM admissions during the study period. When stratified by year, the annual rate of TCM cases rose significantly, from 11.1 to 43.8 per 100,000 hospitalizations from 2007 to 2013.
Although overall in-hospital mortality was 2.5%, it climbed from 1.4% in 2007 to 3.2% in 2013. When compared to patients who did not die during hospitalizations, those who did die were on average older (69.9 vs. 66.4 years; P less than .0001) and had more comorbidities. When a multivariate adjustment was made for baseline clinical risk, the presence of acute kidney injury (AKI), chronic obstructive pulmonary disease (COPD), peripheral artery disease (PAD), pulmonary hypertension, and arrhythmias remained significant predictors of mortality in patients with TCM.
“We found a number of modifiable and nonmodifiable factors that are associated with a significantly increased mortality, and we think clinicians should be aware of these factors when managing this condition,” Dr. Voudris reported.
Of these risk factors, AKI was associated with the greatest increased odds ratio (OR) with a more than fourfold increased risk of death (OR, 4.18; P less than .001). The presence of PAD (OR, 1.87; P less than .0001) and arrhythmia (OR, 1.88; P less than .0001) almost doubled the risk of in-hospital mortality.
Although females represented 89% of the TCM cases collected during the study period, males with comorbid diseases were at particularly high risk of death, an observation that is consistent with previous reports, according to Dr. Voudris. Relative to women, men were more likely to present with unstable hemodynamics and to develop cardiogenic shock.
Although Dr. Voudris acknowledged that the rising number of hospitalizations for TCM is likely due largely to increasing recognition of this condition, he suggested that there may be other contributing factors to the growing incidence, such as the aging of the U.S. population. He noted that the rise in cases persisted throughout the study period when awareness of TCM might be expected to have improved.
“This is still an uncommon disease, but it is important to recognize,” agreed Sachin Kumar, MD, an interventional cardiologist at the University of Texas Health Science Center at Houston. Moderator of the session in which these data were presented, Dr. Kumar indicated that it is important to increase awareness of the condition to accelerate the time to diagnosis and treatment.
Dr. Voudris reported no financial relationships relevant to this study.
SOURCE: Voudris, KV. CRT 2018.
REPORTING FROM CRT 2018
Key clinical point: The Takotsubo cardiomyopathy hospitalization and mortality rates have increased in the United States, according to national data.
Major finding: From 2007 to 2013, Takotsubo cases rose from 11.1 to 43.8 cases per 100,000 hospitalizations and in-hospital mortality more than doubled.
Data source: Retrospective national database analysis.
Disclosures: Dr. Voudris reports no financial relationships relevant to this study.
Source: Voudris, KV. CRT 2018.
VIDEO: Dabigatran effective for myocardial injury after noncardiac surgery
ORLANDO – Treating patients who developed myocardial injury after noncardiac surgery with the anticoagulant dabigatran significantly cut the rate of subsequent major vascular complications in a randomized, multicenter trial with 1,754 patients, a result that gives surgeons and physicians the first evidence-based intervention for treating a common postsurgical condition.
“Because we have not systematically followed noncardiac surgery patients, it’s easy to presume that everyone is okay, but all the epidemiology data show that these patients [who develop myocardial injury after noncardiac surgery] don’t do okay. We need to be aggressive with secondary prophylaxis,” P.J. Devereaux, MD, said at the annual meeting of the American College of Cardiology. “The unfortunate thing is that right now, we don’t do much for these patients,” said Dr. Devereaux, professor of medicine and director of cardiology at McMaster University in Hamilton, Ont.
Results from prior epidemiology studies have shown that, among the roughly 200 million patients who undergo noncardiac surgery worldwide each year, 8% will develop MINS (myocardial injury after noncardiac surgery) (Anesthesiology. 2014 March;120[3]:564-78). The myocardial injury that defines MINS is identified by either an overt MI that meets the universal definition, or an otherwise unexplained rise in serum troponin levels from baseline in the first couple of days after surgery. In the new study, Dr. Devereaux and his associates identified 80% of MINS by a troponin rise and 20% by a diagnosed MI.
The challenge in diagnosing MINS and then administering dabigatran will be implementation of this strategy into routine practice, commented Erin A. Bohula May, MD, a cardiologist at Brigham and Women’s Hospital in Boston. “The problem is, troponin is not routinely measured in postoperative patients. It will be hard to change practice,” she noted.
Dr. Devereaux agreed that a significant barrier is convincing clinicians, especially surgeons, to routinely measure a patient’s troponin levels just before and immediately after surgery. “People are lulled into a false sense of security because patients [who develop MINS] usually don’t have chest pain,” he said in a video interview. “When we first showed that patients with MINS have bad outcomes, that convinced some [surgeons] to measure troponin after surgery. “Showing we can do something about it” is another important step toward fostering more awareness of and interest in diagnosing and treating MINS.
The Management of Myocardial Injury After Noncardiac Surgery Trial (MANAGE) enrolled 1,754 patients at 82 centers in 19 countries. Researchers randomized patients to treatment with either 110 mg dabigatran b.i.d. or placebo. A majority of patients in both arms also received aspirin and a statin, treatments that Dr. Devereaux should be used along with dabigatran in routine practice, based on observational findings, although the efficacy of these drugs for MINS patients has not been tested in randomized studies. The study’s primary endpoint was the incidence of major vascular complications, a composite that included vascular mortality, nonfatal MI, nonfatal and nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, or symptomatic venous thromboembolism.
After an average follow-up of 16 months, the primary endpoint occurred in 11% of the dabigatran-treated patients and in 15% of controls, which represented a 28% risk reduction that was statistically significant. The study’s primary safety endpoint was a composite of life-threatening, major, and critical organ bleeds, which occurred in 3% of the dabigatran-treated patients and in 4% of controls, a nonsignificant difference. The dabigatran-treated patients showed a significant excess of both minor bleeds – 15% compared with 10% in controls – and “nonsignificant” lower gastrointestinal bleeds, 4% with dabigatran and 1% in the controls. The dabigatran-treated patients also had a significantly higher incidence of dyspepsia.
MANAGE was funded by the Population Health Research Institute and had no commercial funding. Dr. Devereaux has received research support from Abbott Diagnostics, Boehringer Ingelheim, Philips Healthcare, and Roche Diagnostics. Dr. May has been a consultant to Daiichi Sankyo, Merck, and Servier and has received research funding from Eisai.
SOURCE: Devereaux P et al. ACC 18.
Dr. Devereaux and his associates are to be congratulated on identifying a new disease entity, MINS (myocardial injury after noncardiac surgery), and now giving us a way to treat it. MINS is extremely common and quite morbid, and there had never before been a trial that studied its treatment. Identifying patients with MINS is extremely important. These are very-high-risk patients, and they are very hard to find. The results from MANAGE give us a way to do something about MINS and an opportunity to improve patient outcomes.
Pamela S. Douglas, MD , is a cardiologist and professor of medicine at Duke University in Durham, N.C. She had no disclosures. She made these comments as a discussant for MANAGE and in an interview.
Dr. Devereaux and his associates are to be congratulated on identifying a new disease entity, MINS (myocardial injury after noncardiac surgery), and now giving us a way to treat it. MINS is extremely common and quite morbid, and there had never before been a trial that studied its treatment. Identifying patients with MINS is extremely important. These are very-high-risk patients, and they are very hard to find. The results from MANAGE give us a way to do something about MINS and an opportunity to improve patient outcomes.
Pamela S. Douglas, MD , is a cardiologist and professor of medicine at Duke University in Durham, N.C. She had no disclosures. She made these comments as a discussant for MANAGE and in an interview.
Dr. Devereaux and his associates are to be congratulated on identifying a new disease entity, MINS (myocardial injury after noncardiac surgery), and now giving us a way to treat it. MINS is extremely common and quite morbid, and there had never before been a trial that studied its treatment. Identifying patients with MINS is extremely important. These are very-high-risk patients, and they are very hard to find. The results from MANAGE give us a way to do something about MINS and an opportunity to improve patient outcomes.
Pamela S. Douglas, MD , is a cardiologist and professor of medicine at Duke University in Durham, N.C. She had no disclosures. She made these comments as a discussant for MANAGE and in an interview.
ORLANDO – Treating patients who developed myocardial injury after noncardiac surgery with the anticoagulant dabigatran significantly cut the rate of subsequent major vascular complications in a randomized, multicenter trial with 1,754 patients, a result that gives surgeons and physicians the first evidence-based intervention for treating a common postsurgical condition.
“Because we have not systematically followed noncardiac surgery patients, it’s easy to presume that everyone is okay, but all the epidemiology data show that these patients [who develop myocardial injury after noncardiac surgery] don’t do okay. We need to be aggressive with secondary prophylaxis,” P.J. Devereaux, MD, said at the annual meeting of the American College of Cardiology. “The unfortunate thing is that right now, we don’t do much for these patients,” said Dr. Devereaux, professor of medicine and director of cardiology at McMaster University in Hamilton, Ont.
Results from prior epidemiology studies have shown that, among the roughly 200 million patients who undergo noncardiac surgery worldwide each year, 8% will develop MINS (myocardial injury after noncardiac surgery) (Anesthesiology. 2014 March;120[3]:564-78). The myocardial injury that defines MINS is identified by either an overt MI that meets the universal definition, or an otherwise unexplained rise in serum troponin levels from baseline in the first couple of days after surgery. In the new study, Dr. Devereaux and his associates identified 80% of MINS by a troponin rise and 20% by a diagnosed MI.
The challenge in diagnosing MINS and then administering dabigatran will be implementation of this strategy into routine practice, commented Erin A. Bohula May, MD, a cardiologist at Brigham and Women’s Hospital in Boston. “The problem is, troponin is not routinely measured in postoperative patients. It will be hard to change practice,” she noted.
Dr. Devereaux agreed that a significant barrier is convincing clinicians, especially surgeons, to routinely measure a patient’s troponin levels just before and immediately after surgery. “People are lulled into a false sense of security because patients [who develop MINS] usually don’t have chest pain,” he said in a video interview. “When we first showed that patients with MINS have bad outcomes, that convinced some [surgeons] to measure troponin after surgery. “Showing we can do something about it” is another important step toward fostering more awareness of and interest in diagnosing and treating MINS.
The Management of Myocardial Injury After Noncardiac Surgery Trial (MANAGE) enrolled 1,754 patients at 82 centers in 19 countries. Researchers randomized patients to treatment with either 110 mg dabigatran b.i.d. or placebo. A majority of patients in both arms also received aspirin and a statin, treatments that Dr. Devereaux should be used along with dabigatran in routine practice, based on observational findings, although the efficacy of these drugs for MINS patients has not been tested in randomized studies. The study’s primary endpoint was the incidence of major vascular complications, a composite that included vascular mortality, nonfatal MI, nonfatal and nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, or symptomatic venous thromboembolism.
After an average follow-up of 16 months, the primary endpoint occurred in 11% of the dabigatran-treated patients and in 15% of controls, which represented a 28% risk reduction that was statistically significant. The study’s primary safety endpoint was a composite of life-threatening, major, and critical organ bleeds, which occurred in 3% of the dabigatran-treated patients and in 4% of controls, a nonsignificant difference. The dabigatran-treated patients showed a significant excess of both minor bleeds – 15% compared with 10% in controls – and “nonsignificant” lower gastrointestinal bleeds, 4% with dabigatran and 1% in the controls. The dabigatran-treated patients also had a significantly higher incidence of dyspepsia.
MANAGE was funded by the Population Health Research Institute and had no commercial funding. Dr. Devereaux has received research support from Abbott Diagnostics, Boehringer Ingelheim, Philips Healthcare, and Roche Diagnostics. Dr. May has been a consultant to Daiichi Sankyo, Merck, and Servier and has received research funding from Eisai.
SOURCE: Devereaux P et al. ACC 18.
ORLANDO – Treating patients who developed myocardial injury after noncardiac surgery with the anticoagulant dabigatran significantly cut the rate of subsequent major vascular complications in a randomized, multicenter trial with 1,754 patients, a result that gives surgeons and physicians the first evidence-based intervention for treating a common postsurgical condition.
“Because we have not systematically followed noncardiac surgery patients, it’s easy to presume that everyone is okay, but all the epidemiology data show that these patients [who develop myocardial injury after noncardiac surgery] don’t do okay. We need to be aggressive with secondary prophylaxis,” P.J. Devereaux, MD, said at the annual meeting of the American College of Cardiology. “The unfortunate thing is that right now, we don’t do much for these patients,” said Dr. Devereaux, professor of medicine and director of cardiology at McMaster University in Hamilton, Ont.
Results from prior epidemiology studies have shown that, among the roughly 200 million patients who undergo noncardiac surgery worldwide each year, 8% will develop MINS (myocardial injury after noncardiac surgery) (Anesthesiology. 2014 March;120[3]:564-78). The myocardial injury that defines MINS is identified by either an overt MI that meets the universal definition, or an otherwise unexplained rise in serum troponin levels from baseline in the first couple of days after surgery. In the new study, Dr. Devereaux and his associates identified 80% of MINS by a troponin rise and 20% by a diagnosed MI.
The challenge in diagnosing MINS and then administering dabigatran will be implementation of this strategy into routine practice, commented Erin A. Bohula May, MD, a cardiologist at Brigham and Women’s Hospital in Boston. “The problem is, troponin is not routinely measured in postoperative patients. It will be hard to change practice,” she noted.
Dr. Devereaux agreed that a significant barrier is convincing clinicians, especially surgeons, to routinely measure a patient’s troponin levels just before and immediately after surgery. “People are lulled into a false sense of security because patients [who develop MINS] usually don’t have chest pain,” he said in a video interview. “When we first showed that patients with MINS have bad outcomes, that convinced some [surgeons] to measure troponin after surgery. “Showing we can do something about it” is another important step toward fostering more awareness of and interest in diagnosing and treating MINS.
The Management of Myocardial Injury After Noncardiac Surgery Trial (MANAGE) enrolled 1,754 patients at 82 centers in 19 countries. Researchers randomized patients to treatment with either 110 mg dabigatran b.i.d. or placebo. A majority of patients in both arms also received aspirin and a statin, treatments that Dr. Devereaux should be used along with dabigatran in routine practice, based on observational findings, although the efficacy of these drugs for MINS patients has not been tested in randomized studies. The study’s primary endpoint was the incidence of major vascular complications, a composite that included vascular mortality, nonfatal MI, nonfatal and nonhemorrhagic stroke, peripheral arterial thrombosis, amputation, or symptomatic venous thromboembolism.
After an average follow-up of 16 months, the primary endpoint occurred in 11% of the dabigatran-treated patients and in 15% of controls, which represented a 28% risk reduction that was statistically significant. The study’s primary safety endpoint was a composite of life-threatening, major, and critical organ bleeds, which occurred in 3% of the dabigatran-treated patients and in 4% of controls, a nonsignificant difference. The dabigatran-treated patients showed a significant excess of both minor bleeds – 15% compared with 10% in controls – and “nonsignificant” lower gastrointestinal bleeds, 4% with dabigatran and 1% in the controls. The dabigatran-treated patients also had a significantly higher incidence of dyspepsia.
MANAGE was funded by the Population Health Research Institute and had no commercial funding. Dr. Devereaux has received research support from Abbott Diagnostics, Boehringer Ingelheim, Philips Healthcare, and Roche Diagnostics. Dr. May has been a consultant to Daiichi Sankyo, Merck, and Servier and has received research funding from Eisai.
SOURCE: Devereaux P et al. ACC 18.
REPORTING FROM ACC 18
Key clinical point: Dabigatran is the first intervention proven to benefit patients with MINS.
Major finding: Major vascular complications occurred in 11% of patients on dabigatran and 15% on placebo.
Study details: MANAGE, a multicenter, randomized trial with 1,754 patients.
Disclosures: MANAGE was funded by the Population Health Research Institute and had no commercial funding. Dr. Devereaux has received research support from Abbott Diagnostics, Boehringer Ingelheim, Philips Healthcare, and Roche Diagnostics. Dr. May has been a consultant to Daiichi Sankyo, Merck, and Servier and has received research funding from Eisai.
Source: Devereaux P et al. ACC 18.
MOMENTUM 3 HeartMate 3 LVAD ‘practice changing’
ORLANDO – of follow-up in patients with advanced heart failure in the large multicenter MOMENTUM 3 trial, Mandeep R. Mehra, MD, reported at the annual meeting of the American College of Cardiology.
HeartMate 3 recipients had a 90% lower risk of undergoing reoperation to replace or remove their device because of malfunction, and a stroke rate half that in the HeartMate II group.
“This was the lowest rate of stroke ever seen in any LVAD trial,” according to Dr. Mehra, medical director of the Brigham and Women’s Hospital Heart and Vascular Center, Boston, and professor of medicine at Harvard Medical School.
“We believe this is a practice-changing result in the field, and that the real implication of our findings is to reassure those who refer or treat patients with advanced heart failure that it is perhaps going to be ignorant not to refer patients for consideration for destination therapy,” he said at a press conference highlighting the MOMENTUM 3 results, also presented in a late-breaking clinical trials session.
The HeartMate 3 is a miniaturized centrifugal-flow device that fits entirely within the chest, whereas the HeartMate II requires creation of a pocket in the abdomen. The HeartMate 3 was designed to prevent pump thrombosis – a common limiting problem with the HeartMate II and other LVADs – by employing three innovations: use of wide blood-flow passages to reduce shear stress and minimize disruption of red blood cells as they pass through the pump; reliance on magnetic levitation technology to create a frictionless pump with no mechanical bearings, which are subject to wear and tear; and incorporation of an artificial fixed pulse that speeds up and slows every 2 seconds in order to minimize blood stasis, which promotes thrombosis, the cardiologist explained in a video interview.
MOMENTUM 3 is the largest-ever randomized trial of LVAD therapy, involving 1,028 advanced heart failure patients at 69 U.S. centers. The study population is a mix of bridge-to-transplant patients and others who weren’t eligible for heart transplantation and are using their device as lifelong destination therapy. In an earlier report on the first 294 patients to reach 6 months of follow-up post implantation, Dr. Mehra and his coinvestigators showed that the HeartMate 3 group had a significantly lower incidence of the composite endpoint of disabling stroke or reoperation to replace or remove the device (N Engl J Med. 2017 Feb 2;376[5]:440-50).
At ACC 2018, he presented the prespecified 2-year analysis of results in the first 366 patients to reach that benchmark. The rate of survival free of disabling stroke or reoperation for device malfunction was 79.5% in the HeartMate 3 group and 60.2% with the HeartMate II, for a highly significant 54% reduction in the risk of bad outcome. Reoperation for device malfunction occurred in 1.6% of HeartMate 3 patients versus 17% of those with a HeartMate II, for a 92% reduction in risk. Two-year survival was 82.8% in the HeartMate 3 group and 76.2% in HeartMate II recipients.
The overall stroke rate was 10% with the HeartMate 3, compared with 19% with the older, axial-flow LVAD. The incidence of disabling stroke was 3% in the HeartMate 3 group and similar at 2% with the HeartMate II; however, nondisabling stroke occurred in only 3% of HeartMate 3 recipients, compared with 14% of patients with the HeartMate II.
“There has always been this notion that, ‘There are so many complications with this device, so let’s suffer with the disease rather than suffer with the pump.’ Now we’re showing that you don’t suffer with the pump as with the earlier-generation devices. I think this is going to open the gates for more referrals and more opportunities for destination therapy in patients who are deemed ineligible for transplant,” Dr. Mehra predicted.
Discussant James L. Janzuzzi Jr., called the MOMENTUM 3 results “a very-much-needed step forward.”
“Perhaps the most dramatic observation in this study is the dramatic reduction in thrombosis events requiring reoperation. In essence, this problem was entirely prevented by the use of this magnetically levitated centrifugal-flow device. Reoperation for thrombosis accounted for two-thirds of the reoperations in the HeartMate II group and the rate was zero in the HeartMate 3 population. Essentially, with this technology we’ve addressed a very important unmet need by reducing the onset of pump thrombosis, which is the precursor to either pump dysfunction or embolic stroke,” commented Dr. Januzzi, professor of medicine at Harvard Medical School, Boston.
Given the 83% survival rate at 2 years in the HeartMate 3 group in the MOMENTUM 3 trial, the on-average 50% survival at 10 years for heart transplant recipients, and the perpetual enormous shortage of donor organs, it’s time to consider a randomized trial of an advanced LVAD such as the HeartMate 3 versus heart transplantation, with quality-of-life outcomes front and center, he asserted.
Dr. Mehra was all for the idea. He noted that within the community of physicians and surgeons who provide care for advanced heart failure patients there is a growing move to replace problematic axial-flow LVADs requiring reoperation with a HeartMate 3 upgrade.
The MOMENTUM 3 trial is funded by Abbott. Dr. Mehra reported receiving research funds from and serving as a consultant to the company.
Simultaneous with his presentation at ACC 2018, the 2-year results of MOMENTUM 3 were published online at NEJM.org (doi: 10.1056/NEJMoa1800866).
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
SOURCE: Mehra M et al. ACC 18.
ORLANDO – of follow-up in patients with advanced heart failure in the large multicenter MOMENTUM 3 trial, Mandeep R. Mehra, MD, reported at the annual meeting of the American College of Cardiology.
HeartMate 3 recipients had a 90% lower risk of undergoing reoperation to replace or remove their device because of malfunction, and a stroke rate half that in the HeartMate II group.
“This was the lowest rate of stroke ever seen in any LVAD trial,” according to Dr. Mehra, medical director of the Brigham and Women’s Hospital Heart and Vascular Center, Boston, and professor of medicine at Harvard Medical School.
“We believe this is a practice-changing result in the field, and that the real implication of our findings is to reassure those who refer or treat patients with advanced heart failure that it is perhaps going to be ignorant not to refer patients for consideration for destination therapy,” he said at a press conference highlighting the MOMENTUM 3 results, also presented in a late-breaking clinical trials session.
The HeartMate 3 is a miniaturized centrifugal-flow device that fits entirely within the chest, whereas the HeartMate II requires creation of a pocket in the abdomen. The HeartMate 3 was designed to prevent pump thrombosis – a common limiting problem with the HeartMate II and other LVADs – by employing three innovations: use of wide blood-flow passages to reduce shear stress and minimize disruption of red blood cells as they pass through the pump; reliance on magnetic levitation technology to create a frictionless pump with no mechanical bearings, which are subject to wear and tear; and incorporation of an artificial fixed pulse that speeds up and slows every 2 seconds in order to minimize blood stasis, which promotes thrombosis, the cardiologist explained in a video interview.
MOMENTUM 3 is the largest-ever randomized trial of LVAD therapy, involving 1,028 advanced heart failure patients at 69 U.S. centers. The study population is a mix of bridge-to-transplant patients and others who weren’t eligible for heart transplantation and are using their device as lifelong destination therapy. In an earlier report on the first 294 patients to reach 6 months of follow-up post implantation, Dr. Mehra and his coinvestigators showed that the HeartMate 3 group had a significantly lower incidence of the composite endpoint of disabling stroke or reoperation to replace or remove the device (N Engl J Med. 2017 Feb 2;376[5]:440-50).
At ACC 2018, he presented the prespecified 2-year analysis of results in the first 366 patients to reach that benchmark. The rate of survival free of disabling stroke or reoperation for device malfunction was 79.5% in the HeartMate 3 group and 60.2% with the HeartMate II, for a highly significant 54% reduction in the risk of bad outcome. Reoperation for device malfunction occurred in 1.6% of HeartMate 3 patients versus 17% of those with a HeartMate II, for a 92% reduction in risk. Two-year survival was 82.8% in the HeartMate 3 group and 76.2% in HeartMate II recipients.
The overall stroke rate was 10% with the HeartMate 3, compared with 19% with the older, axial-flow LVAD. The incidence of disabling stroke was 3% in the HeartMate 3 group and similar at 2% with the HeartMate II; however, nondisabling stroke occurred in only 3% of HeartMate 3 recipients, compared with 14% of patients with the HeartMate II.
“There has always been this notion that, ‘There are so many complications with this device, so let’s suffer with the disease rather than suffer with the pump.’ Now we’re showing that you don’t suffer with the pump as with the earlier-generation devices. I think this is going to open the gates for more referrals and more opportunities for destination therapy in patients who are deemed ineligible for transplant,” Dr. Mehra predicted.
Discussant James L. Janzuzzi Jr., called the MOMENTUM 3 results “a very-much-needed step forward.”
“Perhaps the most dramatic observation in this study is the dramatic reduction in thrombosis events requiring reoperation. In essence, this problem was entirely prevented by the use of this magnetically levitated centrifugal-flow device. Reoperation for thrombosis accounted for two-thirds of the reoperations in the HeartMate II group and the rate was zero in the HeartMate 3 population. Essentially, with this technology we’ve addressed a very important unmet need by reducing the onset of pump thrombosis, which is the precursor to either pump dysfunction or embolic stroke,” commented Dr. Januzzi, professor of medicine at Harvard Medical School, Boston.
Given the 83% survival rate at 2 years in the HeartMate 3 group in the MOMENTUM 3 trial, the on-average 50% survival at 10 years for heart transplant recipients, and the perpetual enormous shortage of donor organs, it’s time to consider a randomized trial of an advanced LVAD such as the HeartMate 3 versus heart transplantation, with quality-of-life outcomes front and center, he asserted.
Dr. Mehra was all for the idea. He noted that within the community of physicians and surgeons who provide care for advanced heart failure patients there is a growing move to replace problematic axial-flow LVADs requiring reoperation with a HeartMate 3 upgrade.
The MOMENTUM 3 trial is funded by Abbott. Dr. Mehra reported receiving research funds from and serving as a consultant to the company.
Simultaneous with his presentation at ACC 2018, the 2-year results of MOMENTUM 3 were published online at NEJM.org (doi: 10.1056/NEJMoa1800866).
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
SOURCE: Mehra M et al. ACC 18.
ORLANDO – of follow-up in patients with advanced heart failure in the large multicenter MOMENTUM 3 trial, Mandeep R. Mehra, MD, reported at the annual meeting of the American College of Cardiology.
HeartMate 3 recipients had a 90% lower risk of undergoing reoperation to replace or remove their device because of malfunction, and a stroke rate half that in the HeartMate II group.
“This was the lowest rate of stroke ever seen in any LVAD trial,” according to Dr. Mehra, medical director of the Brigham and Women’s Hospital Heart and Vascular Center, Boston, and professor of medicine at Harvard Medical School.
“We believe this is a practice-changing result in the field, and that the real implication of our findings is to reassure those who refer or treat patients with advanced heart failure that it is perhaps going to be ignorant not to refer patients for consideration for destination therapy,” he said at a press conference highlighting the MOMENTUM 3 results, also presented in a late-breaking clinical trials session.
The HeartMate 3 is a miniaturized centrifugal-flow device that fits entirely within the chest, whereas the HeartMate II requires creation of a pocket in the abdomen. The HeartMate 3 was designed to prevent pump thrombosis – a common limiting problem with the HeartMate II and other LVADs – by employing three innovations: use of wide blood-flow passages to reduce shear stress and minimize disruption of red blood cells as they pass through the pump; reliance on magnetic levitation technology to create a frictionless pump with no mechanical bearings, which are subject to wear and tear; and incorporation of an artificial fixed pulse that speeds up and slows every 2 seconds in order to minimize blood stasis, which promotes thrombosis, the cardiologist explained in a video interview.
MOMENTUM 3 is the largest-ever randomized trial of LVAD therapy, involving 1,028 advanced heart failure patients at 69 U.S. centers. The study population is a mix of bridge-to-transplant patients and others who weren’t eligible for heart transplantation and are using their device as lifelong destination therapy. In an earlier report on the first 294 patients to reach 6 months of follow-up post implantation, Dr. Mehra and his coinvestigators showed that the HeartMate 3 group had a significantly lower incidence of the composite endpoint of disabling stroke or reoperation to replace or remove the device (N Engl J Med. 2017 Feb 2;376[5]:440-50).
At ACC 2018, he presented the prespecified 2-year analysis of results in the first 366 patients to reach that benchmark. The rate of survival free of disabling stroke or reoperation for device malfunction was 79.5% in the HeartMate 3 group and 60.2% with the HeartMate II, for a highly significant 54% reduction in the risk of bad outcome. Reoperation for device malfunction occurred in 1.6% of HeartMate 3 patients versus 17% of those with a HeartMate II, for a 92% reduction in risk. Two-year survival was 82.8% in the HeartMate 3 group and 76.2% in HeartMate II recipients.
The overall stroke rate was 10% with the HeartMate 3, compared with 19% with the older, axial-flow LVAD. The incidence of disabling stroke was 3% in the HeartMate 3 group and similar at 2% with the HeartMate II; however, nondisabling stroke occurred in only 3% of HeartMate 3 recipients, compared with 14% of patients with the HeartMate II.
“There has always been this notion that, ‘There are so many complications with this device, so let’s suffer with the disease rather than suffer with the pump.’ Now we’re showing that you don’t suffer with the pump as with the earlier-generation devices. I think this is going to open the gates for more referrals and more opportunities for destination therapy in patients who are deemed ineligible for transplant,” Dr. Mehra predicted.
Discussant James L. Janzuzzi Jr., called the MOMENTUM 3 results “a very-much-needed step forward.”
“Perhaps the most dramatic observation in this study is the dramatic reduction in thrombosis events requiring reoperation. In essence, this problem was entirely prevented by the use of this magnetically levitated centrifugal-flow device. Reoperation for thrombosis accounted for two-thirds of the reoperations in the HeartMate II group and the rate was zero in the HeartMate 3 population. Essentially, with this technology we’ve addressed a very important unmet need by reducing the onset of pump thrombosis, which is the precursor to either pump dysfunction or embolic stroke,” commented Dr. Januzzi, professor of medicine at Harvard Medical School, Boston.
Given the 83% survival rate at 2 years in the HeartMate 3 group in the MOMENTUM 3 trial, the on-average 50% survival at 10 years for heart transplant recipients, and the perpetual enormous shortage of donor organs, it’s time to consider a randomized trial of an advanced LVAD such as the HeartMate 3 versus heart transplantation, with quality-of-life outcomes front and center, he asserted.
Dr. Mehra was all for the idea. He noted that within the community of physicians and surgeons who provide care for advanced heart failure patients there is a growing move to replace problematic axial-flow LVADs requiring reoperation with a HeartMate 3 upgrade.
The MOMENTUM 3 trial is funded by Abbott. Dr. Mehra reported receiving research funds from and serving as a consultant to the company.
Simultaneous with his presentation at ACC 2018, the 2-year results of MOMENTUM 3 were published online at NEJM.org (doi: 10.1056/NEJMoa1800866).
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
SOURCE: Mehra M et al. ACC 18.
REPORTING FROM ACC 18
Key clinical point: Landmark trial paves way to much wider use of LVADs as destination therapy.
Major finding: The 2-year rate of survival free of disabling stroke or reoperation to replace or remove a malfunctioning LVAD was 79.5% with the novel HeartMate 3 LVAD, compared with 60.2% with the commonly used HeartMate II axial-flow device.
Study details: This was a randomized, unblinded, multicenter study of more than 1,000 patients with advanced heart failure.
Disclosures: The MOMENTUM 3 trial was funded by Abbott. The presenter reported receiving research grants from and serving as a consultant to the company.
Source: Mehra MR et al. ACC 18.
CECCY: Carvedilol didn’t curb cardiotoxicity in breast cancer patients
ORLANDO – Anthracycline chemotherapy was associated with a cardiotoxicity incidence of roughly 14% of breast cancer patients regardless of treatment with carvedilol, based on data from a randomized trial of 200 patients.
“Cardio-oncology has been neglected,” Monica Samuel Avila, MD, of Hospital das Clínicas da Faculdade de Medicina da Universidade in São Paulo, Brazil, said in a video interview at the annual meeting of the American College of Cardiology. “We have seen improvement of survival in patients with cancer, but with that comes complications related to treatment. I think that the interactions between cardiologists and oncologists are increasing in a more important way,” she said.
In the Carvedilol for Prevention of Chemotherapy-Induced Cardiotoxicity (CECCY) Trial, Dr. Avila and colleagues evaluated primary prevention of cardiotoxicity in women with normal hearts who were undergoing chemotherapy for breast cancer.
Patients in the treatment group received a median carvedilol dose of 18.4 mg/day. The primary endpoint of cardiotoxicity, defined as a decrease in left ventricular ejection fraction (LVEF) of at least 10% at 6 months, occurred in 15% of carvedilol patients and 14% placebo patients, a nonsignificant difference. No significant differences occurred in diastolic dysfunction or in B-type natriuretic peptide (BNP) levels at 6 weeks, 12 weeks, or 24 weeks between the groups.
However, carvedilol patients showed significantly reduced troponin 1 levels compared with placebo, which suggests protection against myocardial injury, Dr. Avila said.
“In short follow up, we can see cardiotoxicity appearing, and we know we have to treat it promptly to prevent cardiac events,” she said.
Dr. Avila and colleagues identified 200 women older than 18 years with HER2-negative breast cancer tumor status and normal left ventricular ejection fraction. The patients were undergoing chemotherapy with 240 mg/m2 of anthracycline and were randomized to treatment with carvedilol or a placebo. Baseline characteristics were similar between the two groups.
Adverse effects were not significantly different between the groups, and the most common events in each group included dizziness, dry mouth, symptomatic hypertension, stomachache, and nausea. Although the results suggest that carvedilol can reduce the risk of myocardial injury, more research is needed to address the question of the increase in troponin without change in the LVEF, Dr. Avila noted. The study is ongoing and the research team intends to follow the low-risk patient population for a total of 2 years. “For high-risk patients, I am already giving carvedilol,” she said. “We believe if we find a difference in LVEF or clinical events, we could encourage cardiologists to give carvedilol in a low-risk population,” she said.
“This study highlights that there is no safe dose of anthracycline,” commented Bonnie Ky, MD of the University of Pennsylvania, Philadelphia, at a press briefing. She emphasized the value of carvedilol for a high-risk population, and stressed the importance of following long-term changes in heart injury markers after 1-2 years for low-risk patients.
Dr. Avila had no financial conflicts to disclose. Dr. Ky disclosed relationships with multiple companies including Bioinvent and Bristol Myers.
The findings were published simultaneously in the Journal of the American College of Cardiology.
SOURCE: Avila, M. ACC 18
ORLANDO – Anthracycline chemotherapy was associated with a cardiotoxicity incidence of roughly 14% of breast cancer patients regardless of treatment with carvedilol, based on data from a randomized trial of 200 patients.
“Cardio-oncology has been neglected,” Monica Samuel Avila, MD, of Hospital das Clínicas da Faculdade de Medicina da Universidade in São Paulo, Brazil, said in a video interview at the annual meeting of the American College of Cardiology. “We have seen improvement of survival in patients with cancer, but with that comes complications related to treatment. I think that the interactions between cardiologists and oncologists are increasing in a more important way,” she said.
In the Carvedilol for Prevention of Chemotherapy-Induced Cardiotoxicity (CECCY) Trial, Dr. Avila and colleagues evaluated primary prevention of cardiotoxicity in women with normal hearts who were undergoing chemotherapy for breast cancer.
Patients in the treatment group received a median carvedilol dose of 18.4 mg/day. The primary endpoint of cardiotoxicity, defined as a decrease in left ventricular ejection fraction (LVEF) of at least 10% at 6 months, occurred in 15% of carvedilol patients and 14% placebo patients, a nonsignificant difference. No significant differences occurred in diastolic dysfunction or in B-type natriuretic peptide (BNP) levels at 6 weeks, 12 weeks, or 24 weeks between the groups.
However, carvedilol patients showed significantly reduced troponin 1 levels compared with placebo, which suggests protection against myocardial injury, Dr. Avila said.
“In short follow up, we can see cardiotoxicity appearing, and we know we have to treat it promptly to prevent cardiac events,” she said.
Dr. Avila and colleagues identified 200 women older than 18 years with HER2-negative breast cancer tumor status and normal left ventricular ejection fraction. The patients were undergoing chemotherapy with 240 mg/m2 of anthracycline and were randomized to treatment with carvedilol or a placebo. Baseline characteristics were similar between the two groups.
Adverse effects were not significantly different between the groups, and the most common events in each group included dizziness, dry mouth, symptomatic hypertension, stomachache, and nausea. Although the results suggest that carvedilol can reduce the risk of myocardial injury, more research is needed to address the question of the increase in troponin without change in the LVEF, Dr. Avila noted. The study is ongoing and the research team intends to follow the low-risk patient population for a total of 2 years. “For high-risk patients, I am already giving carvedilol,” she said. “We believe if we find a difference in LVEF or clinical events, we could encourage cardiologists to give carvedilol in a low-risk population,” she said.
“This study highlights that there is no safe dose of anthracycline,” commented Bonnie Ky, MD of the University of Pennsylvania, Philadelphia, at a press briefing. She emphasized the value of carvedilol for a high-risk population, and stressed the importance of following long-term changes in heart injury markers after 1-2 years for low-risk patients.
Dr. Avila had no financial conflicts to disclose. Dr. Ky disclosed relationships with multiple companies including Bioinvent and Bristol Myers.
The findings were published simultaneously in the Journal of the American College of Cardiology.
SOURCE: Avila, M. ACC 18
ORLANDO – Anthracycline chemotherapy was associated with a cardiotoxicity incidence of roughly 14% of breast cancer patients regardless of treatment with carvedilol, based on data from a randomized trial of 200 patients.
“Cardio-oncology has been neglected,” Monica Samuel Avila, MD, of Hospital das Clínicas da Faculdade de Medicina da Universidade in São Paulo, Brazil, said in a video interview at the annual meeting of the American College of Cardiology. “We have seen improvement of survival in patients with cancer, but with that comes complications related to treatment. I think that the interactions between cardiologists and oncologists are increasing in a more important way,” she said.
In the Carvedilol for Prevention of Chemotherapy-Induced Cardiotoxicity (CECCY) Trial, Dr. Avila and colleagues evaluated primary prevention of cardiotoxicity in women with normal hearts who were undergoing chemotherapy for breast cancer.
Patients in the treatment group received a median carvedilol dose of 18.4 mg/day. The primary endpoint of cardiotoxicity, defined as a decrease in left ventricular ejection fraction (LVEF) of at least 10% at 6 months, occurred in 15% of carvedilol patients and 14% placebo patients, a nonsignificant difference. No significant differences occurred in diastolic dysfunction or in B-type natriuretic peptide (BNP) levels at 6 weeks, 12 weeks, or 24 weeks between the groups.
However, carvedilol patients showed significantly reduced troponin 1 levels compared with placebo, which suggests protection against myocardial injury, Dr. Avila said.
“In short follow up, we can see cardiotoxicity appearing, and we know we have to treat it promptly to prevent cardiac events,” she said.
Dr. Avila and colleagues identified 200 women older than 18 years with HER2-negative breast cancer tumor status and normal left ventricular ejection fraction. The patients were undergoing chemotherapy with 240 mg/m2 of anthracycline and were randomized to treatment with carvedilol or a placebo. Baseline characteristics were similar between the two groups.
Adverse effects were not significantly different between the groups, and the most common events in each group included dizziness, dry mouth, symptomatic hypertension, stomachache, and nausea. Although the results suggest that carvedilol can reduce the risk of myocardial injury, more research is needed to address the question of the increase in troponin without change in the LVEF, Dr. Avila noted. The study is ongoing and the research team intends to follow the low-risk patient population for a total of 2 years. “For high-risk patients, I am already giving carvedilol,” she said. “We believe if we find a difference in LVEF or clinical events, we could encourage cardiologists to give carvedilol in a low-risk population,” she said.
“This study highlights that there is no safe dose of anthracycline,” commented Bonnie Ky, MD of the University of Pennsylvania, Philadelphia, at a press briefing. She emphasized the value of carvedilol for a high-risk population, and stressed the importance of following long-term changes in heart injury markers after 1-2 years for low-risk patients.
Dr. Avila had no financial conflicts to disclose. Dr. Ky disclosed relationships with multiple companies including Bioinvent and Bristol Myers.
The findings were published simultaneously in the Journal of the American College of Cardiology.
SOURCE: Avila, M. ACC 18
REPORTING FROM ACC 18
Key clinical point:
Major finding: Cardiotoxicity was roughly 14% in breast cancer patients treated with anthracycline whether they received carvedilol or placebo.
Study details: CECCY was a randomized, placebo-controlled trial of 200 patients with HER2-negative breast cancer tumor status.
Disclosures: Dr. Avila had no financial conflicts to disclose.
Source: Avila M. ACC 2018.
Wearable defibrillator cuts mortality in post-MI patients
ORLANDO – Wearable cardioverter defibrillator vests failed to significantly cut the rate of arrhythmic death in at-risk post-MI patients but succeeded in significantly dropping total mortality during a median of 84 days of use in the first randomized trial of nonimplanted defibrillators in such patients.
But despite this overall mortality benefit, the 1,524 patients randomized to the WCD group failed to show a significant improvement in the rate of sudden and ventricular tachycardia death, the primary endpoint for the study, said Dr. Olgin, chief of cardiology at the University of California, San Francisco. Total mortality was a secondary endpoint in the study. Based on the total mortality benefit observed and the “totality of evidence” from prior, uncontrolled observational studies, Dr. Olgin concluded that it is now “reasonable” to protect post-MI patients with ejection fractions of 35% or less during the first 40-90 days following an MI when patients can then be assessed for receiving an implantable cardioverter defibrillator.
That would be an upgrade from the current American College of Cardiology/American Heart Association guidelines on managing ventricular arrhythmias and preventing sudden cardiac death, issued in 2017, that classified WCDs as a class IIb recommendations – “may be reasonable” – for post-MI patients with a reduced left ventricular ejection fraction (Circulation. 2017 Oct 30;doi:10.1161/CIR.0000000000000549).
WCDs are currently approved for routine prescribing by U.S. physicians, but their use is very variable in post-MI patients. Just before Dr. Olgin delivered his report at the meeting, a poll of the several thousand meeting attendees who heard his talk showed that roughly a third reported routinely prescribing WCDs, with the other two thirds saying they did not.
Several electrophysiologists who heard the report agreed that further research needs to better tease out which post-MI patients get the most benefit from this treatment.
The patients enrolled in the study “were not a sick population; they had a low event rate,” commented Sana M. Al-Khatib, MD, professor of medicine at Duke University in Durham, N.C. and chair of the panel that wrote the 2017 ventricular arrhythmia guidelines. She suggested testing the efficacy of WCDs in post-MI patients with lower ejection fractions or those with a greater history of heart disease prior to their index MI. Nearly half of the patients enrolled in the study had New York Heart Association class I symptoms, indicating that they had mild heart disease, she noted in an interview. Another issue left unresolved by the results Dr. Olgin reported was how much of the mortality benefit was attributable to the shocks delivered by the tested WCDs and how much derived from the arrhythmia monitoring that the WCDs provided.
Another way to better target WCDs to post-MI patients who could derive the most benefit might be to focus on patients with frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dhanunjaya Lakkireddy, MD, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City. But Dr. Lakkireddy acknowledged that currently left ventricular ejection fraction is the primary surrogate marker cardiologists rely on to identify post-MI patients who are at increased risk for ventricular arrhythmia.
Dr. Olgin countered that the total mortality rate seen among the control, usual care patients in his study, 4.9% during the median 84 day follow-up, closely matched the 5% rate reported in prior trials of at-risk patients who received implantable cardioverter defibrillators.
During follow-up, total mortality occurred in 3.1% of the patients randomized to WCD use and 4.9% among the control patients.
The results also showed that 19% of the patients randomized to the WCD arm failed to ever use the device, and that over the course of follow-up the usage rate fell below 50%. Patients who used the device generally wore it as directed, however, with an average 22 hours a day of use at the start of treatment that subsequently dipped to 21 hours a day near the end of the 90-day treatment period, Dr. Olgin reported.
The most likely explanation for the disparity between the significant effect on total mortality and the insignificant effect on arrhythmia mortality is misclassification of some deaths. “Any small number of misclassified sudden deaths would have dramatically reduced our power to see a difference” in arrhythmia deaths, Dr. Olgin noted.
VEST was sponsored by Zoll, the company that markets the tested device. Dr. Olgin has no personal disclosures. Dr. Al-Khatib and Dr. Lakkireddy had no disclosures. Dr. Wilber is a consultant to Biosense Webster and Medtronic.
mzoler@frontlinemedcom.com
SOURCE: Olgin J et al. ACC 18.
ORLANDO – Wearable cardioverter defibrillator vests failed to significantly cut the rate of arrhythmic death in at-risk post-MI patients but succeeded in significantly dropping total mortality during a median of 84 days of use in the first randomized trial of nonimplanted defibrillators in such patients.
But despite this overall mortality benefit, the 1,524 patients randomized to the WCD group failed to show a significant improvement in the rate of sudden and ventricular tachycardia death, the primary endpoint for the study, said Dr. Olgin, chief of cardiology at the University of California, San Francisco. Total mortality was a secondary endpoint in the study. Based on the total mortality benefit observed and the “totality of evidence” from prior, uncontrolled observational studies, Dr. Olgin concluded that it is now “reasonable” to protect post-MI patients with ejection fractions of 35% or less during the first 40-90 days following an MI when patients can then be assessed for receiving an implantable cardioverter defibrillator.
That would be an upgrade from the current American College of Cardiology/American Heart Association guidelines on managing ventricular arrhythmias and preventing sudden cardiac death, issued in 2017, that classified WCDs as a class IIb recommendations – “may be reasonable” – for post-MI patients with a reduced left ventricular ejection fraction (Circulation. 2017 Oct 30;doi:10.1161/CIR.0000000000000549).
WCDs are currently approved for routine prescribing by U.S. physicians, but their use is very variable in post-MI patients. Just before Dr. Olgin delivered his report at the meeting, a poll of the several thousand meeting attendees who heard his talk showed that roughly a third reported routinely prescribing WCDs, with the other two thirds saying they did not.
Several electrophysiologists who heard the report agreed that further research needs to better tease out which post-MI patients get the most benefit from this treatment.
The patients enrolled in the study “were not a sick population; they had a low event rate,” commented Sana M. Al-Khatib, MD, professor of medicine at Duke University in Durham, N.C. and chair of the panel that wrote the 2017 ventricular arrhythmia guidelines. She suggested testing the efficacy of WCDs in post-MI patients with lower ejection fractions or those with a greater history of heart disease prior to their index MI. Nearly half of the patients enrolled in the study had New York Heart Association class I symptoms, indicating that they had mild heart disease, she noted in an interview. Another issue left unresolved by the results Dr. Olgin reported was how much of the mortality benefit was attributable to the shocks delivered by the tested WCDs and how much derived from the arrhythmia monitoring that the WCDs provided.
Another way to better target WCDs to post-MI patients who could derive the most benefit might be to focus on patients with frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dhanunjaya Lakkireddy, MD, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City. But Dr. Lakkireddy acknowledged that currently left ventricular ejection fraction is the primary surrogate marker cardiologists rely on to identify post-MI patients who are at increased risk for ventricular arrhythmia.
Dr. Olgin countered that the total mortality rate seen among the control, usual care patients in his study, 4.9% during the median 84 day follow-up, closely matched the 5% rate reported in prior trials of at-risk patients who received implantable cardioverter defibrillators.
During follow-up, total mortality occurred in 3.1% of the patients randomized to WCD use and 4.9% among the control patients.
The results also showed that 19% of the patients randomized to the WCD arm failed to ever use the device, and that over the course of follow-up the usage rate fell below 50%. Patients who used the device generally wore it as directed, however, with an average 22 hours a day of use at the start of treatment that subsequently dipped to 21 hours a day near the end of the 90-day treatment period, Dr. Olgin reported.
The most likely explanation for the disparity between the significant effect on total mortality and the insignificant effect on arrhythmia mortality is misclassification of some deaths. “Any small number of misclassified sudden deaths would have dramatically reduced our power to see a difference” in arrhythmia deaths, Dr. Olgin noted.
VEST was sponsored by Zoll, the company that markets the tested device. Dr. Olgin has no personal disclosures. Dr. Al-Khatib and Dr. Lakkireddy had no disclosures. Dr. Wilber is a consultant to Biosense Webster and Medtronic.
mzoler@frontlinemedcom.com
SOURCE: Olgin J et al. ACC 18.
ORLANDO – Wearable cardioverter defibrillator vests failed to significantly cut the rate of arrhythmic death in at-risk post-MI patients but succeeded in significantly dropping total mortality during a median of 84 days of use in the first randomized trial of nonimplanted defibrillators in such patients.
But despite this overall mortality benefit, the 1,524 patients randomized to the WCD group failed to show a significant improvement in the rate of sudden and ventricular tachycardia death, the primary endpoint for the study, said Dr. Olgin, chief of cardiology at the University of California, San Francisco. Total mortality was a secondary endpoint in the study. Based on the total mortality benefit observed and the “totality of evidence” from prior, uncontrolled observational studies, Dr. Olgin concluded that it is now “reasonable” to protect post-MI patients with ejection fractions of 35% or less during the first 40-90 days following an MI when patients can then be assessed for receiving an implantable cardioverter defibrillator.
That would be an upgrade from the current American College of Cardiology/American Heart Association guidelines on managing ventricular arrhythmias and preventing sudden cardiac death, issued in 2017, that classified WCDs as a class IIb recommendations – “may be reasonable” – for post-MI patients with a reduced left ventricular ejection fraction (Circulation. 2017 Oct 30;doi:10.1161/CIR.0000000000000549).
WCDs are currently approved for routine prescribing by U.S. physicians, but their use is very variable in post-MI patients. Just before Dr. Olgin delivered his report at the meeting, a poll of the several thousand meeting attendees who heard his talk showed that roughly a third reported routinely prescribing WCDs, with the other two thirds saying they did not.
Several electrophysiologists who heard the report agreed that further research needs to better tease out which post-MI patients get the most benefit from this treatment.
The patients enrolled in the study “were not a sick population; they had a low event rate,” commented Sana M. Al-Khatib, MD, professor of medicine at Duke University in Durham, N.C. and chair of the panel that wrote the 2017 ventricular arrhythmia guidelines. She suggested testing the efficacy of WCDs in post-MI patients with lower ejection fractions or those with a greater history of heart disease prior to their index MI. Nearly half of the patients enrolled in the study had New York Heart Association class I symptoms, indicating that they had mild heart disease, she noted in an interview. Another issue left unresolved by the results Dr. Olgin reported was how much of the mortality benefit was attributable to the shocks delivered by the tested WCDs and how much derived from the arrhythmia monitoring that the WCDs provided.
Another way to better target WCDs to post-MI patients who could derive the most benefit might be to focus on patients with frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dhanunjaya Lakkireddy, MD, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City. But Dr. Lakkireddy acknowledged that currently left ventricular ejection fraction is the primary surrogate marker cardiologists rely on to identify post-MI patients who are at increased risk for ventricular arrhythmia.
Dr. Olgin countered that the total mortality rate seen among the control, usual care patients in his study, 4.9% during the median 84 day follow-up, closely matched the 5% rate reported in prior trials of at-risk patients who received implantable cardioverter defibrillators.
During follow-up, total mortality occurred in 3.1% of the patients randomized to WCD use and 4.9% among the control patients.
The results also showed that 19% of the patients randomized to the WCD arm failed to ever use the device, and that over the course of follow-up the usage rate fell below 50%. Patients who used the device generally wore it as directed, however, with an average 22 hours a day of use at the start of treatment that subsequently dipped to 21 hours a day near the end of the 90-day treatment period, Dr. Olgin reported.
The most likely explanation for the disparity between the significant effect on total mortality and the insignificant effect on arrhythmia mortality is misclassification of some deaths. “Any small number of misclassified sudden deaths would have dramatically reduced our power to see a difference” in arrhythmia deaths, Dr. Olgin noted.
VEST was sponsored by Zoll, the company that markets the tested device. Dr. Olgin has no personal disclosures. Dr. Al-Khatib and Dr. Lakkireddy had no disclosures. Dr. Wilber is a consultant to Biosense Webster and Medtronic.
mzoler@frontlinemedcom.com
SOURCE: Olgin J et al. ACC 18.
REPORTING FROM ACC18
Key clinical point: The first RCT of a wearable defibrillator in post-MI patients showed reduced total mortality.
Major finding: Total mortality was 3.2% in patients treated with a wearable cardioverter defibrillator and 4.9% in controls after a median of 84 days.
Study details: VEST, a multicenter, randomized trial with 2,302 patients.
Disclosures: VEST was sponsored by Zoll, the company that markets the tested device. Dr. Olgin has no personal disclosures.
Source: Olgin J. ACC 18.
VEST: Closer tailoring might boost wearable cardioverter defibrillator’s benefit
ORLANDO – , the findings failed to show a statistically significant reduction in sudden death or death from ventricular tachycardia. This suggests better targeting of the device is needed, commented Dhanunjaya Lakkireddy, MD, in a video interview at the annual meeting of the American College of Cardiology.
The Vest Prevention of Early Sudden Death Trial (VEST) randomized 2,302 patients within the first 7 days following an acute MI who also had a left ventricular ejection fraction of 35% or less to either 90 days of treatment with a wearable cardioverter defibrillator (WCD) or usual care. After a median of 84 days, the results showed no statistically significant reduction from WCD use in the primary endpoint of sudden death or death from ventricular tachyarrhythmias, but a statistically significant reduction in the secondary endpoint of all-cause death: 3.1% in the patients randomized to WCD use and 4.9% among the control patients, reported Jeffrey Olgin, MD, chief of cardiology at the University of California, San Francisco.
The results suggest that a more robust benefit might occur in post-MI, low ejection fraction patients who undergo additional selection based on having frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dr. Lakkireddy, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City.
VEST was sponsored by Zoll, a company that markets a WCD. Dr. Lakkireddy had no relevant disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
Source: Olgin J and Lakkireddy D ACC 18.
ORLANDO – , the findings failed to show a statistically significant reduction in sudden death or death from ventricular tachycardia. This suggests better targeting of the device is needed, commented Dhanunjaya Lakkireddy, MD, in a video interview at the annual meeting of the American College of Cardiology.
The Vest Prevention of Early Sudden Death Trial (VEST) randomized 2,302 patients within the first 7 days following an acute MI who also had a left ventricular ejection fraction of 35% or less to either 90 days of treatment with a wearable cardioverter defibrillator (WCD) or usual care. After a median of 84 days, the results showed no statistically significant reduction from WCD use in the primary endpoint of sudden death or death from ventricular tachyarrhythmias, but a statistically significant reduction in the secondary endpoint of all-cause death: 3.1% in the patients randomized to WCD use and 4.9% among the control patients, reported Jeffrey Olgin, MD, chief of cardiology at the University of California, San Francisco.
The results suggest that a more robust benefit might occur in post-MI, low ejection fraction patients who undergo additional selection based on having frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dr. Lakkireddy, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City.
VEST was sponsored by Zoll, a company that markets a WCD. Dr. Lakkireddy had no relevant disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
Source: Olgin J and Lakkireddy D ACC 18.
ORLANDO – , the findings failed to show a statistically significant reduction in sudden death or death from ventricular tachycardia. This suggests better targeting of the device is needed, commented Dhanunjaya Lakkireddy, MD, in a video interview at the annual meeting of the American College of Cardiology.
The Vest Prevention of Early Sudden Death Trial (VEST) randomized 2,302 patients within the first 7 days following an acute MI who also had a left ventricular ejection fraction of 35% or less to either 90 days of treatment with a wearable cardioverter defibrillator (WCD) or usual care. After a median of 84 days, the results showed no statistically significant reduction from WCD use in the primary endpoint of sudden death or death from ventricular tachyarrhythmias, but a statistically significant reduction in the secondary endpoint of all-cause death: 3.1% in the patients randomized to WCD use and 4.9% among the control patients, reported Jeffrey Olgin, MD, chief of cardiology at the University of California, San Francisco.
The results suggest that a more robust benefit might occur in post-MI, low ejection fraction patients who undergo additional selection based on having frequent premature ventricular contractions and nonsustained ventricular tachycardia, suggested Dr. Lakkireddy, professor of medicine and director of the Center for Excellence in AF and Complex Arrhythmias at the University of Kansas Medical Center in Kansas City.
VEST was sponsored by Zoll, a company that markets a WCD. Dr. Lakkireddy had no relevant disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
Source: Olgin J and Lakkireddy D ACC 18.
EXPERT ANALYSIS FROM ACC 18
