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Metabolically healthy obese still at elevated cardiovascular risk
Obese individuals with no metabolic abnormalities, such as dyslipidemia, high blood pressure, or high blood sugar levels, still have a higher risk of cardiovascular disease than do metabolically healthy people of normal weight, new data suggests.
“Our study robustly challenges the assertion that MHO [metabolically healthy obese] is a benign condition and adds to the evidence base that MHO is a high-risk state for future CVD events,” wrote Rishi Caleyachetty, MD, of the University of Birmingham, England, and his coauthors online (J Am Coll Cardiol. 2017, Sep 11. doi. 10.1016/j.jacc.2017.07.763).
Dr. Caleyachetty and his associates reported findings from a population-based study using the electronic health records of nearly 3.5 million individuals aged 18 years or older who were free of cardiovascular disease at baseline.
Overall, 15% of the population were classified as being metabolically healthy obese, meaning that they had a body mass index (BMI) of at least 30 kg/m2 with no sign of diabetes, hypertension, or hyperlipidemia, and 26% were overweight with no metabolic abnormalities. Despite their lack of metabolic disease, these obese individuals still had a significant 49% higher risk of coronary heart disease, 7% higher risk of cerebrovascular disease, and 96% higher risk of heart failure, compared with normal-weight individuals with no metabolic disease, after researchers adjusted for age, sex, smoking status, and social deprivation.
Individuals who were overweight but metabolically healthy had a 30% increased risk of ischemic heart disease, 11% increased risk of heart failure, and the same risk of cerebrovascular disease as normal-weight, healthy individuals.
They also saw an increasing risk of ischemic heart disease, cerebrovascular disease, heart failure, and peripheral vascular disease with each additional metabolic abnormality, even among underweight and normal-weight individuals, and suggested that a focus on screening overweight and obese individuals only could miss metabolic abnormalities in many patients.
Overweight and obese individuals without metabolic disease had a significantly lower risk of peripheral vascular disease, compared with healthy normal-weight individuals. The authors said this was a surprising finding but suggested cigarette smoking could be a confounding factor, as this is associated with both peripheral vascular disease and lower BMI.
“In sensitivity analyses restricted to individuals who were obese with no metabolic abnormalities and reported never smoking cigarettes, risk for PVD [peripheral vascular disease] was increased, compared [with] normal-weight individuals with no metabolic abnormalities,” Dr. Caleyachetty and his coinvestigators wrote.
Over the mean follow-up of 5.4 years, 5.6% of initially metabolically healthy obese individuals developed diabetes, 11.5% developed hyperlipidemia and 10.5% developed hypertension. In contrast, among the metabolically healthy overweight individuals at baseline, 1.9% developed diabetes, 9.4% developed hyperlipidemia, and 7.2% developed hypertension.
While the analysis adjusted for sex, the authors did note that women who were overweight or obese but metabolically healthy had stronger positive associations than did males with cerebrovascular disease and heart failure.
“Clinicians need to be aware that individuals who would otherwise be considered nonobese, based on a normal BMI, can have metabolic abnormalities, and therefore also be at high risk for CVD events,” the investigators concluded.
No conflicts of interest were declared.
Recently, studies have consistently placed metabolically healthy obese individuals between metabolically healthy lean and metabolically unhealthy obese individuals in terms of cardiovascular disease risk, occult cardiac dysfunction, and type 2 diabetes. Thus, either metabolic dysfunction or elevated body mass index appears to increases CVD risk factors.
Often, one or two metabolic risk factors in normal weight individuals are dismissed as unimportant because they are of healthy weight; however, these data suggest that the normal-weight group is at similar risk, compared with overweight, and at times, obese individuals, when metabolic abnormalities are present. The study not only definitively counters the concept of metabolically benign obesity but also demonstrates great risk to normal weight individuals if metabolic dysfunction is present. Thus, we would suggest an increased need for screening in the normal-weight population.
Jennifer W. Bea, PhD, is from the Collaboratory for Metabolic Disease Prevention and Treatment in Tucson, Ariz., and Nancy K. Sweitzer, MD, is chief of the division of cardiology at the Sarver Heart Center. These comments are taken from an accompanying editorial (J Am Coll Cardiol. 2017 Sep 19;70:1438-40. doi. org/10.1016/j.jacc.2017.07.742). No conflicts of interest were declared.
Recently, studies have consistently placed metabolically healthy obese individuals between metabolically healthy lean and metabolically unhealthy obese individuals in terms of cardiovascular disease risk, occult cardiac dysfunction, and type 2 diabetes. Thus, either metabolic dysfunction or elevated body mass index appears to increases CVD risk factors.
Often, one or two metabolic risk factors in normal weight individuals are dismissed as unimportant because they are of healthy weight; however, these data suggest that the normal-weight group is at similar risk, compared with overweight, and at times, obese individuals, when metabolic abnormalities are present. The study not only definitively counters the concept of metabolically benign obesity but also demonstrates great risk to normal weight individuals if metabolic dysfunction is present. Thus, we would suggest an increased need for screening in the normal-weight population.
Jennifer W. Bea, PhD, is from the Collaboratory for Metabolic Disease Prevention and Treatment in Tucson, Ariz., and Nancy K. Sweitzer, MD, is chief of the division of cardiology at the Sarver Heart Center. These comments are taken from an accompanying editorial (J Am Coll Cardiol. 2017 Sep 19;70:1438-40. doi. org/10.1016/j.jacc.2017.07.742). No conflicts of interest were declared.
Recently, studies have consistently placed metabolically healthy obese individuals between metabolically healthy lean and metabolically unhealthy obese individuals in terms of cardiovascular disease risk, occult cardiac dysfunction, and type 2 diabetes. Thus, either metabolic dysfunction or elevated body mass index appears to increases CVD risk factors.
Often, one or two metabolic risk factors in normal weight individuals are dismissed as unimportant because they are of healthy weight; however, these data suggest that the normal-weight group is at similar risk, compared with overweight, and at times, obese individuals, when metabolic abnormalities are present. The study not only definitively counters the concept of metabolically benign obesity but also demonstrates great risk to normal weight individuals if metabolic dysfunction is present. Thus, we would suggest an increased need for screening in the normal-weight population.
Jennifer W. Bea, PhD, is from the Collaboratory for Metabolic Disease Prevention and Treatment in Tucson, Ariz., and Nancy K. Sweitzer, MD, is chief of the division of cardiology at the Sarver Heart Center. These comments are taken from an accompanying editorial (J Am Coll Cardiol. 2017 Sep 19;70:1438-40. doi. org/10.1016/j.jacc.2017.07.742). No conflicts of interest were declared.
Obese individuals with no metabolic abnormalities, such as dyslipidemia, high blood pressure, or high blood sugar levels, still have a higher risk of cardiovascular disease than do metabolically healthy people of normal weight, new data suggests.
“Our study robustly challenges the assertion that MHO [metabolically healthy obese] is a benign condition and adds to the evidence base that MHO is a high-risk state for future CVD events,” wrote Rishi Caleyachetty, MD, of the University of Birmingham, England, and his coauthors online (J Am Coll Cardiol. 2017, Sep 11. doi. 10.1016/j.jacc.2017.07.763).
Dr. Caleyachetty and his associates reported findings from a population-based study using the electronic health records of nearly 3.5 million individuals aged 18 years or older who were free of cardiovascular disease at baseline.
Overall, 15% of the population were classified as being metabolically healthy obese, meaning that they had a body mass index (BMI) of at least 30 kg/m2 with no sign of diabetes, hypertension, or hyperlipidemia, and 26% were overweight with no metabolic abnormalities. Despite their lack of metabolic disease, these obese individuals still had a significant 49% higher risk of coronary heart disease, 7% higher risk of cerebrovascular disease, and 96% higher risk of heart failure, compared with normal-weight individuals with no metabolic disease, after researchers adjusted for age, sex, smoking status, and social deprivation.
Individuals who were overweight but metabolically healthy had a 30% increased risk of ischemic heart disease, 11% increased risk of heart failure, and the same risk of cerebrovascular disease as normal-weight, healthy individuals.
They also saw an increasing risk of ischemic heart disease, cerebrovascular disease, heart failure, and peripheral vascular disease with each additional metabolic abnormality, even among underweight and normal-weight individuals, and suggested that a focus on screening overweight and obese individuals only could miss metabolic abnormalities in many patients.
Overweight and obese individuals without metabolic disease had a significantly lower risk of peripheral vascular disease, compared with healthy normal-weight individuals. The authors said this was a surprising finding but suggested cigarette smoking could be a confounding factor, as this is associated with both peripheral vascular disease and lower BMI.
“In sensitivity analyses restricted to individuals who were obese with no metabolic abnormalities and reported never smoking cigarettes, risk for PVD [peripheral vascular disease] was increased, compared [with] normal-weight individuals with no metabolic abnormalities,” Dr. Caleyachetty and his coinvestigators wrote.
Over the mean follow-up of 5.4 years, 5.6% of initially metabolically healthy obese individuals developed diabetes, 11.5% developed hyperlipidemia and 10.5% developed hypertension. In contrast, among the metabolically healthy overweight individuals at baseline, 1.9% developed diabetes, 9.4% developed hyperlipidemia, and 7.2% developed hypertension.
While the analysis adjusted for sex, the authors did note that women who were overweight or obese but metabolically healthy had stronger positive associations than did males with cerebrovascular disease and heart failure.
“Clinicians need to be aware that individuals who would otherwise be considered nonobese, based on a normal BMI, can have metabolic abnormalities, and therefore also be at high risk for CVD events,” the investigators concluded.
No conflicts of interest were declared.
Obese individuals with no metabolic abnormalities, such as dyslipidemia, high blood pressure, or high blood sugar levels, still have a higher risk of cardiovascular disease than do metabolically healthy people of normal weight, new data suggests.
“Our study robustly challenges the assertion that MHO [metabolically healthy obese] is a benign condition and adds to the evidence base that MHO is a high-risk state for future CVD events,” wrote Rishi Caleyachetty, MD, of the University of Birmingham, England, and his coauthors online (J Am Coll Cardiol. 2017, Sep 11. doi. 10.1016/j.jacc.2017.07.763).
Dr. Caleyachetty and his associates reported findings from a population-based study using the electronic health records of nearly 3.5 million individuals aged 18 years or older who were free of cardiovascular disease at baseline.
Overall, 15% of the population were classified as being metabolically healthy obese, meaning that they had a body mass index (BMI) of at least 30 kg/m2 with no sign of diabetes, hypertension, or hyperlipidemia, and 26% were overweight with no metabolic abnormalities. Despite their lack of metabolic disease, these obese individuals still had a significant 49% higher risk of coronary heart disease, 7% higher risk of cerebrovascular disease, and 96% higher risk of heart failure, compared with normal-weight individuals with no metabolic disease, after researchers adjusted for age, sex, smoking status, and social deprivation.
Individuals who were overweight but metabolically healthy had a 30% increased risk of ischemic heart disease, 11% increased risk of heart failure, and the same risk of cerebrovascular disease as normal-weight, healthy individuals.
They also saw an increasing risk of ischemic heart disease, cerebrovascular disease, heart failure, and peripheral vascular disease with each additional metabolic abnormality, even among underweight and normal-weight individuals, and suggested that a focus on screening overweight and obese individuals only could miss metabolic abnormalities in many patients.
Overweight and obese individuals without metabolic disease had a significantly lower risk of peripheral vascular disease, compared with healthy normal-weight individuals. The authors said this was a surprising finding but suggested cigarette smoking could be a confounding factor, as this is associated with both peripheral vascular disease and lower BMI.
“In sensitivity analyses restricted to individuals who were obese with no metabolic abnormalities and reported never smoking cigarettes, risk for PVD [peripheral vascular disease] was increased, compared [with] normal-weight individuals with no metabolic abnormalities,” Dr. Caleyachetty and his coinvestigators wrote.
Over the mean follow-up of 5.4 years, 5.6% of initially metabolically healthy obese individuals developed diabetes, 11.5% developed hyperlipidemia and 10.5% developed hypertension. In contrast, among the metabolically healthy overweight individuals at baseline, 1.9% developed diabetes, 9.4% developed hyperlipidemia, and 7.2% developed hypertension.
While the analysis adjusted for sex, the authors did note that women who were overweight or obese but metabolically healthy had stronger positive associations than did males with cerebrovascular disease and heart failure.
“Clinicians need to be aware that individuals who would otherwise be considered nonobese, based on a normal BMI, can have metabolic abnormalities, and therefore also be at high risk for CVD events,” the investigators concluded.
No conflicts of interest were declared.
FROM THE JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Key clinical point: Obese individuals without any sign of metabolic disease, such as hypertension or dyslipidemia, still have a greater risk of cardiovascular disease than do normal weight individuals.
Major finding: Metabolically healthy obese individuals have a 49% higher risk of coronary heart disease and 96% higher risk of heart failure than metabolically healthy normal weight individuals.
Data source: Population-based electronic health record study of 3.5 million people.
Disclosures: No conflicts of interest were declared.
Ivabradine cut mortality in HFrEF patients not on beta-blocker
BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.
He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.
“I think there would be ethical equipoise,” he added. “If patients are unwilling or unable to take a beta-blocker, or their cardiologist feels it’s not in their best interest, then I certainly think a placebo-controlled trial would not only be appropriate, but there’s also an onus on the cardiology community to do such a trial.”
Ivabradine slows heart rate by a unique mechanism that doesn’t involve blockade of adrenergic receptors. In the SHIFT trial (Lancet. 2010 Sep 11;376[9744]:875-85), more than 6,500 patients with heart failure with reduced ejection fraction (HFrEF) in sinus rhythm and with a heart rate greater than 70 bpm were randomized to ivabradine or placebo on top of guideline-directed medical therapy for heart failure. During a median 23 months of follow-up, heart failure hospitalizations were significantly reduced by 26% in the ivabradine group, although cardiovascular deaths were not significantly affected.
As a result of the SHIFT findings, the drug was approved with an indication for use only in combination with a beta-blocker in patients with HFrEF whose on-treatment heart rate exceeds 70 bpm. Ivabradine is not currently recommended as an alternative to beta-blocker therapy. However, in real-world clinical practice a large number of heart failure patients are not managed with a beta-blocker, the cardiologist noted.
His post-hoc analysis focused on the 685 SHIFT participants who were not on a beta-blocker at randomization. During follow-up, there were 93 deaths among patients who were on placebo and only 71 in those randomized to ivabradine, for a statistically significant 30% reduction in all-cause mortality. Cardiovascular mortality was reduced to a similar extent. These hazard ratios remained similar after adjusting for differences in heart rate and other clinical characteristics.
“Beta-blockers are a highly effective therapy for heart failure with reduced ejection fraction, but the mechanism of benefit remains uncertain. It might simply be due to heart rate reduction. And I would point out that we have no evidence of a dose response for beta-blockers: It may well be that you get most of the effect of a beta-blocker with the lowest dose. Titrating to the full dose of a beta-blocker might only be helpful in that it lowers your heart rate. I would argue that 6.25 mg/day of carvedilol plus ivabradine might be as good as 50 mg twice daily of carvedilol but with much higher patient acceptability. We don’t know,” said Dr. Cleland.
“This is an interesting, hypothesis-generating analysis, and we need confirmation now that ivabradine reduces mortality in heart failure patients who are unwilling or unable to take a beta-blocker,” he concluded.
The SHIFT trial was sponsored by Servier. Dr. Cleland reported serving as a consultant to and receiving research funding from that company and others.
BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.
He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.
“I think there would be ethical equipoise,” he added. “If patients are unwilling or unable to take a beta-blocker, or their cardiologist feels it’s not in their best interest, then I certainly think a placebo-controlled trial would not only be appropriate, but there’s also an onus on the cardiology community to do such a trial.”
Ivabradine slows heart rate by a unique mechanism that doesn’t involve blockade of adrenergic receptors. In the SHIFT trial (Lancet. 2010 Sep 11;376[9744]:875-85), more than 6,500 patients with heart failure with reduced ejection fraction (HFrEF) in sinus rhythm and with a heart rate greater than 70 bpm were randomized to ivabradine or placebo on top of guideline-directed medical therapy for heart failure. During a median 23 months of follow-up, heart failure hospitalizations were significantly reduced by 26% in the ivabradine group, although cardiovascular deaths were not significantly affected.
As a result of the SHIFT findings, the drug was approved with an indication for use only in combination with a beta-blocker in patients with HFrEF whose on-treatment heart rate exceeds 70 bpm. Ivabradine is not currently recommended as an alternative to beta-blocker therapy. However, in real-world clinical practice a large number of heart failure patients are not managed with a beta-blocker, the cardiologist noted.
His post-hoc analysis focused on the 685 SHIFT participants who were not on a beta-blocker at randomization. During follow-up, there were 93 deaths among patients who were on placebo and only 71 in those randomized to ivabradine, for a statistically significant 30% reduction in all-cause mortality. Cardiovascular mortality was reduced to a similar extent. These hazard ratios remained similar after adjusting for differences in heart rate and other clinical characteristics.
“Beta-blockers are a highly effective therapy for heart failure with reduced ejection fraction, but the mechanism of benefit remains uncertain. It might simply be due to heart rate reduction. And I would point out that we have no evidence of a dose response for beta-blockers: It may well be that you get most of the effect of a beta-blocker with the lowest dose. Titrating to the full dose of a beta-blocker might only be helpful in that it lowers your heart rate. I would argue that 6.25 mg/day of carvedilol plus ivabradine might be as good as 50 mg twice daily of carvedilol but with much higher patient acceptability. We don’t know,” said Dr. Cleland.
“This is an interesting, hypothesis-generating analysis, and we need confirmation now that ivabradine reduces mortality in heart failure patients who are unwilling or unable to take a beta-blocker,” he concluded.
The SHIFT trial was sponsored by Servier. Dr. Cleland reported serving as a consultant to and receiving research funding from that company and others.
BARCELONA – The time is right for a placebo-controlled, randomized trial of ivabradine in patients with heart failure with reduced ejection fraction who are unwilling or unable to take a beta-blocker as recommended in the guidelines, John G.F. Cleland, MD, asserted at the annual congress of the European Society of Cardiology.
He cited as the rationale for such a study a new post-hoc analysis of data from the SHIFT trial showing that ivabradine (Corlanor) significantly reduced both cardiovascular and all-cause mortality, as well as hospitalizations for heart failure, in the subset of study participants who weren’t on beta-blocker therapy.
“I think there would be ethical equipoise,” he added. “If patients are unwilling or unable to take a beta-blocker, or their cardiologist feels it’s not in their best interest, then I certainly think a placebo-controlled trial would not only be appropriate, but there’s also an onus on the cardiology community to do such a trial.”
Ivabradine slows heart rate by a unique mechanism that doesn’t involve blockade of adrenergic receptors. In the SHIFT trial (Lancet. 2010 Sep 11;376[9744]:875-85), more than 6,500 patients with heart failure with reduced ejection fraction (HFrEF) in sinus rhythm and with a heart rate greater than 70 bpm were randomized to ivabradine or placebo on top of guideline-directed medical therapy for heart failure. During a median 23 months of follow-up, heart failure hospitalizations were significantly reduced by 26% in the ivabradine group, although cardiovascular deaths were not significantly affected.
As a result of the SHIFT findings, the drug was approved with an indication for use only in combination with a beta-blocker in patients with HFrEF whose on-treatment heart rate exceeds 70 bpm. Ivabradine is not currently recommended as an alternative to beta-blocker therapy. However, in real-world clinical practice a large number of heart failure patients are not managed with a beta-blocker, the cardiologist noted.
His post-hoc analysis focused on the 685 SHIFT participants who were not on a beta-blocker at randomization. During follow-up, there were 93 deaths among patients who were on placebo and only 71 in those randomized to ivabradine, for a statistically significant 30% reduction in all-cause mortality. Cardiovascular mortality was reduced to a similar extent. These hazard ratios remained similar after adjusting for differences in heart rate and other clinical characteristics.
“Beta-blockers are a highly effective therapy for heart failure with reduced ejection fraction, but the mechanism of benefit remains uncertain. It might simply be due to heart rate reduction. And I would point out that we have no evidence of a dose response for beta-blockers: It may well be that you get most of the effect of a beta-blocker with the lowest dose. Titrating to the full dose of a beta-blocker might only be helpful in that it lowers your heart rate. I would argue that 6.25 mg/day of carvedilol plus ivabradine might be as good as 50 mg twice daily of carvedilol but with much higher patient acceptability. We don’t know,” said Dr. Cleland.
“This is an interesting, hypothesis-generating analysis, and we need confirmation now that ivabradine reduces mortality in heart failure patients who are unwilling or unable to take a beta-blocker,” he concluded.
The SHIFT trial was sponsored by Servier. Dr. Cleland reported serving as a consultant to and receiving research funding from that company and others.
AT THE ESC CONGRESS 2017
Key clinical point:
Major finding: All-cause mortality was reduced by 30%, compared with placebo, in ivabradine-treated patients with heart failure with reduced ejection fraction who were not on a beta-blocker.
Data source: A post-hoc analysis of the 685 patients in a much larger randomized, placebo-controlled clinical trial of ivabradine in patients with heart failure with reduced ejection fraction.
Disclosures: The SHIFT trial was funded by Servier. The presenter reported serving as a consultant to and recipient of research grants from that and other companies.
Preventive upstream therapy prevents progression of atrial fib
BARCELONA – Aggressive treatment of known risk factors for atrial fibrillation resulted in improved 1-year maintenance of sinus rhythm in patients with recent-onset atrial fibrillation and heart failure in the randomized multicenter RACE 3 trial, Isabelle C. van Gelder, MD, reported at the annual congress of the European Society of Cardiology.
“We now screen for AF, making it possible to catch patients early. That’s what we’ve learned from this trial: if we start treating patients after their first episode of AF and aggressively reduce risk factors for AF, it may help the sinus rhythm. I think that’s an important message: do not wait too long, start treatment early,” said Dr. van Gelder, professor of cardiology at the University of Groningen, the Netherlands.
She calls the interventional strategy tested in RACE 3 “risk factor-driven upstream therapy.” The four-pronged strategy consisted of statin therapy, a mineralcorticoid receptor antagonist, an ACE inhibitor and/or an angiotensin receptor blocker, and a 9- to 11-week supervised cardiac rehabilitation program emphasizing lifestyle modification through physical training and dietary changes supported by professional counseling to promote adherence.
“These are interventions designed to improve the atrial substrate,” Dr. van Gelder explained.
RACE 3 (Routine versus Aggressive Upstream Rhythm Control for Prevention of Early Atrial Fibrillation in Heart Failure 3) was a multicenter, randomized, nonblinded clinical trial including 245 patients with, on average, a 3-month history of AF, a 2-month history of persistent AF, and a 2-month history of mild to moderate heart failure, either with preserved or reduced ejection fraction. All participants received guideline-directed rhythm control and heart failure therapies. In addition, half of participants were randomized to the upstream intervention. Three weeks after enrollment, all patients underwent electrical cardioversion.
The primary outcome was maintenance of sinus rhythm at 1 year as determined by 7-day Holter monitoring analyzed in blinded fashion at a central laboratory. The rate was 75% in the upstream intervention group, significantly better than the 63% in controls. This represented a 76% greater likelihood of sinus rhythm at 1 year in the upstream intervention group. They also showed significant reductions in systolic and diastolic blood pressure, N-terminal pro-brain natriuretic peptide, and LDL cholesterol, compared with controls. However, at 1 year, the two groups didn’t differ significantly in body mass index or left atrial volume. The lack of impact on left atrial volume was disappointing, Dr. van Gelder said.
“The remodeling process starts long before the first episode of AF, although we don’t know exactly when. Although we intended to intervene early in the remodeling process, I think we weren’t that early,” according to the cardiologist.
Discussant Josep Brugada, MD, applauded the Dutch investigators for opening the door to evidence-based preventive upstream therapy for AF, which he declared is vital given the worsening AF epidemic. 
“In recent years enormous efforts have been put into treating symptoms of AF, but clearly we have failed to control the epidemic of AF in our societies, probably because we’ve been aiming only at treating symptoms, not treating the causes,” observed Dr. Brugada of the University of Barcelona.
He added, however, that the RACE 3 intervention didn’t go far enough.
“It’s a bit of a disappointment that there is no change in BMI seen after 1 year. Zero. That probably means the rehabilitation program wasn’t strong enough. Yet, the study results are positive, so if we used physical training in a stronger way to get a reduction in body weight and BMI, probably the outcome would be even greater,” he said.
To be maximally effective, an upstream intervention for AF should also address two other important risk factors for the arrhythmia: heavy alcohol drinking and obstructive sleep apnea, the electrophysiologist added.
The RACE 3 trial was supported by the Netherlands Heart Foundation and the Netherlands Heart Institute. Dr. van Gelder reported having no relevant financial interests.
Dr. van Gelder discussed the RACE 3 trial and results in a video interview.
BARCELONA – Aggressive treatment of known risk factors for atrial fibrillation resulted in improved 1-year maintenance of sinus rhythm in patients with recent-onset atrial fibrillation and heart failure in the randomized multicenter RACE 3 trial, Isabelle C. van Gelder, MD, reported at the annual congress of the European Society of Cardiology.
“We now screen for AF, making it possible to catch patients early. That’s what we’ve learned from this trial: if we start treating patients after their first episode of AF and aggressively reduce risk factors for AF, it may help the sinus rhythm. I think that’s an important message: do not wait too long, start treatment early,” said Dr. van Gelder, professor of cardiology at the University of Groningen, the Netherlands.
She calls the interventional strategy tested in RACE 3 “risk factor-driven upstream therapy.” The four-pronged strategy consisted of statin therapy, a mineralcorticoid receptor antagonist, an ACE inhibitor and/or an angiotensin receptor blocker, and a 9- to 11-week supervised cardiac rehabilitation program emphasizing lifestyle modification through physical training and dietary changes supported by professional counseling to promote adherence.
“These are interventions designed to improve the atrial substrate,” Dr. van Gelder explained.
RACE 3 (Routine versus Aggressive Upstream Rhythm Control for Prevention of Early Atrial Fibrillation in Heart Failure 3) was a multicenter, randomized, nonblinded clinical trial including 245 patients with, on average, a 3-month history of AF, a 2-month history of persistent AF, and a 2-month history of mild to moderate heart failure, either with preserved or reduced ejection fraction. All participants received guideline-directed rhythm control and heart failure therapies. In addition, half of participants were randomized to the upstream intervention. Three weeks after enrollment, all patients underwent electrical cardioversion.
The primary outcome was maintenance of sinus rhythm at 1 year as determined by 7-day Holter monitoring analyzed in blinded fashion at a central laboratory. The rate was 75% in the upstream intervention group, significantly better than the 63% in controls. This represented a 76% greater likelihood of sinus rhythm at 1 year in the upstream intervention group. They also showed significant reductions in systolic and diastolic blood pressure, N-terminal pro-brain natriuretic peptide, and LDL cholesterol, compared with controls. However, at 1 year, the two groups didn’t differ significantly in body mass index or left atrial volume. The lack of impact on left atrial volume was disappointing, Dr. van Gelder said.
“The remodeling process starts long before the first episode of AF, although we don’t know exactly when. Although we intended to intervene early in the remodeling process, I think we weren’t that early,” according to the cardiologist.
Discussant Josep Brugada, MD, applauded the Dutch investigators for opening the door to evidence-based preventive upstream therapy for AF, which he declared is vital given the worsening AF epidemic.
“In recent years enormous efforts have been put into treating symptoms of AF, but clearly we have failed to control the epidemic of AF in our societies, probably because we’ve been aiming only at treating symptoms, not treating the causes,” observed Dr. Brugada of the University of Barcelona.
He added, however, that the RACE 3 intervention didn’t go far enough.
“It’s a bit of a disappointment that there is no change in BMI seen after 1 year. Zero. That probably means the rehabilitation program wasn’t strong enough. Yet, the study results are positive, so if we used physical training in a stronger way to get a reduction in body weight and BMI, probably the outcome would be even greater,” he said.
To be maximally effective, an upstream intervention for AF should also address two other important risk factors for the arrhythmia: heavy alcohol drinking and obstructive sleep apnea, the electrophysiologist added.
The RACE 3 trial was supported by the Netherlands Heart Foundation and the Netherlands Heart Institute. Dr. van Gelder reported having no relevant financial interests.
Dr. van Gelder discussed the RACE 3 trial and results in a video interview.
BARCELONA – Aggressive treatment of known risk factors for atrial fibrillation resulted in improved 1-year maintenance of sinus rhythm in patients with recent-onset atrial fibrillation and heart failure in the randomized multicenter RACE 3 trial, Isabelle C. van Gelder, MD, reported at the annual congress of the European Society of Cardiology.
“We now screen for AF, making it possible to catch patients early. That’s what we’ve learned from this trial: if we start treating patients after their first episode of AF and aggressively reduce risk factors for AF, it may help the sinus rhythm. I think that’s an important message: do not wait too long, start treatment early,” said Dr. van Gelder, professor of cardiology at the University of Groningen, the Netherlands.
She calls the interventional strategy tested in RACE 3 “risk factor-driven upstream therapy.” The four-pronged strategy consisted of statin therapy, a mineralcorticoid receptor antagonist, an ACE inhibitor and/or an angiotensin receptor blocker, and a 9- to 11-week supervised cardiac rehabilitation program emphasizing lifestyle modification through physical training and dietary changes supported by professional counseling to promote adherence.
“These are interventions designed to improve the atrial substrate,” Dr. van Gelder explained.
RACE 3 (Routine versus Aggressive Upstream Rhythm Control for Prevention of Early Atrial Fibrillation in Heart Failure 3) was a multicenter, randomized, nonblinded clinical trial including 245 patients with, on average, a 3-month history of AF, a 2-month history of persistent AF, and a 2-month history of mild to moderate heart failure, either with preserved or reduced ejection fraction. All participants received guideline-directed rhythm control and heart failure therapies. In addition, half of participants were randomized to the upstream intervention. Three weeks after enrollment, all patients underwent electrical cardioversion.
The primary outcome was maintenance of sinus rhythm at 1 year as determined by 7-day Holter monitoring analyzed in blinded fashion at a central laboratory. The rate was 75% in the upstream intervention group, significantly better than the 63% in controls. This represented a 76% greater likelihood of sinus rhythm at 1 year in the upstream intervention group. They also showed significant reductions in systolic and diastolic blood pressure, N-terminal pro-brain natriuretic peptide, and LDL cholesterol, compared with controls. However, at 1 year, the two groups didn’t differ significantly in body mass index or left atrial volume. The lack of impact on left atrial volume was disappointing, Dr. van Gelder said.
“The remodeling process starts long before the first episode of AF, although we don’t know exactly when. Although we intended to intervene early in the remodeling process, I think we weren’t that early,” according to the cardiologist.
Discussant Josep Brugada, MD, applauded the Dutch investigators for opening the door to evidence-based preventive upstream therapy for AF, which he declared is vital given the worsening AF epidemic.
“In recent years enormous efforts have been put into treating symptoms of AF, but clearly we have failed to control the epidemic of AF in our societies, probably because we’ve been aiming only at treating symptoms, not treating the causes,” observed Dr. Brugada of the University of Barcelona.
He added, however, that the RACE 3 intervention didn’t go far enough.
“It’s a bit of a disappointment that there is no change in BMI seen after 1 year. Zero. That probably means the rehabilitation program wasn’t strong enough. Yet, the study results are positive, so if we used physical training in a stronger way to get a reduction in body weight and BMI, probably the outcome would be even greater,” he said.
To be maximally effective, an upstream intervention for AF should also address two other important risk factors for the arrhythmia: heavy alcohol drinking and obstructive sleep apnea, the electrophysiologist added.
The RACE 3 trial was supported by the Netherlands Heart Foundation and the Netherlands Heart Institute. Dr. van Gelder reported having no relevant financial interests.
Dr. van Gelder discussed the RACE 3 trial and results in a video interview.
AT THE ESC CONGRESS 2017
Key clinical point:
Major finding: At 1 year, 75% of patients with baseline persistent atrial fibrillation who received a four-pronged program of upstream risk factor modification were in sinus rhythm, compared with 63% of controls.
Data source: RACE 3 was a multicenter, randomized, nonblinded clinical trial including 245 patients with a recent history of persistent atrial fibrillation and heart failure.
Disclosures: The RACE 3 trial was supported by the Netherlands Heart Foundation and the Netherlands Heart Institute. The presenter reported having no relevant financial interests.
Big risk of serious falls after first episode of syncope
BARCELONA – Patients have an exorbitant 80% increased risk of hospitalization for falls resulting in fracture or head injury in the first year after discharge following a first-ever episode of syncope, according to a Danish national cohort study. One in five patients who sustained a fall resulting in hospitalization experienced a hip fracture, according to Anna-Karin Nume, MD, of the University of Copenhagen.
In this interview at the annual congress of the European Society of Cardiology, Dr. Nume highlights findings from her study, which included 125,763 Danish adults with first-time syncope.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
BARCELONA – Patients have an exorbitant 80% increased risk of hospitalization for falls resulting in fracture or head injury in the first year after discharge following a first-ever episode of syncope, according to a Danish national cohort study. One in five patients who sustained a fall resulting in hospitalization experienced a hip fracture, according to Anna-Karin Nume, MD, of the University of Copenhagen.
In this interview at the annual congress of the European Society of Cardiology, Dr. Nume highlights findings from her study, which included 125,763 Danish adults with first-time syncope.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
BARCELONA – Patients have an exorbitant 80% increased risk of hospitalization for falls resulting in fracture or head injury in the first year after discharge following a first-ever episode of syncope, according to a Danish national cohort study. One in five patients who sustained a fall resulting in hospitalization experienced a hip fracture, according to Anna-Karin Nume, MD, of the University of Copenhagen.
In this interview at the annual congress of the European Society of Cardiology, Dr. Nume highlights findings from her study, which included 125,763 Danish adults with first-time syncope.
The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
AT THE ESC CONGRESS 2017
Despite global decline, rheumatic heart disease persists in poorest regions
Global mortality due to rheumatic heart disease fell by about 48% during a recent 25-year-period, but some of the poorest areas of the world were left behind, according to a report in the New England Journal of Medicine.
Those regions included Oceania, South Asia, and central sub-Saharan Africa, where rheumatic heart disease remains endemic, wrote David A. Watkins, MD, MPH, of the University of Washington, Seattle, and his coinvestigators. “We estimate that 10 persons per 1,000 population living in South Asia and central sub-Saharan Africa and 15 persons per 1,000 population in Oceania were living with rheumatic heart disease in the year 2015,” they wrote. “Improvements in the measurement of the burden of rheumatic heart disease will assist in planning for its control and will help identify countries where further investments are needed.”
To better define the problem, Dr. Watkins and his associates analyzed epidemiologic studies of rheumatic heart disease from 1990 through 2015. They used the Cause of Death Ensemble model, which estimates mortality more reliably than older methods, and DisMod-MR (version 2.1), which sums epidemiologic data from multiple sources and corrects for gaps and inconsistencies (N Engl J Med. 2017;377:713-22).
Worldwide, about 319,400 individuals died of rheumatic heart disease in 2015, the researchers reported. Age-adjusted death rates fell by about 48% (95% confidence interval, 45%-51%), from 9.2 deaths per 100,000 population in 1990 to 4.8 deaths per 100,000 population in 2015. But this global trend masked striking regional disparities. In 1990, 77% of deaths from rheumatic heart disease occurred in endemic areas of Africa, South Asia, Oceania, and the Caribbean; by 2015, 82% of deaths occurred in endemic regions. Oceania, South Asia, and central sub-Saharan Africa had the highest death rates and were the only regions where the 95% confidence intervals for 1990 and 2015 overlapped, the investigators noted.
In 2015, age-standardized death rates exceeded 10 deaths per 100,000 population in the Solomon Islands, Pakistan, Papua New Guinea, Kiribati, Vanuatu, Fiji, India, Federated States of Micronesia, Marshall Islands, Central African Republic, and Lesotho, they reported. Estimated fatalities were highest in India (119,100 deaths), China (72,600), and Pakistan (18,900). They estimated that in 2015, there were 33.2 million cases of rheumatic heart disease and 10.5 million associated disability-adjusted life-years globally.
The study excluded “borderline” or subclinical rheumatic heart disease, which is detected by echocardiography and whose management remains unclear. “Better data for low-income and middle-income countries are needed to guide policies for the control of rheumatic heart disease,” the investigators wrote. They recommended studying death certificate misclassifications, disease prevalence among adults, and longitudinal trends in nonfatal outcomes and excess mortality.
Funders of the study included the Bill and Melinda Gates Foundation and the Medtronic Foundation. Dr. Watkins disclosed grants from the Medtronic Foundation during the conduct of the study and grants from the Bill and Melinda Gates Foundation outside the submitted work.
Rheumatic heart disease ranks as one of the most serious cardiovascular scourges of the past century. As a result of improvements in living conditions and the introduction of penicillin, the disease was almost eradicated in the developed world by the 1980s. However, it remains a force to be reckoned with in the developing world, as demonstrated by an assessment from the 2015 Global Burden of Disease study (GBD 2015), painstakingly performed by Dr. Watkins and his colleagues.
Several key messages emerge from this important study. It confirms the marked global heterogeneity of the burden of rheumatic heart disease, with near-zero prevalence in developed countries sharply contrasting with substantial prevalence and mortality in developing areas. In addition, however, the study documents the scarcity of accurately measured data in many locations, especially in areas with the highest prevalence (such as sub-Saharan Africa).
Although the “headline news” of a global decline in the prevalence of rheumatic heart disease described by Watkins et al. may give cause for optimism, the burden remains great for those parts of the world least able to afford it. Without sustained re-engagement of clinicians, researchers, funders, and public health bodies, the menace of rheumatic heart disease is unlikely to be eliminated in the near future. Rheumatic heart disease remains a problematic iceberg, yet undissolved, in warm tropical waters.
Eloi Marijon, MD, PhD, and Xavier Jouven, MD, PhD, are at European Georges Pompidou Hospital, Paris. David S. Celermajer, PhD, is at Sydney (Australia) Medical School. They reported having no conflicts of interest. Their editorial accompanied the report by Dr. Watkins and his colleagues (N Engl J Med. 2017;377:780-1).
Rheumatic heart disease ranks as one of the most serious cardiovascular scourges of the past century. As a result of improvements in living conditions and the introduction of penicillin, the disease was almost eradicated in the developed world by the 1980s. However, it remains a force to be reckoned with in the developing world, as demonstrated by an assessment from the 2015 Global Burden of Disease study (GBD 2015), painstakingly performed by Dr. Watkins and his colleagues.
Several key messages emerge from this important study. It confirms the marked global heterogeneity of the burden of rheumatic heart disease, with near-zero prevalence in developed countries sharply contrasting with substantial prevalence and mortality in developing areas. In addition, however, the study documents the scarcity of accurately measured data in many locations, especially in areas with the highest prevalence (such as sub-Saharan Africa).
Although the “headline news” of a global decline in the prevalence of rheumatic heart disease described by Watkins et al. may give cause for optimism, the burden remains great for those parts of the world least able to afford it. Without sustained re-engagement of clinicians, researchers, funders, and public health bodies, the menace of rheumatic heart disease is unlikely to be eliminated in the near future. Rheumatic heart disease remains a problematic iceberg, yet undissolved, in warm tropical waters.
Eloi Marijon, MD, PhD, and Xavier Jouven, MD, PhD, are at European Georges Pompidou Hospital, Paris. David S. Celermajer, PhD, is at Sydney (Australia) Medical School. They reported having no conflicts of interest. Their editorial accompanied the report by Dr. Watkins and his colleagues (N Engl J Med. 2017;377:780-1).
Rheumatic heart disease ranks as one of the most serious cardiovascular scourges of the past century. As a result of improvements in living conditions and the introduction of penicillin, the disease was almost eradicated in the developed world by the 1980s. However, it remains a force to be reckoned with in the developing world, as demonstrated by an assessment from the 2015 Global Burden of Disease study (GBD 2015), painstakingly performed by Dr. Watkins and his colleagues.
Several key messages emerge from this important study. It confirms the marked global heterogeneity of the burden of rheumatic heart disease, with near-zero prevalence in developed countries sharply contrasting with substantial prevalence and mortality in developing areas. In addition, however, the study documents the scarcity of accurately measured data in many locations, especially in areas with the highest prevalence (such as sub-Saharan Africa).
Although the “headline news” of a global decline in the prevalence of rheumatic heart disease described by Watkins et al. may give cause for optimism, the burden remains great for those parts of the world least able to afford it. Without sustained re-engagement of clinicians, researchers, funders, and public health bodies, the menace of rheumatic heart disease is unlikely to be eliminated in the near future. Rheumatic heart disease remains a problematic iceberg, yet undissolved, in warm tropical waters.
Eloi Marijon, MD, PhD, and Xavier Jouven, MD, PhD, are at European Georges Pompidou Hospital, Paris. David S. Celermajer, PhD, is at Sydney (Australia) Medical School. They reported having no conflicts of interest. Their editorial accompanied the report by Dr. Watkins and his colleagues (N Engl J Med. 2017;377:780-1).
Global mortality due to rheumatic heart disease fell by about 48% during a recent 25-year-period, but some of the poorest areas of the world were left behind, according to a report in the New England Journal of Medicine.
Those regions included Oceania, South Asia, and central sub-Saharan Africa, where rheumatic heart disease remains endemic, wrote David A. Watkins, MD, MPH, of the University of Washington, Seattle, and his coinvestigators. “We estimate that 10 persons per 1,000 population living in South Asia and central sub-Saharan Africa and 15 persons per 1,000 population in Oceania were living with rheumatic heart disease in the year 2015,” they wrote. “Improvements in the measurement of the burden of rheumatic heart disease will assist in planning for its control and will help identify countries where further investments are needed.”
To better define the problem, Dr. Watkins and his associates analyzed epidemiologic studies of rheumatic heart disease from 1990 through 2015. They used the Cause of Death Ensemble model, which estimates mortality more reliably than older methods, and DisMod-MR (version 2.1), which sums epidemiologic data from multiple sources and corrects for gaps and inconsistencies (N Engl J Med. 2017;377:713-22).
Worldwide, about 319,400 individuals died of rheumatic heart disease in 2015, the researchers reported. Age-adjusted death rates fell by about 48% (95% confidence interval, 45%-51%), from 9.2 deaths per 100,000 population in 1990 to 4.8 deaths per 100,000 population in 2015. But this global trend masked striking regional disparities. In 1990, 77% of deaths from rheumatic heart disease occurred in endemic areas of Africa, South Asia, Oceania, and the Caribbean; by 2015, 82% of deaths occurred in endemic regions. Oceania, South Asia, and central sub-Saharan Africa had the highest death rates and were the only regions where the 95% confidence intervals for 1990 and 2015 overlapped, the investigators noted.
In 2015, age-standardized death rates exceeded 10 deaths per 100,000 population in the Solomon Islands, Pakistan, Papua New Guinea, Kiribati, Vanuatu, Fiji, India, Federated States of Micronesia, Marshall Islands, Central African Republic, and Lesotho, they reported. Estimated fatalities were highest in India (119,100 deaths), China (72,600), and Pakistan (18,900). They estimated that in 2015, there were 33.2 million cases of rheumatic heart disease and 10.5 million associated disability-adjusted life-years globally.
The study excluded “borderline” or subclinical rheumatic heart disease, which is detected by echocardiography and whose management remains unclear. “Better data for low-income and middle-income countries are needed to guide policies for the control of rheumatic heart disease,” the investigators wrote. They recommended studying death certificate misclassifications, disease prevalence among adults, and longitudinal trends in nonfatal outcomes and excess mortality.
Funders of the study included the Bill and Melinda Gates Foundation and the Medtronic Foundation. Dr. Watkins disclosed grants from the Medtronic Foundation during the conduct of the study and grants from the Bill and Melinda Gates Foundation outside the submitted work.
Global mortality due to rheumatic heart disease fell by about 48% during a recent 25-year-period, but some of the poorest areas of the world were left behind, according to a report in the New England Journal of Medicine.
Those regions included Oceania, South Asia, and central sub-Saharan Africa, where rheumatic heart disease remains endemic, wrote David A. Watkins, MD, MPH, of the University of Washington, Seattle, and his coinvestigators. “We estimate that 10 persons per 1,000 population living in South Asia and central sub-Saharan Africa and 15 persons per 1,000 population in Oceania were living with rheumatic heart disease in the year 2015,” they wrote. “Improvements in the measurement of the burden of rheumatic heart disease will assist in planning for its control and will help identify countries where further investments are needed.”
To better define the problem, Dr. Watkins and his associates analyzed epidemiologic studies of rheumatic heart disease from 1990 through 2015. They used the Cause of Death Ensemble model, which estimates mortality more reliably than older methods, and DisMod-MR (version 2.1), which sums epidemiologic data from multiple sources and corrects for gaps and inconsistencies (N Engl J Med. 2017;377:713-22).
Worldwide, about 319,400 individuals died of rheumatic heart disease in 2015, the researchers reported. Age-adjusted death rates fell by about 48% (95% confidence interval, 45%-51%), from 9.2 deaths per 100,000 population in 1990 to 4.8 deaths per 100,000 population in 2015. But this global trend masked striking regional disparities. In 1990, 77% of deaths from rheumatic heart disease occurred in endemic areas of Africa, South Asia, Oceania, and the Caribbean; by 2015, 82% of deaths occurred in endemic regions. Oceania, South Asia, and central sub-Saharan Africa had the highest death rates and were the only regions where the 95% confidence intervals for 1990 and 2015 overlapped, the investigators noted.
In 2015, age-standardized death rates exceeded 10 deaths per 100,000 population in the Solomon Islands, Pakistan, Papua New Guinea, Kiribati, Vanuatu, Fiji, India, Federated States of Micronesia, Marshall Islands, Central African Republic, and Lesotho, they reported. Estimated fatalities were highest in India (119,100 deaths), China (72,600), and Pakistan (18,900). They estimated that in 2015, there were 33.2 million cases of rheumatic heart disease and 10.5 million associated disability-adjusted life-years globally.
The study excluded “borderline” or subclinical rheumatic heart disease, which is detected by echocardiography and whose management remains unclear. “Better data for low-income and middle-income countries are needed to guide policies for the control of rheumatic heart disease,” the investigators wrote. They recommended studying death certificate misclassifications, disease prevalence among adults, and longitudinal trends in nonfatal outcomes and excess mortality.
Funders of the study included the Bill and Melinda Gates Foundation and the Medtronic Foundation. Dr. Watkins disclosed grants from the Medtronic Foundation during the conduct of the study and grants from the Bill and Melinda Gates Foundation outside the submitted work.
FROM NEW ENGLAND JOURNAL OF MEDICINE
Key clinical point:
Major finding: Globally, age-adjusted death rates fell by about 48% between 1990 and 2015. Oceania, South Asia, and central sub-Saharan Africa had the highest death rates in 2015, and were the only regions where the 95% confidence intervals overlapped with those for 1990.
Data source: A systematic review and analysis of morbidity and mortality data from 1990 through 2015.
Disclosures: Funders included the Bill and Melinda Gates Foundation and the Medtronic Foundation. Dr. Watkins disclosed grants from the Medtronic Foundation during the conduct of the study and grants from the Bill and Melinda Gates Foundation outside the submitted work.
First trial of TAVR vs. SAVR in low-risk patients
PARIS – Five-year hemodynamic results of the first randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with severe aortic stenosis showed continued superior valve performance in the TAVR group, Lars Sondergaard, MD, reported at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.
“The durability results are very encouraging. We can’t see that the TAVR patients are doing worse. So I think this is setting the scene to try to move forward in patients at low risk and also in younger patients,” declared Dr. Sondergaard, professor of cardiology at the University of Copenhagen.
He presented an update from the Nordic Aortic Valve Intervention (NOTION) trial, a prospective, multicenter, randomized, all-comers clinical trial in which 280 patients with symptomatic severe aortic stenosis at low surgical risk were assigned to surgical aortic valve replacement (SAVR) or to TAVR with the self-expanding CoreValve. Their mean age was 79 years, with an average Society of Thoracic Surgeons projected risk of mortality score of 3%. Eighty-two percent of participants had an STS score below 4%. Roughly 40% of TAVR patients got the first-generation CoreValve in the 26-mm size, 40% received the 29-mm version, and the rest got the 31-mm CoreValve.
Among patients in the lowest-surgical-risk and youngest subgroup – those aged 70-75 with a Society of Thoracic Surgeons risk score below 4% – the composite primary endpoint rate at 4 years was 15.6% with TAVR compared with 27.2% with SAVR. However, only 62 NOTION participants fell into this category, so the between-group difference, while sizable, didn’t achieve statistical significance, according to Dr. Sondergaard.
There was a trade-off between the two valve replacement strategies with regard to procedural complications. The rate of new-onset atrial fibrillation was far higher in the SAVR group: 59.4% at 1 year and 60.2% at 4 years of follow-up, compared with 21.2% and 24.5% at 1 and 4 years, respectively, in the TAVR group.
On the other hand, 38% of the TAVR patients got a new pacemaker within the first year of follow-up, compared with only 2.4% in the SAVR group. At 4 years, 43.7% of the TAVR group had a pacemaker, versus 9% of the SAVR group.
Turning to the hemodynamic data, the cardiologist noted that the effective orifice area in the TAVR group went from 0.71 cm2 at baseline to 1.66 at 1 year and remained steady thereafter at 1.67 cm2 through 5 years. The TAVR group’s mean gradient improved from 45.4 mm Hg at baseline to 8.6 mm Hg at 1 year and 7.9 mm Hg at 5 years. These outcomes were significantly better than in the SAVR group, where the effective orifice area went from 0.74 cm2 at baseline to 1.32 at 1 year and 1.24 cm2 at 5 years, while the mean gradient fell from 44.9 mm Hg to 12.5 at 1 year and 13.6 mm Hg at 5 years.
Moderate hemodynamic structural valve deterioration was significantly more common in the SAVR group: 20.7% at 5 years, compared with 2.9% in the TAVR patients. The opposite was true with regard to moderate paravalvular leak, which occurred in 20.9% of the TAVI group but only 1.5% of SAVR patients.
Late complications were rare following either procedure. There were no cases of valve thrombosis through 5 years. The incidence of endocarditis at 5 years was 4.3% in the TAVR patients and similar at 5.9% in the SAVR group.
Discussant Samer Mansour, MD, of the University of Montreal, remarked that the rate of new pacemaker implantation following TAVR seemed extraordinarily high.
“This was early days,” Dr. Sondergaard explained. “We had a lower threshold for putting in a pacemaker and we put the valves in a little deeper.”
About half of new pacemaker recipients didn’t use the device after the first year, he added. Also, neither getting a new pacemaker nor moderate paravalvular leak was associated with increased mortality in the TAVR group.
Dr. Mansour observed that subtle but real differences in mortality probably wouldn’t show up in a 280-patient trial. Dr. Sondergaard concurred.
“We designed the NOTION trial in 2008-2009. Knowing what we know now, we should have had a larger study, but at that time TAVR volume wasn’t that big and it wasn’t realistic as a Nordic trial to include 1,000 patients. This was the best we could do,” he said.
Follow-up in the NOTION study will continue out to 10 years.
The study is funded by Medtronic. Dr. Sondergaard reported serving as a consultant to and receiving research grant support from the company.
PARIS – Five-year hemodynamic results of the first randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with severe aortic stenosis showed continued superior valve performance in the TAVR group, Lars Sondergaard, MD, reported at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.
“The durability results are very encouraging. We can’t see that the TAVR patients are doing worse. So I think this is setting the scene to try to move forward in patients at low risk and also in younger patients,” declared Dr. Sondergaard, professor of cardiology at the University of Copenhagen.
He presented an update from the Nordic Aortic Valve Intervention (NOTION) trial, a prospective, multicenter, randomized, all-comers clinical trial in which 280 patients with symptomatic severe aortic stenosis at low surgical risk were assigned to surgical aortic valve replacement (SAVR) or to TAVR with the self-expanding CoreValve. Their mean age was 79 years, with an average Society of Thoracic Surgeons projected risk of mortality score of 3%. Eighty-two percent of participants had an STS score below 4%. Roughly 40% of TAVR patients got the first-generation CoreValve in the 26-mm size, 40% received the 29-mm version, and the rest got the 31-mm CoreValve.
Among patients in the lowest-surgical-risk and youngest subgroup – those aged 70-75 with a Society of Thoracic Surgeons risk score below 4% – the composite primary endpoint rate at 4 years was 15.6% with TAVR compared with 27.2% with SAVR. However, only 62 NOTION participants fell into this category, so the between-group difference, while sizable, didn’t achieve statistical significance, according to Dr. Sondergaard.
There was a trade-off between the two valve replacement strategies with regard to procedural complications. The rate of new-onset atrial fibrillation was far higher in the SAVR group: 59.4% at 1 year and 60.2% at 4 years of follow-up, compared with 21.2% and 24.5% at 1 and 4 years, respectively, in the TAVR group.
On the other hand, 38% of the TAVR patients got a new pacemaker within the first year of follow-up, compared with only 2.4% in the SAVR group. At 4 years, 43.7% of the TAVR group had a pacemaker, versus 9% of the SAVR group.
Turning to the hemodynamic data, the cardiologist noted that the effective orifice area in the TAVR group went from 0.71 cm2 at baseline to 1.66 at 1 year and remained steady thereafter at 1.67 cm2 through 5 years. The TAVR group’s mean gradient improved from 45.4 mm Hg at baseline to 8.6 mm Hg at 1 year and 7.9 mm Hg at 5 years. These outcomes were significantly better than in the SAVR group, where the effective orifice area went from 0.74 cm2 at baseline to 1.32 at 1 year and 1.24 cm2 at 5 years, while the mean gradient fell from 44.9 mm Hg to 12.5 at 1 year and 13.6 mm Hg at 5 years.
Moderate hemodynamic structural valve deterioration was significantly more common in the SAVR group: 20.7% at 5 years, compared with 2.9% in the TAVR patients. The opposite was true with regard to moderate paravalvular leak, which occurred in 20.9% of the TAVI group but only 1.5% of SAVR patients.
Late complications were rare following either procedure. There were no cases of valve thrombosis through 5 years. The incidence of endocarditis at 5 years was 4.3% in the TAVR patients and similar at 5.9% in the SAVR group.
Discussant Samer Mansour, MD, of the University of Montreal, remarked that the rate of new pacemaker implantation following TAVR seemed extraordinarily high.
“This was early days,” Dr. Sondergaard explained. “We had a lower threshold for putting in a pacemaker and we put the valves in a little deeper.”
About half of new pacemaker recipients didn’t use the device after the first year, he added. Also, neither getting a new pacemaker nor moderate paravalvular leak was associated with increased mortality in the TAVR group.
Dr. Mansour observed that subtle but real differences in mortality probably wouldn’t show up in a 280-patient trial. Dr. Sondergaard concurred.
“We designed the NOTION trial in 2008-2009. Knowing what we know now, we should have had a larger study, but at that time TAVR volume wasn’t that big and it wasn’t realistic as a Nordic trial to include 1,000 patients. This was the best we could do,” he said.
Follow-up in the NOTION study will continue out to 10 years.
The study is funded by Medtronic. Dr. Sondergaard reported serving as a consultant to and receiving research grant support from the company.
PARIS – Five-year hemodynamic results of the first randomized trial of transcatheter versus surgical aortic valve replacement in low-surgical-risk patients with severe aortic stenosis showed continued superior valve performance in the TAVR group, Lars Sondergaard, MD, reported at the annual congress of the European Association of Percutaneous Cardiovascular Interventions.
“The durability results are very encouraging. We can’t see that the TAVR patients are doing worse. So I think this is setting the scene to try to move forward in patients at low risk and also in younger patients,” declared Dr. Sondergaard, professor of cardiology at the University of Copenhagen.
He presented an update from the Nordic Aortic Valve Intervention (NOTION) trial, a prospective, multicenter, randomized, all-comers clinical trial in which 280 patients with symptomatic severe aortic stenosis at low surgical risk were assigned to surgical aortic valve replacement (SAVR) or to TAVR with the self-expanding CoreValve. Their mean age was 79 years, with an average Society of Thoracic Surgeons projected risk of mortality score of 3%. Eighty-two percent of participants had an STS score below 4%. Roughly 40% of TAVR patients got the first-generation CoreValve in the 26-mm size, 40% received the 29-mm version, and the rest got the 31-mm CoreValve.
Among patients in the lowest-surgical-risk and youngest subgroup – those aged 70-75 with a Society of Thoracic Surgeons risk score below 4% – the composite primary endpoint rate at 4 years was 15.6% with TAVR compared with 27.2% with SAVR. However, only 62 NOTION participants fell into this category, so the between-group difference, while sizable, didn’t achieve statistical significance, according to Dr. Sondergaard.
There was a trade-off between the two valve replacement strategies with regard to procedural complications. The rate of new-onset atrial fibrillation was far higher in the SAVR group: 59.4% at 1 year and 60.2% at 4 years of follow-up, compared with 21.2% and 24.5% at 1 and 4 years, respectively, in the TAVR group.
On the other hand, 38% of the TAVR patients got a new pacemaker within the first year of follow-up, compared with only 2.4% in the SAVR group. At 4 years, 43.7% of the TAVR group had a pacemaker, versus 9% of the SAVR group.
Turning to the hemodynamic data, the cardiologist noted that the effective orifice area in the TAVR group went from 0.71 cm2 at baseline to 1.66 at 1 year and remained steady thereafter at 1.67 cm2 through 5 years. The TAVR group’s mean gradient improved from 45.4 mm Hg at baseline to 8.6 mm Hg at 1 year and 7.9 mm Hg at 5 years. These outcomes were significantly better than in the SAVR group, where the effective orifice area went from 0.74 cm2 at baseline to 1.32 at 1 year and 1.24 cm2 at 5 years, while the mean gradient fell from 44.9 mm Hg to 12.5 at 1 year and 13.6 mm Hg at 5 years.
Moderate hemodynamic structural valve deterioration was significantly more common in the SAVR group: 20.7% at 5 years, compared with 2.9% in the TAVR patients. The opposite was true with regard to moderate paravalvular leak, which occurred in 20.9% of the TAVI group but only 1.5% of SAVR patients.
Late complications were rare following either procedure. There were no cases of valve thrombosis through 5 years. The incidence of endocarditis at 5 years was 4.3% in the TAVR patients and similar at 5.9% in the SAVR group.
Discussant Samer Mansour, MD, of the University of Montreal, remarked that the rate of new pacemaker implantation following TAVR seemed extraordinarily high.
“This was early days,” Dr. Sondergaard explained. “We had a lower threshold for putting in a pacemaker and we put the valves in a little deeper.”
About half of new pacemaker recipients didn’t use the device after the first year, he added. Also, neither getting a new pacemaker nor moderate paravalvular leak was associated with increased mortality in the TAVR group.
Dr. Mansour observed that subtle but real differences in mortality probably wouldn’t show up in a 280-patient trial. Dr. Sondergaard concurred.
“We designed the NOTION trial in 2008-2009. Knowing what we know now, we should have had a larger study, but at that time TAVR volume wasn’t that big and it wasn’t realistic as a Nordic trial to include 1,000 patients. This was the best we could do,” he said.
Follow-up in the NOTION study will continue out to 10 years.
The study is funded by Medtronic. Dr. Sondergaard reported serving as a consultant to and receiving research grant support from the company.
AT EuroPCR
Key clinical point:
Major finding: At 4 years of follow-up, the composite endpoint of all-cause mortality, MI, or stroke occurred in 29% of low-surgical-risk patients with severe aortic stenosis who were randomized to transcatheter aortic valve replacement (TAVR) and 30% of those who underwent surgical valve replacement.
Data source: NOTION, a prospective multicenter randomized trial in which 280 Nordic patients with symptomatic severe aortic stenosis at low surgical risk were assigned to surgical aortic valve replacement (SAVR) or to TAVR with the self-expanding CoreValve.
Disclosures: The study is funded by Medtronic. The presenter reported serving as a consultant to and receiving research grant support from the company.
FDA approves first spironolactone oral suspension
The Food and Drug Administration has approved CaroSpir, the first oral suspension form of spironolactone, the aldosterone antagonist that was first approved in 1960, according to an announcement from CMP Pharma.
CaroSpir is intended for the treatment of New York Heart Association class III-IV heart failure and reduced ejection fraction, usually in combination with other treatments. CaroSpir is also indicated as an add-on medication for the treatment of hypertension, and for the treatment of edema in cirrhotic patients who have not adequately responded to fluid and sodium restriction.
“CaroSpir provides a stable, ready to use, and consistent liquid treatment option for adult patients. Up until now, these patients have been prescribed a pharmacy-compounded liquid form of spironolactone. The dosing inconsistencies of compounded liquids have long been a persistent challenge for physicians,” Gerald Sakowski, CEO at CMP Pharma, said in the press release.
Find the full press release on the CMP Pharma website.
The Food and Drug Administration has approved CaroSpir, the first oral suspension form of spironolactone, the aldosterone antagonist that was first approved in 1960, according to an announcement from CMP Pharma.
CaroSpir is intended for the treatment of New York Heart Association class III-IV heart failure and reduced ejection fraction, usually in combination with other treatments. CaroSpir is also indicated as an add-on medication for the treatment of hypertension, and for the treatment of edema in cirrhotic patients who have not adequately responded to fluid and sodium restriction.
“CaroSpir provides a stable, ready to use, and consistent liquid treatment option for adult patients. Up until now, these patients have been prescribed a pharmacy-compounded liquid form of spironolactone. The dosing inconsistencies of compounded liquids have long been a persistent challenge for physicians,” Gerald Sakowski, CEO at CMP Pharma, said in the press release.
Find the full press release on the CMP Pharma website.
The Food and Drug Administration has approved CaroSpir, the first oral suspension form of spironolactone, the aldosterone antagonist that was first approved in 1960, according to an announcement from CMP Pharma.
CaroSpir is intended for the treatment of New York Heart Association class III-IV heart failure and reduced ejection fraction, usually in combination with other treatments. CaroSpir is also indicated as an add-on medication for the treatment of hypertension, and for the treatment of edema in cirrhotic patients who have not adequately responded to fluid and sodium restriction.
“CaroSpir provides a stable, ready to use, and consistent liquid treatment option for adult patients. Up until now, these patients have been prescribed a pharmacy-compounded liquid form of spironolactone. The dosing inconsistencies of compounded liquids have long been a persistent challenge for physicians,” Gerald Sakowski, CEO at CMP Pharma, said in the press release.
Find the full press release on the CMP Pharma website.
Ventricular assist devices linked to sepsis
NEW ORLEANS – Back in 2008, there was only one case.
Since then, however, the number of patients with ventricular assist devices who developed sepsis while being treated in the cardiac unit at Queen Elizabeth Hospital in Birmingham, England, appeared to be noticeably growing. So, investigators launched a study to confirm their suspicions and to learn more about the underlying causes.
“Bloodstream infection is a serious infection, so I thought, ‘Let’s see what’s happening,’ ” explained Ira Das, MD, a consultant microbiologist at Queen Elizabeth Hospital.
Coagulase-negative staphylococci were the most common cause, present in 32% of the 25 cases. Sepsis was caused by Enterococcus faecium in 12%, Candida parapsilosis in 8%, and Staphylococcus aureus in 2%. Another 4% were either Enterococcus faecalis, Serratia marcescens, Pseudomonas aeruginosa, C. guilliermondii, or C. orthopsilosis. The remaining 16% of bloodstream infections were polymicrobial.
Less certain was the source of these infections.
“In the majority of cases, we didn’t know where it was coming from,” Dr. Das said at the annual meeting of the American Society for Microbiology. In 6 of the 25 cases, VAD was confirmed to be the focus of infection, either through imaging or because a failing component of the explanted device was examined later. An intravascular catheter was the source in another 5 patients, and in 14 cases, the source remained a mystery.
“Some of these infections just might have been hard to see,” Dr. Das said. “If the infection is inside the device, it’s not always easy to visualize.”
The study supports earlier findings from a review article that points to a significant infection risk associated with the implantation of VADs (Expert Rev Med Devices. 2011 Sep;8[5]:627-34). That article’s authors noted, “Despite recent improvements in outcomes, device-related infections remain a significant complication of LVAD [left ventricular assist device] therapy.”
In a previous study of people with end-stage heart failure, other investigators noted that, “despite the substantial survival benefit, the morbidity and mortality associated with the use of the left ventricular assist device were considerable. In particular, infection and mechanical failure of the device were major factors in the 2-year survival rate of only 23%” (N Engl J Med. 2001 Nov 15;345[20]:1435-43).
Similarly, in the current study, mortality was higher among those with sepsis and a VAD. Mortality was 39% – including eight patients who died with a VAD in situ and one following cardiac transplantation. However, Dr. Das cautioned, “It’s a small number, and there are other factors that could have contributed. They all go on anticoagulants so they have bleeding tendencies, and many of the patients are in the ICU with multiorgan failure.”
Infection prevention remains paramount to minimize mortality and other adverse events associated with a patient’s having a VAD. “We have to make sure that infection control procedures and our treatments are up to the optimal standard,” Dr. Das said. “It’s not easy to remove the device.”
Of the 129 VADs implanted, 68 were long-term LVADs, 11 were short-term LVADs, 15 were right ventricular devices, and 35 were biventricular devices.
The study is ongoing. The data presented at the meeting were collected up until December 2016.
“Since then, I’ve seen two more cases, and – very interestingly – one was Haemophilus influenzae,” Dr. Das said. “The patient was on the device, he was at home, and he came in with bacteremia.” Again, the source of infection proved elusive. “With H. influenzae, you would think it was coming from his chest, but the chest x-ray was normal.”
The second case, a patient with a coagulase-negative staphylococci bloodstream infection, was scheduled for a PET scan at the time of Dr. Das’ presentation to try to identify the source of infection.
Dr. Das had no relevant disclosures.
Modern technology saves our patients' lives, but there is always another side to the coin. Reports that LVAD devices are associated with a high incidence of bloodstream infections is important for future clinical practice. The fact that the causes and risk factors for these infections are unknown make this phenomena one of high interest.
Modern technology saves our patients' lives, but there is always another side to the coin. Reports that LVAD devices are associated with a high incidence of bloodstream infections is important for future clinical practice. The fact that the causes and risk factors for these infections are unknown make this phenomena one of high interest.
Modern technology saves our patients' lives, but there is always another side to the coin. Reports that LVAD devices are associated with a high incidence of bloodstream infections is important for future clinical practice. The fact that the causes and risk factors for these infections are unknown make this phenomena one of high interest.
NEW ORLEANS – Back in 2008, there was only one case.
Since then, however, the number of patients with ventricular assist devices who developed sepsis while being treated in the cardiac unit at Queen Elizabeth Hospital in Birmingham, England, appeared to be noticeably growing. So, investigators launched a study to confirm their suspicions and to learn more about the underlying causes.
“Bloodstream infection is a serious infection, so I thought, ‘Let’s see what’s happening,’ ” explained Ira Das, MD, a consultant microbiologist at Queen Elizabeth Hospital.
Coagulase-negative staphylococci were the most common cause, present in 32% of the 25 cases. Sepsis was caused by Enterococcus faecium in 12%, Candida parapsilosis in 8%, and Staphylococcus aureus in 2%. Another 4% were either Enterococcus faecalis, Serratia marcescens, Pseudomonas aeruginosa, C. guilliermondii, or C. orthopsilosis. The remaining 16% of bloodstream infections were polymicrobial.
Less certain was the source of these infections.
“In the majority of cases, we didn’t know where it was coming from,” Dr. Das said at the annual meeting of the American Society for Microbiology. In 6 of the 25 cases, VAD was confirmed to be the focus of infection, either through imaging or because a failing component of the explanted device was examined later. An intravascular catheter was the source in another 5 patients, and in 14 cases, the source remained a mystery.
“Some of these infections just might have been hard to see,” Dr. Das said. “If the infection is inside the device, it’s not always easy to visualize.”
The study supports earlier findings from a review article that points to a significant infection risk associated with the implantation of VADs (Expert Rev Med Devices. 2011 Sep;8[5]:627-34). That article’s authors noted, “Despite recent improvements in outcomes, device-related infections remain a significant complication of LVAD [left ventricular assist device] therapy.”
In a previous study of people with end-stage heart failure, other investigators noted that, “despite the substantial survival benefit, the morbidity and mortality associated with the use of the left ventricular assist device were considerable. In particular, infection and mechanical failure of the device were major factors in the 2-year survival rate of only 23%” (N Engl J Med. 2001 Nov 15;345[20]:1435-43).
Similarly, in the current study, mortality was higher among those with sepsis and a VAD. Mortality was 39% – including eight patients who died with a VAD in situ and one following cardiac transplantation. However, Dr. Das cautioned, “It’s a small number, and there are other factors that could have contributed. They all go on anticoagulants so they have bleeding tendencies, and many of the patients are in the ICU with multiorgan failure.”
Infection prevention remains paramount to minimize mortality and other adverse events associated with a patient’s having a VAD. “We have to make sure that infection control procedures and our treatments are up to the optimal standard,” Dr. Das said. “It’s not easy to remove the device.”
Of the 129 VADs implanted, 68 were long-term LVADs, 11 were short-term LVADs, 15 were right ventricular devices, and 35 were biventricular devices.
The study is ongoing. The data presented at the meeting were collected up until December 2016.
“Since then, I’ve seen two more cases, and – very interestingly – one was Haemophilus influenzae,” Dr. Das said. “The patient was on the device, he was at home, and he came in with bacteremia.” Again, the source of infection proved elusive. “With H. influenzae, you would think it was coming from his chest, but the chest x-ray was normal.”
The second case, a patient with a coagulase-negative staphylococci bloodstream infection, was scheduled for a PET scan at the time of Dr. Das’ presentation to try to identify the source of infection.
Dr. Das had no relevant disclosures.
NEW ORLEANS – Back in 2008, there was only one case.
Since then, however, the number of patients with ventricular assist devices who developed sepsis while being treated in the cardiac unit at Queen Elizabeth Hospital in Birmingham, England, appeared to be noticeably growing. So, investigators launched a study to confirm their suspicions and to learn more about the underlying causes.
“Bloodstream infection is a serious infection, so I thought, ‘Let’s see what’s happening,’ ” explained Ira Das, MD, a consultant microbiologist at Queen Elizabeth Hospital.
Coagulase-negative staphylococci were the most common cause, present in 32% of the 25 cases. Sepsis was caused by Enterococcus faecium in 12%, Candida parapsilosis in 8%, and Staphylococcus aureus in 2%. Another 4% were either Enterococcus faecalis, Serratia marcescens, Pseudomonas aeruginosa, C. guilliermondii, or C. orthopsilosis. The remaining 16% of bloodstream infections were polymicrobial.
Less certain was the source of these infections.
“In the majority of cases, we didn’t know where it was coming from,” Dr. Das said at the annual meeting of the American Society for Microbiology. In 6 of the 25 cases, VAD was confirmed to be the focus of infection, either through imaging or because a failing component of the explanted device was examined later. An intravascular catheter was the source in another 5 patients, and in 14 cases, the source remained a mystery.
“Some of these infections just might have been hard to see,” Dr. Das said. “If the infection is inside the device, it’s not always easy to visualize.”
The study supports earlier findings from a review article that points to a significant infection risk associated with the implantation of VADs (Expert Rev Med Devices. 2011 Sep;8[5]:627-34). That article’s authors noted, “Despite recent improvements in outcomes, device-related infections remain a significant complication of LVAD [left ventricular assist device] therapy.”
In a previous study of people with end-stage heart failure, other investigators noted that, “despite the substantial survival benefit, the morbidity and mortality associated with the use of the left ventricular assist device were considerable. In particular, infection and mechanical failure of the device were major factors in the 2-year survival rate of only 23%” (N Engl J Med. 2001 Nov 15;345[20]:1435-43).
Similarly, in the current study, mortality was higher among those with sepsis and a VAD. Mortality was 39% – including eight patients who died with a VAD in situ and one following cardiac transplantation. However, Dr. Das cautioned, “It’s a small number, and there are other factors that could have contributed. They all go on anticoagulants so they have bleeding tendencies, and many of the patients are in the ICU with multiorgan failure.”
Infection prevention remains paramount to minimize mortality and other adverse events associated with a patient’s having a VAD. “We have to make sure that infection control procedures and our treatments are up to the optimal standard,” Dr. Das said. “It’s not easy to remove the device.”
Of the 129 VADs implanted, 68 were long-term LVADs, 11 were short-term LVADs, 15 were right ventricular devices, and 35 were biventricular devices.
The study is ongoing. The data presented at the meeting were collected up until December 2016.
“Since then, I’ve seen two more cases, and – very interestingly – one was Haemophilus influenzae,” Dr. Das said. “The patient was on the device, he was at home, and he came in with bacteremia.” Again, the source of infection proved elusive. “With H. influenzae, you would think it was coming from his chest, but the chest x-ray was normal.”
The second case, a patient with a coagulase-negative staphylococci bloodstream infection, was scheduled for a PET scan at the time of Dr. Das’ presentation to try to identify the source of infection.
Dr. Das had no relevant disclosures.
AT ASM MICROBE 2017
Key clinical point: There may be a significant rate of bloodstream infections among people with a ventricular assist device.
Major finding: A total of 20% of the 118 people with a VAD had a bloodstream infection.
Data source: A retrospective study of 129 ventricular assist devices placed in 118 people between 2008 and 2016.
Disclosures: Dr. Das had no relevant disclosures.
Study: No increased mortality with ACA-prompted readmission declines
Concerns that efforts to reduce 30-day hospital readmission rates under the Affordable Care Act’s Hospital Readmission Reduction Program might lead to unintended increases in mortality rates appear to be unfounded, according to a review of more than 6.7 million hospitalizations for heart failure, acute myocardial infarction, or pneumonia between 2008 and 2014.
In fact, reductions in 30-day readmission rates among Medicare fee-for-service beneficiaries are weakly but significantly correlated with reductions in hospital 30-day mortality rates after discharge, according to Kumar Dharmarajan, MD, of Yale New Haven (Conn.) Health, and colleagues (JAMA 2017 Jul 18;318[3]:270-8. doi: 10.1001/jama.2017.8444).
From 2008 to 2014, the RARRs declined in aggregate across hospitals (–0.053% for heart failure, –0.044% for acute MI, and –0.033% for pneumonia).
“In contrast, monthly aggregate trends across hospitals in 30-day risk-adjusted mortality rates after discharge varied by admitting condition” the investigators said.
For heart failure, acute MI, and pneumonia, there was an increase of 0.008%, a decrease of 0.003%, and an increase of 0.001%, respectively, they said. However, paired monthly trends in 30-day RARRs and 30-day RAMRs after discharge “identified concomitant reduction in readmission and mortality rates within hospitals.”
Correlation coefficients of the paired monthly trends for heart failure, acute MI, and pneumonia in 2008-2014 were 0.066, 0.067, and 0.108, respectively.
“Paired trends in hospital 30-day risk-adjusted readmission rates and both 90-day risk-adjusted mortality rates after discharge and 90-day risk-adjusted mortality rates after the admission date also identified concomitant reductions in readmission and mortality rates within hospitals,” the authors wrote.
The findings “do not support increasing postdischarge mortality related to reducing hospital readmissions,” they concluded.
The authors work under contract with the Centers for Medicare & Medicaid Services to develop and maintain performance measures. Dr. Dharmarajan reported serving as a consultant and scientific advisory board member for Clover Health at the time this research was performed. He is supported by grants from the National Institute on Aging and the American Federation for Aging Research, and the Yale Claude D. Pepper Older Americans Independence Center.
The findings by Dharmarajan and colleagues are “certainly good news,” Karen E. Joynt Maddox, MD, wrote in an editorial.
The study provides support for strategies that hospitals are using to reduce readmissions, and also underscores the importance of evaluating unintended consequences of policy changes such as the Affordable Care Act’s Hospital Readmissions Reduction Program (HRRP), she said (JAMA. 2017 Jul 18;318[3]:243-4).
The study did not address the possibility that attention to reducing readmissions has taken priority over reducing mortality, which could have the unintended consequence of slowing improvements in mortality, she noted, suggesting that for this and other reasons it may be “time to reexamine and reengineer the HRRP to avoid unintended consequences and to ensure that its incentives are fully aligned with the ultimate goal of improving the health outcomes of patients.
“Only with full knowledge of the advantages and disadvantages of a particular policy decision can policy makers and advocates work to craft statutes and rules that maximize benefits while minimizing harms,” she wrote.
Dr. Joynt Maddox is with Brigham and Women’s Hospital, Boston. She is supported by a grant from the National Heart, Lung, and Blood Institute.
The findings by Dharmarajan and colleagues are “certainly good news,” Karen E. Joynt Maddox, MD, wrote in an editorial.
The study provides support for strategies that hospitals are using to reduce readmissions, and also underscores the importance of evaluating unintended consequences of policy changes such as the Affordable Care Act’s Hospital Readmissions Reduction Program (HRRP), she said (JAMA. 2017 Jul 18;318[3]:243-4).
The study did not address the possibility that attention to reducing readmissions has taken priority over reducing mortality, which could have the unintended consequence of slowing improvements in mortality, she noted, suggesting that for this and other reasons it may be “time to reexamine and reengineer the HRRP to avoid unintended consequences and to ensure that its incentives are fully aligned with the ultimate goal of improving the health outcomes of patients.
“Only with full knowledge of the advantages and disadvantages of a particular policy decision can policy makers and advocates work to craft statutes and rules that maximize benefits while minimizing harms,” she wrote.
Dr. Joynt Maddox is with Brigham and Women’s Hospital, Boston. She is supported by a grant from the National Heart, Lung, and Blood Institute.
The findings by Dharmarajan and colleagues are “certainly good news,” Karen E. Joynt Maddox, MD, wrote in an editorial.
The study provides support for strategies that hospitals are using to reduce readmissions, and also underscores the importance of evaluating unintended consequences of policy changes such as the Affordable Care Act’s Hospital Readmissions Reduction Program (HRRP), she said (JAMA. 2017 Jul 18;318[3]:243-4).
The study did not address the possibility that attention to reducing readmissions has taken priority over reducing mortality, which could have the unintended consequence of slowing improvements in mortality, she noted, suggesting that for this and other reasons it may be “time to reexamine and reengineer the HRRP to avoid unintended consequences and to ensure that its incentives are fully aligned with the ultimate goal of improving the health outcomes of patients.
“Only with full knowledge of the advantages and disadvantages of a particular policy decision can policy makers and advocates work to craft statutes and rules that maximize benefits while minimizing harms,” she wrote.
Dr. Joynt Maddox is with Brigham and Women’s Hospital, Boston. She is supported by a grant from the National Heart, Lung, and Blood Institute.
Concerns that efforts to reduce 30-day hospital readmission rates under the Affordable Care Act’s Hospital Readmission Reduction Program might lead to unintended increases in mortality rates appear to be unfounded, according to a review of more than 6.7 million hospitalizations for heart failure, acute myocardial infarction, or pneumonia between 2008 and 2014.
In fact, reductions in 30-day readmission rates among Medicare fee-for-service beneficiaries are weakly but significantly correlated with reductions in hospital 30-day mortality rates after discharge, according to Kumar Dharmarajan, MD, of Yale New Haven (Conn.) Health, and colleagues (JAMA 2017 Jul 18;318[3]:270-8. doi: 10.1001/jama.2017.8444).
From 2008 to 2014, the RARRs declined in aggregate across hospitals (–0.053% for heart failure, –0.044% for acute MI, and –0.033% for pneumonia).
“In contrast, monthly aggregate trends across hospitals in 30-day risk-adjusted mortality rates after discharge varied by admitting condition” the investigators said.
For heart failure, acute MI, and pneumonia, there was an increase of 0.008%, a decrease of 0.003%, and an increase of 0.001%, respectively, they said. However, paired monthly trends in 30-day RARRs and 30-day RAMRs after discharge “identified concomitant reduction in readmission and mortality rates within hospitals.”
Correlation coefficients of the paired monthly trends for heart failure, acute MI, and pneumonia in 2008-2014 were 0.066, 0.067, and 0.108, respectively.
“Paired trends in hospital 30-day risk-adjusted readmission rates and both 90-day risk-adjusted mortality rates after discharge and 90-day risk-adjusted mortality rates after the admission date also identified concomitant reductions in readmission and mortality rates within hospitals,” the authors wrote.
The findings “do not support increasing postdischarge mortality related to reducing hospital readmissions,” they concluded.
The authors work under contract with the Centers for Medicare & Medicaid Services to develop and maintain performance measures. Dr. Dharmarajan reported serving as a consultant and scientific advisory board member for Clover Health at the time this research was performed. He is supported by grants from the National Institute on Aging and the American Federation for Aging Research, and the Yale Claude D. Pepper Older Americans Independence Center.
Concerns that efforts to reduce 30-day hospital readmission rates under the Affordable Care Act’s Hospital Readmission Reduction Program might lead to unintended increases in mortality rates appear to be unfounded, according to a review of more than 6.7 million hospitalizations for heart failure, acute myocardial infarction, or pneumonia between 2008 and 2014.
In fact, reductions in 30-day readmission rates among Medicare fee-for-service beneficiaries are weakly but significantly correlated with reductions in hospital 30-day mortality rates after discharge, according to Kumar Dharmarajan, MD, of Yale New Haven (Conn.) Health, and colleagues (JAMA 2017 Jul 18;318[3]:270-8. doi: 10.1001/jama.2017.8444).
From 2008 to 2014, the RARRs declined in aggregate across hospitals (–0.053% for heart failure, –0.044% for acute MI, and –0.033% for pneumonia).
“In contrast, monthly aggregate trends across hospitals in 30-day risk-adjusted mortality rates after discharge varied by admitting condition” the investigators said.
For heart failure, acute MI, and pneumonia, there was an increase of 0.008%, a decrease of 0.003%, and an increase of 0.001%, respectively, they said. However, paired monthly trends in 30-day RARRs and 30-day RAMRs after discharge “identified concomitant reduction in readmission and mortality rates within hospitals.”
Correlation coefficients of the paired monthly trends for heart failure, acute MI, and pneumonia in 2008-2014 were 0.066, 0.067, and 0.108, respectively.
“Paired trends in hospital 30-day risk-adjusted readmission rates and both 90-day risk-adjusted mortality rates after discharge and 90-day risk-adjusted mortality rates after the admission date also identified concomitant reductions in readmission and mortality rates within hospitals,” the authors wrote.
The findings “do not support increasing postdischarge mortality related to reducing hospital readmissions,” they concluded.
The authors work under contract with the Centers for Medicare & Medicaid Services to develop and maintain performance measures. Dr. Dharmarajan reported serving as a consultant and scientific advisory board member for Clover Health at the time this research was performed. He is supported by grants from the National Institute on Aging and the American Federation for Aging Research, and the Yale Claude D. Pepper Older Americans Independence Center.
FROM JAMA
Key clinical point:
Major finding: Correlation coefficients of the paired monthly trends for heart failure, acute myocardial infarction, and pneumonia in 2008-2014 were 0.066, 0.067, and 0.108, respectively.
Data source: A retrospective review of more than 6.7 million hospitalized Medicare fee-for-service beneficiaries.
Disclosures: The authors work under contract with the Centers for Medicare & Medicaid Services to develop and maintain performance measures. Dr. Dharmarajan reported serving as a consultant and scientific advisory board member for Clover Health at the time this research was performed. He is supported by grants from the National Institute on Aging and the American Federation for Aging Research, and the Yale Claude D. Pepper Older Americans Independence Center.
Plasma biomarker distinguishes ARDS, acute heart failure
WASHINGTON – Plasma levels of an interleukin-33 receptor that’s involved in inflammation regulation appeared able to discriminate between acute respiratory distress syndrome and acute decompensated heart failure in an analysis with 72 patients.
In a second study, high plasma levels of the same interleukin-33 receptor, known as soluble suppressor of tumorgenicity 2 (sST2), identified acute respiratory distress syndrome (ARDS) patients who were sicker and more responsive to conservative fluid management, Sean D. Levy, MD, said at an international conference of the American Thoracic Society.
In order to assess the ability of sST2 to reliably distinguish patients with ARDS from those with acute decompensated heart failure, he and his associates selected 72 patients seen at the Massachusetts General Hospital in Boston with an initial diagnosis of acute decompensated heart failure accompanied by bilateral lung infiltrates and acute hypoxemia respiratory failure requiring endotracheal intubation and mechanical ventilation. The investigators measured the sST2 level in a plasma specimen from each patient. In addition, after each patient either left the hospital or died, their case underwent review by two critical care physicians who retrospectively rediagnosed the patients as either having ARDS or acute decompensated heart failure. This divided the cohort into 30 patients with ARDS and 42 with true acute heart failure. The two subgroups matched up fairly closely for most clinical measures and comorbidities, but APACHE III (Acute Physiology and Chronic Health Evaluation III) scores averaged significantly higher in the ARDS patients.
The plasma levels of sST2 showed a dramatic split between the two subgroups. The 30 patients retrospectively diagnosed with ARDS had an average level of 386 ng/mL with an interquartile range of 318-611 ng/mL. The 42 acute decompensated heart failure patients averaged a sST2 level of 148 ng/mL, with an interquartile range of 84-225 ng/mL. The area under the receiver operator curve for discriminating between ARDS and acute heart failure using a cutpoint of 271 mg/mL was 0.86, showing “good” discrimination, Dr. Levy said. This cutpoint had a sensitivity of 83% and specificity of 88% for correctly distinguishing between ARDS and acute heart failure.
In a second analysis, Dr. Levy and his associates looked at the ability of sST2 levels to separate out patients with acute lung injury who had a more robust response to either the conservative or liberal fluid-management strategies tested in the Fluid and Catheter Treatment Trial (FACTT), run by the National Heart, Lung, and Blood Institute’s ARDS Clinical Trials Network. The primary outcome of FACTT was death from any cause 60 days after entry, and this showed no significant difference between conservative (restricted fluids and increased urine output) and liberal (the reverse) fluid management strategies in acute lung injury patients (N Engl J Med. 2006 Jun 15;354[14]:2564-75). From among the 1,001 patients enrolled in FACTT, 826 had specimens available for measuring sST2 (Crit Care Med. 2013 Nov;41[11]:2521-31),
The researchers applied the sST2 cut point they derived in the first analysis to the FACTT cohort and identified 133 (16%) patients with a low sST2 level and 693 (84%) with a high level. The patients with high sST2 were sicker, with significantly higher APACHE III scores, worse acidemia, and worse renal function.
Patients with high sST2 levels had a significant increase in ventilator-free days on conservative fluid management, compared with liberal management, while the two management strategies produced virtually identical results in the patients with low levels of sST2. Patients with high sST2 also had a significantly quicker time to extubation on a conservative strategy compared with the liberal strategy, and again this correlation did not exist among patients with low sST2. However, as in the overall trial a conservative strategy had no discernible impact on 60-day mortality, compared with the liberal strategy, even in the subgroup with high sST2.
Dr. Levy had no disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
WASHINGTON – Plasma levels of an interleukin-33 receptor that’s involved in inflammation regulation appeared able to discriminate between acute respiratory distress syndrome and acute decompensated heart failure in an analysis with 72 patients.
In a second study, high plasma levels of the same interleukin-33 receptor, known as soluble suppressor of tumorgenicity 2 (sST2), identified acute respiratory distress syndrome (ARDS) patients who were sicker and more responsive to conservative fluid management, Sean D. Levy, MD, said at an international conference of the American Thoracic Society.
In order to assess the ability of sST2 to reliably distinguish patients with ARDS from those with acute decompensated heart failure, he and his associates selected 72 patients seen at the Massachusetts General Hospital in Boston with an initial diagnosis of acute decompensated heart failure accompanied by bilateral lung infiltrates and acute hypoxemia respiratory failure requiring endotracheal intubation and mechanical ventilation. The investigators measured the sST2 level in a plasma specimen from each patient. In addition, after each patient either left the hospital or died, their case underwent review by two critical care physicians who retrospectively rediagnosed the patients as either having ARDS or acute decompensated heart failure. This divided the cohort into 30 patients with ARDS and 42 with true acute heart failure. The two subgroups matched up fairly closely for most clinical measures and comorbidities, but APACHE III (Acute Physiology and Chronic Health Evaluation III) scores averaged significantly higher in the ARDS patients.
The plasma levels of sST2 showed a dramatic split between the two subgroups. The 30 patients retrospectively diagnosed with ARDS had an average level of 386 ng/mL with an interquartile range of 318-611 ng/mL. The 42 acute decompensated heart failure patients averaged a sST2 level of 148 ng/mL, with an interquartile range of 84-225 ng/mL. The area under the receiver operator curve for discriminating between ARDS and acute heart failure using a cutpoint of 271 mg/mL was 0.86, showing “good” discrimination, Dr. Levy said. This cutpoint had a sensitivity of 83% and specificity of 88% for correctly distinguishing between ARDS and acute heart failure.
In a second analysis, Dr. Levy and his associates looked at the ability of sST2 levels to separate out patients with acute lung injury who had a more robust response to either the conservative or liberal fluid-management strategies tested in the Fluid and Catheter Treatment Trial (FACTT), run by the National Heart, Lung, and Blood Institute’s ARDS Clinical Trials Network. The primary outcome of FACTT was death from any cause 60 days after entry, and this showed no significant difference between conservative (restricted fluids and increased urine output) and liberal (the reverse) fluid management strategies in acute lung injury patients (N Engl J Med. 2006 Jun 15;354[14]:2564-75). From among the 1,001 patients enrolled in FACTT, 826 had specimens available for measuring sST2 (Crit Care Med. 2013 Nov;41[11]:2521-31),
The researchers applied the sST2 cut point they derived in the first analysis to the FACTT cohort and identified 133 (16%) patients with a low sST2 level and 693 (84%) with a high level. The patients with high sST2 were sicker, with significantly higher APACHE III scores, worse acidemia, and worse renal function.
Patients with high sST2 levels had a significant increase in ventilator-free days on conservative fluid management, compared with liberal management, while the two management strategies produced virtually identical results in the patients with low levels of sST2. Patients with high sST2 also had a significantly quicker time to extubation on a conservative strategy compared with the liberal strategy, and again this correlation did not exist among patients with low sST2. However, as in the overall trial a conservative strategy had no discernible impact on 60-day mortality, compared with the liberal strategy, even in the subgroup with high sST2.
Dr. Levy had no disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
WASHINGTON – Plasma levels of an interleukin-33 receptor that’s involved in inflammation regulation appeared able to discriminate between acute respiratory distress syndrome and acute decompensated heart failure in an analysis with 72 patients.
In a second study, high plasma levels of the same interleukin-33 receptor, known as soluble suppressor of tumorgenicity 2 (sST2), identified acute respiratory distress syndrome (ARDS) patients who were sicker and more responsive to conservative fluid management, Sean D. Levy, MD, said at an international conference of the American Thoracic Society.
In order to assess the ability of sST2 to reliably distinguish patients with ARDS from those with acute decompensated heart failure, he and his associates selected 72 patients seen at the Massachusetts General Hospital in Boston with an initial diagnosis of acute decompensated heart failure accompanied by bilateral lung infiltrates and acute hypoxemia respiratory failure requiring endotracheal intubation and mechanical ventilation. The investigators measured the sST2 level in a plasma specimen from each patient. In addition, after each patient either left the hospital or died, their case underwent review by two critical care physicians who retrospectively rediagnosed the patients as either having ARDS or acute decompensated heart failure. This divided the cohort into 30 patients with ARDS and 42 with true acute heart failure. The two subgroups matched up fairly closely for most clinical measures and comorbidities, but APACHE III (Acute Physiology and Chronic Health Evaluation III) scores averaged significantly higher in the ARDS patients.
The plasma levels of sST2 showed a dramatic split between the two subgroups. The 30 patients retrospectively diagnosed with ARDS had an average level of 386 ng/mL with an interquartile range of 318-611 ng/mL. The 42 acute decompensated heart failure patients averaged a sST2 level of 148 ng/mL, with an interquartile range of 84-225 ng/mL. The area under the receiver operator curve for discriminating between ARDS and acute heart failure using a cutpoint of 271 mg/mL was 0.86, showing “good” discrimination, Dr. Levy said. This cutpoint had a sensitivity of 83% and specificity of 88% for correctly distinguishing between ARDS and acute heart failure.
In a second analysis, Dr. Levy and his associates looked at the ability of sST2 levels to separate out patients with acute lung injury who had a more robust response to either the conservative or liberal fluid-management strategies tested in the Fluid and Catheter Treatment Trial (FACTT), run by the National Heart, Lung, and Blood Institute’s ARDS Clinical Trials Network. The primary outcome of FACTT was death from any cause 60 days after entry, and this showed no significant difference between conservative (restricted fluids and increased urine output) and liberal (the reverse) fluid management strategies in acute lung injury patients (N Engl J Med. 2006 Jun 15;354[14]:2564-75). From among the 1,001 patients enrolled in FACTT, 826 had specimens available for measuring sST2 (Crit Care Med. 2013 Nov;41[11]:2521-31),
The researchers applied the sST2 cut point they derived in the first analysis to the FACTT cohort and identified 133 (16%) patients with a low sST2 level and 693 (84%) with a high level. The patients with high sST2 were sicker, with significantly higher APACHE III scores, worse acidemia, and worse renal function.
Patients with high sST2 levels had a significant increase in ventilator-free days on conservative fluid management, compared with liberal management, while the two management strategies produced virtually identical results in the patients with low levels of sST2. Patients with high sST2 also had a significantly quicker time to extubation on a conservative strategy compared with the liberal strategy, and again this correlation did not exist among patients with low sST2. However, as in the overall trial a conservative strategy had no discernible impact on 60-day mortality, compared with the liberal strategy, even in the subgroup with high sST2.
Dr. Levy had no disclosures.
mzoler@frontlinemedcom.com
On Twitter @mitchelzoler
AT ATS 2017
Key clinical point:
Major finding: An sST2 cutpoint of 271 ng/mL discriminated between ARDS and acute heart failure with 83% sensitivity and 88% specificity.
Data source: Review of 72 patients admitted for acute decompensated heart failure at one U.S. center.
Disclosures: Dr. Levy had no disclosures.