Heart Failure

Severe heart failure can be reversed in some cases by using a left ventricular assist device to temporarily “unload” the myocardium plus a drug regimen to promote reverse remodeling, reported Dr. Emma J. Birks of the Royal Brompton and Harefield (England) National Health Service Trust and her associates.

In a study of 15 patients who received this treatment for nonischemic cardiomyopathy, 11 recovered sufficiently after a mean of 320 days to qualify for removal of the device. Ten of them survived with marked improvement that has persisted for over 4 years, the researchers said.

Following LVAD implantation, the patients received an ACE inhibitor (lisinopril), angiotensin-receptor blocker (losartan), a nonselective β-blocker (carvedilol), and an aldosterone antagonist (spironolactone) to enhance reverse remodeling. After maximal regression in the left ventricular end-diastolic diameter was achieved, the nonselective β-blocker was replaced with a selective β₁-blocker together with clenbuterol, a selective β₂-agonist, to prevent myocardial atrophy.

Eleven patients showed significant clinical improvement accompanied by marked functional changes in the myocardium and improved hemodynamics, exercise capacity, and quality of life. Ten (75%) fully recovered after the device was removed (N. Engl. J. Med. 2006;355:1873–84).

This study was supported in part by Thoratec, manufacturer of the HeartMate LVAD.

Severe heart failure can be reversed in some cases by using a left ventricular assist device to temporarily “unload” the myocardium plus a drug regimen to promote reverse remodeling, reported Dr. Emma J. Birks of the Royal Brompton and Harefield (England) National Health Service Trust and her associates.

In a study of 15 patients who received this treatment for nonischemic cardiomyopathy, 11 recovered sufficiently after a mean of 320 days to qualify for removal of the device. Ten of them survived with marked improvement that has persisted for over 4 years, the researchers said.

Following LVAD implantation, the patients received an ACE inhibitor (lisinopril), angiotensin-receptor blocker (losartan), a nonselective β-blocker (carvedilol), and an aldosterone antagonist (spironolactone) to enhance reverse remodeling. After maximal regression in the left ventricular end-diastolic diameter was achieved, the nonselective β-blocker was replaced with a selective β₁-blocker together with clenbuterol, a selective β₂-agonist, to prevent myocardial atrophy.

Eleven patients showed significant clinical improvement accompanied by marked functional changes in the myocardium and improved hemodynamics, exercise capacity, and quality of life. Ten (75%) fully recovered after the device was removed (N. Engl. J. Med. 2006;355:1873–84).

This study was supported in part by Thoratec, manufacturer of the HeartMate LVAD.

Severe heart failure can be reversed in some cases by using a left ventricular assist device to temporarily “unload” the myocardium plus a drug regimen to promote reverse remodeling, reported Dr. Emma J. Birks of the Royal Brompton and Harefield (England) National Health Service Trust and her associates.

In a study of 15 patients who received this treatment for nonischemic cardiomyopathy, 11 recovered sufficiently after a mean of 320 days to qualify for removal of the device. Ten of them survived with marked improvement that has persisted for over 4 years, the researchers said.

Following LVAD implantation, the patients received an ACE inhibitor (lisinopril), angiotensin-receptor blocker (losartan), a nonselective β-blocker (carvedilol), and an aldosterone antagonist (spironolactone) to enhance reverse remodeling. After maximal regression in the left ventricular end-diastolic diameter was achieved, the nonselective β-blocker was replaced with a selective β₁-blocker together with clenbuterol, a selective β₂-agonist, to prevent myocardial atrophy.

Eleven patients showed significant clinical improvement accompanied by marked functional changes in the myocardium and improved hemodynamics, exercise capacity, and quality of life. Ten (75%) fully recovered after the device was removed (N. Engl. J. Med. 2006;355:1873–84).

This study was supported in part by Thoratec, manufacturer of the HeartMate LVAD.

SEATTLE — Immune modulation therapy for patients with chronic heart failure did not reduce deaths or hospitalizations but was helpful in two subsets of patients in a 2,426-patient trial, Dr. Guillermo Torre-Amione reported.

Prespecified subgroup analyses found fewer deaths or hospitalizations with Celacade immune modulation therapy than with placebo in patients with New York Heart Association (NYHA) class II heart failure and in patients with class III-IV heart failure but no history of MI, he said at the annual meeting of the Heart Failure Society of America.

The randomized, double-blind, placebo-controlled Advanced Chronic Heart Failure Clinical Assessment of Immune Modulation Therapy (ACCLAIM) trial showed that the Celacade technology was safe and well tolerated and “helpful in heart failure from nonischemic etiology, and in patients with ischemic etiology who have not yet reached more advanced disease stages,” said Dr. Torre-Amione, medical director at the Methodist DeBakey Heart Center, Houston, and his associates.

Dr. Torre-Amione has received honoraria and research funding from Vasogen Inc., which funded the trial and owns the experimental Celacade technology.

Celacade therapy targets the chronic inflammation associated with cardiovascular disease. Samples of whole blood taken from patients randomized to Celacade therapy were subjected to oxidative stress and returned to patients via intramuscular injection. The oxidative stress induces cell apoptosis and triggers other reactions that increase production of anti-inflammatory cytokines and regulatory T cells that help reduce chronic inflammation, the investigators said.

Outpatient treatment with the 10-mL blood samples took place on days 1, 2, and 14, then every 30 days for 22 weeks or longer during June 2003-November 2005. All patients were on standard medications for heart failure, as tolerated. The mean follow-up in the study was 10 months.

There was no significant difference at 600 days between the Celacade and placebo groups in the primary combined end point of death from any cause or hospitalization for cardiovascular reasons. Quality-of-life scores were significantly better in the Celacade group than in placebo patients in preplanned analyses of secondary end points. The number of serious adverse events was similar between groups, as was the number of patients with more than one serious adverse event.

Among 900 patients with no prior MI, however, there were 26% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo, and patients fared better on secondary end points with Celacade as well, Dr. Torre-Amione said.

Among 700 patients with NYHA class II heart failure, there were 29% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo.

In a separate analysis of a combined group of 1,300 patients (about half of all patients in the study) with either class II heart failure or class III-IV but no history of MI, there were 165 deaths or heart failure hospitalizations in the Celacade group, compared with 226 in the placebo group, a highly statistically significant difference. In addition, the Celacade group had fewer mean days in the hospital for heart failure or for any cause, he said.

The study took place in 177 centers in North America, Europe, and Israel. Patients predominantly were white males and had a mean age of 64 years. All had a baseline ejection fraction of 30% or less and prior hospitalization (or outpatient treatment with IV medication) for heart failure within the previous 12 months. Sixty-two percent of patients had a history of MI.

SEATTLE — Immune modulation therapy for patients with chronic heart failure did not reduce deaths or hospitalizations but was helpful in two subsets of patients in a 2,426-patient trial, Dr. Guillermo Torre-Amione reported.

Prespecified subgroup analyses found fewer deaths or hospitalizations with Celacade immune modulation therapy than with placebo in patients with New York Heart Association (NYHA) class II heart failure and in patients with class III-IV heart failure but no history of MI, he said at the annual meeting of the Heart Failure Society of America.

The randomized, double-blind, placebo-controlled Advanced Chronic Heart Failure Clinical Assessment of Immune Modulation Therapy (ACCLAIM) trial showed that the Celacade technology was safe and well tolerated and “helpful in heart failure from nonischemic etiology, and in patients with ischemic etiology who have not yet reached more advanced disease stages,” said Dr. Torre-Amione, medical director at the Methodist DeBakey Heart Center, Houston, and his associates.

Dr. Torre-Amione has received honoraria and research funding from Vasogen Inc., which funded the trial and owns the experimental Celacade technology.

Celacade therapy targets the chronic inflammation associated with cardiovascular disease. Samples of whole blood taken from patients randomized to Celacade therapy were subjected to oxidative stress and returned to patients via intramuscular injection. The oxidative stress induces cell apoptosis and triggers other reactions that increase production of anti-inflammatory cytokines and regulatory T cells that help reduce chronic inflammation, the investigators said.

Outpatient treatment with the 10-mL blood samples took place on days 1, 2, and 14, then every 30 days for 22 weeks or longer during June 2003-November 2005. All patients were on standard medications for heart failure, as tolerated. The mean follow-up in the study was 10 months.

There was no significant difference at 600 days between the Celacade and placebo groups in the primary combined end point of death from any cause or hospitalization for cardiovascular reasons. Quality-of-life scores were significantly better in the Celacade group than in placebo patients in preplanned analyses of secondary end points. The number of serious adverse events was similar between groups, as was the number of patients with more than one serious adverse event.

Among 900 patients with no prior MI, however, there were 26% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo, and patients fared better on secondary end points with Celacade as well, Dr. Torre-Amione said.

Among 700 patients with NYHA class II heart failure, there were 29% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo.

In a separate analysis of a combined group of 1,300 patients (about half of all patients in the study) with either class II heart failure or class III-IV but no history of MI, there were 165 deaths or heart failure hospitalizations in the Celacade group, compared with 226 in the placebo group, a highly statistically significant difference. In addition, the Celacade group had fewer mean days in the hospital for heart failure or for any cause, he said.

The study took place in 177 centers in North America, Europe, and Israel. Patients predominantly were white males and had a mean age of 64 years. All had a baseline ejection fraction of 30% or less and prior hospitalization (or outpatient treatment with IV medication) for heart failure within the previous 12 months. Sixty-two percent of patients had a history of MI.

SEATTLE — Immune modulation therapy for patients with chronic heart failure did not reduce deaths or hospitalizations but was helpful in two subsets of patients in a 2,426-patient trial, Dr. Guillermo Torre-Amione reported.

Prespecified subgroup analyses found fewer deaths or hospitalizations with Celacade immune modulation therapy than with placebo in patients with New York Heart Association (NYHA) class II heart failure and in patients with class III-IV heart failure but no history of MI, he said at the annual meeting of the Heart Failure Society of America.

The randomized, double-blind, placebo-controlled Advanced Chronic Heart Failure Clinical Assessment of Immune Modulation Therapy (ACCLAIM) trial showed that the Celacade technology was safe and well tolerated and “helpful in heart failure from nonischemic etiology, and in patients with ischemic etiology who have not yet reached more advanced disease stages,” said Dr. Torre-Amione, medical director at the Methodist DeBakey Heart Center, Houston, and his associates.

Dr. Torre-Amione has received honoraria and research funding from Vasogen Inc., which funded the trial and owns the experimental Celacade technology.

Celacade therapy targets the chronic inflammation associated with cardiovascular disease. Samples of whole blood taken from patients randomized to Celacade therapy were subjected to oxidative stress and returned to patients via intramuscular injection. The oxidative stress induces cell apoptosis and triggers other reactions that increase production of anti-inflammatory cytokines and regulatory T cells that help reduce chronic inflammation, the investigators said.

Outpatient treatment with the 10-mL blood samples took place on days 1, 2, and 14, then every 30 days for 22 weeks or longer during June 2003-November 2005. All patients were on standard medications for heart failure, as tolerated. The mean follow-up in the study was 10 months.

There was no significant difference at 600 days between the Celacade and placebo groups in the primary combined end point of death from any cause or hospitalization for cardiovascular reasons. Quality-of-life scores were significantly better in the Celacade group than in placebo patients in preplanned analyses of secondary end points. The number of serious adverse events was similar between groups, as was the number of patients with more than one serious adverse event.

Among 900 patients with no prior MI, however, there were 26% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo, and patients fared better on secondary end points with Celacade as well, Dr. Torre-Amione said.

Among 700 patients with NYHA class II heart failure, there were 29% fewer deaths or cardiovascular hospitalizations with Celacade compared with placebo.

In a separate analysis of a combined group of 1,300 patients (about half of all patients in the study) with either class II heart failure or class III-IV but no history of MI, there were 165 deaths or heart failure hospitalizations in the Celacade group, compared with 226 in the placebo group, a highly statistically significant difference. In addition, the Celacade group had fewer mean days in the hospital for heart failure or for any cause, he said.

The study took place in 177 centers in North America, Europe, and Israel. Patients predominantly were white males and had a mean age of 64 years. All had a baseline ejection fraction of 30% or less and prior hospitalization (or outpatient treatment with IV medication) for heart failure within the previous 12 months. Sixty-two percent of patients had a history of MI.

CHICAGO — Most heart failure patients greatly overestimate the survival benefit provided by implantable cardioverter defibrillators, according to a new survey, Dr. Garrick C. Stewart reported at the annual scientific sessions of the American Heart Association.

The problem stems in part from the common practice of reporting clinical trial outcomes in terms of percent reduction in mortality. It creates confusion among patients, the public, and even physicians. This figure is actually a percent of a percent and is far greater than the number of deaths prevented or delayed, which is what really matters, added Dr. Stewart of Brigham and Women's Hospital, Boston.

“We advocate reporting event rates in persons per 100 to translate more clearly such information for our patients. We cannot stop reminding our patients and ourselves that heart failure remains a fatal disease from which most deaths occur slowly,” he stressed.

Dr. Stewart presented the results of a written survey completed by 104 patients with symptomatic heart failure who fit the profile of the study population in the landmark Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) which established the efficacy of ICDs for primary prevention of cardiac arrest. These were patients with a left ventricular ejection fraction below 35% and no history of cardiac arrest or syncope. Two-thirds already had an ICD.

More than half of those surveyed indicated they expected an ICD would save at least 50 lives per 100 recipients over a 5-year period. In reality, Dr. Stewart noted, SCD-HeFT showed the benefit is 7–8 lives saved.

“Frankly, the benefit is just not as big as we think,” observed coinvestigator Dr. Lynne Warner Stevenson, codirector of the cardiomyopathy and heart failure clinic at Brigham and Women's Hospital and professor of medicine at Harvard Medical School, Boston.

“We frequently have patients referred to us from other centers where they've been told that they must have an ICD put in place or they'll die. We think that's quite a disservice because it implies that the ICD will make them immortal,” she continued.

Two-thirds of survey participants who actually had an ICD thought the device would save their own lives. Fifty-five percent indicated they wouldn't deactivate it even if they were getting daily shocks, 70% would keep it on if they were dying of cancer, and 100% would keep the device on even if they were continuously struggling to breathe.

Dr. Stewart and Dr. Stevenson advocate a highly systematic approach to consenting patients for an ICD if they've never had a life-threatening arrhythmia.

“We actually have a script we use that says if we put an ICD in 100 patients with heart disease like yours, over the next 5 years we would expect that 30 patients would die anyway, 7 or 8 would be saved by the ICD, 10–20 would have a shock they don't need, 5–15 would have other complications, and the rest would not experience their device at all,” Dr. Stevenson said.

After hearing all of this, roughly one-third of patients still want a device, one-third decide they definitely don't, and one-third want to think it over some more.

Underscoring the point that ICDs partially protect against sudden arrhythmic death but don't prevent a slower death from pump failure, Dr. Jean-Yves F. Le Heuzey presented outcome data on 2,418 patients who got an ICD at 22 French hospitals during 2001–2003.

Mortality was 11.3% by 2005. Forty-two percent of deaths resulted from pump failure, 8.7% from cardiac arrest with electromechanical dissociation, and 6.2% were due to arrhythmic storm. Cancer and septic shock each accounted for 6.5% of deaths, said Dr. Le Heuzey, professor of cardiology at George Pompidou European Hospital, Paris.

More than half of those surveyed said they expected an ICD would save at least 50 lives per 100 recipients over 5 years. DR. STEWART

CHICAGO — Most heart failure patients greatly overestimate the survival benefit provided by implantable cardioverter defibrillators, according to a new survey, Dr. Garrick C. Stewart reported at the annual scientific sessions of the American Heart Association.

The problem stems in part from the common practice of reporting clinical trial outcomes in terms of percent reduction in mortality. It creates confusion among patients, the public, and even physicians. This figure is actually a percent of a percent and is far greater than the number of deaths prevented or delayed, which is what really matters, added Dr. Stewart of Brigham and Women's Hospital, Boston.

“We advocate reporting event rates in persons per 100 to translate more clearly such information for our patients. We cannot stop reminding our patients and ourselves that heart failure remains a fatal disease from which most deaths occur slowly,” he stressed.

Dr. Stewart presented the results of a written survey completed by 104 patients with symptomatic heart failure who fit the profile of the study population in the landmark Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) which established the efficacy of ICDs for primary prevention of cardiac arrest. These were patients with a left ventricular ejection fraction below 35% and no history of cardiac arrest or syncope. Two-thirds already had an ICD.

More than half of those surveyed indicated they expected an ICD would save at least 50 lives per 100 recipients over a 5-year period. In reality, Dr. Stewart noted, SCD-HeFT showed the benefit is 7–8 lives saved.

“Frankly, the benefit is just not as big as we think,” observed coinvestigator Dr. Lynne Warner Stevenson, codirector of the cardiomyopathy and heart failure clinic at Brigham and Women's Hospital and professor of medicine at Harvard Medical School, Boston.

“We frequently have patients referred to us from other centers where they've been told that they must have an ICD put in place or they'll die. We think that's quite a disservice because it implies that the ICD will make them immortal,” she continued.

Two-thirds of survey participants who actually had an ICD thought the device would save their own lives. Fifty-five percent indicated they wouldn't deactivate it even if they were getting daily shocks, 70% would keep it on if they were dying of cancer, and 100% would keep the device on even if they were continuously struggling to breathe.

Dr. Stewart and Dr. Stevenson advocate a highly systematic approach to consenting patients for an ICD if they've never had a life-threatening arrhythmia.

“We actually have a script we use that says if we put an ICD in 100 patients with heart disease like yours, over the next 5 years we would expect that 30 patients would die anyway, 7 or 8 would be saved by the ICD, 10–20 would have a shock they don't need, 5–15 would have other complications, and the rest would not experience their device at all,” Dr. Stevenson said.

After hearing all of this, roughly one-third of patients still want a device, one-third decide they definitely don't, and one-third want to think it over some more.

Underscoring the point that ICDs partially protect against sudden arrhythmic death but don't prevent a slower death from pump failure, Dr. Jean-Yves F. Le Heuzey presented outcome data on 2,418 patients who got an ICD at 22 French hospitals during 2001–2003.

Mortality was 11.3% by 2005. Forty-two percent of deaths resulted from pump failure, 8.7% from cardiac arrest with electromechanical dissociation, and 6.2% were due to arrhythmic storm. Cancer and septic shock each accounted for 6.5% of deaths, said Dr. Le Heuzey, professor of cardiology at George Pompidou European Hospital, Paris.

More than half of those surveyed said they expected an ICD would save at least 50 lives per 100 recipients over 5 years. DR. STEWART

CHICAGO — Most heart failure patients greatly overestimate the survival benefit provided by implantable cardioverter defibrillators, according to a new survey, Dr. Garrick C. Stewart reported at the annual scientific sessions of the American Heart Association.

The problem stems in part from the common practice of reporting clinical trial outcomes in terms of percent reduction in mortality. It creates confusion among patients, the public, and even physicians. This figure is actually a percent of a percent and is far greater than the number of deaths prevented or delayed, which is what really matters, added Dr. Stewart of Brigham and Women's Hospital, Boston.

“We advocate reporting event rates in persons per 100 to translate more clearly such information for our patients. We cannot stop reminding our patients and ourselves that heart failure remains a fatal disease from which most deaths occur slowly,” he stressed.

Dr. Stewart presented the results of a written survey completed by 104 patients with symptomatic heart failure who fit the profile of the study population in the landmark Sudden Cardiac Death in Heart Failure Trial (SCD-HeFT) which established the efficacy of ICDs for primary prevention of cardiac arrest. These were patients with a left ventricular ejection fraction below 35% and no history of cardiac arrest or syncope. Two-thirds already had an ICD.

More than half of those surveyed indicated they expected an ICD would save at least 50 lives per 100 recipients over a 5-year period. In reality, Dr. Stewart noted, SCD-HeFT showed the benefit is 7–8 lives saved.

“Frankly, the benefit is just not as big as we think,” observed coinvestigator Dr. Lynne Warner Stevenson, codirector of the cardiomyopathy and heart failure clinic at Brigham and Women's Hospital and professor of medicine at Harvard Medical School, Boston.

“We frequently have patients referred to us from other centers where they've been told that they must have an ICD put in place or they'll die. We think that's quite a disservice because it implies that the ICD will make them immortal,” she continued.

Two-thirds of survey participants who actually had an ICD thought the device would save their own lives. Fifty-five percent indicated they wouldn't deactivate it even if they were getting daily shocks, 70% would keep it on if they were dying of cancer, and 100% would keep the device on even if they were continuously struggling to breathe.

Dr. Stewart and Dr. Stevenson advocate a highly systematic approach to consenting patients for an ICD if they've never had a life-threatening arrhythmia.

“We actually have a script we use that says if we put an ICD in 100 patients with heart disease like yours, over the next 5 years we would expect that 30 patients would die anyway, 7 or 8 would be saved by the ICD, 10–20 would have a shock they don't need, 5–15 would have other complications, and the rest would not experience their device at all,” Dr. Stevenson said.

After hearing all of this, roughly one-third of patients still want a device, one-third decide they definitely don't, and one-third want to think it over some more.

Underscoring the point that ICDs partially protect against sudden arrhythmic death but don't prevent a slower death from pump failure, Dr. Jean-Yves F. Le Heuzey presented outcome data on 2,418 patients who got an ICD at 22 French hospitals during 2001–2003.

Mortality was 11.3% by 2005. Forty-two percent of deaths resulted from pump failure, 8.7% from cardiac arrest with electromechanical dissociation, and 6.2% were due to arrhythmic storm. Cancer and septic shock each accounted for 6.5% of deaths, said Dr. Le Heuzey, professor of cardiology at George Pompidou European Hospital, Paris.

More than half of those surveyed said they expected an ICD would save at least 50 lives per 100 recipients over 5 years. DR. STEWART

SEATTLE — A heart rate of 90 beats per minute was detrimental in a study of pacemaker-dependent patients with heart failure, Krishnamurti Rao reported at the annual meeting of the Heart Failure Society of America.

Thirteen patients in a crossover study spent 2 months with the heart rate set at 60, 75, or 90 beats per minute (bpm), then were randomized to 2 months at one of the other settings, and then 2 months at the third of the three settings. At 90 bpm, patients had significantly lower ejection fractions and reduced exercise tolerance as measured by maximal oxygen consumption (peak VO₂) and walked significantly shorter distances on 6-minute walk tests, compared with the periods when heart rates were set to 75 or 60 bpm.

“These findings suggest that a mild tachycardia of even 90 [bpm], when chronic, can lead to left ventricular dysfunction,” said Mr. Rao, who conducted the study with associates on the faculty of the University of Maryland, Baltimore, and currently is a student at Boston University. He has no affiliation with the companies that make pacemakers or heart medications.

Patients also fared worse clinically at a setting of 90 bpm, compared with the other two settings. Clinical deterioration caused four patients in the 90-bpm period and one patient in the 60-bpm period to discontinue that setting before the end of the 2 months. Symptoms worsened in some patients immediately upon starting the 90-bpm rate and in others several weeks after changing rates, he noted. Two patients had their rates turned down to 85 or 80 bpm 3–4 weeks into the 90-bpm period.

The study could not determine the optimal heart rate. Based on the data available, the investigators suggest that pacemaker rates should not be set at more than 75 bpm.

Mean peak VO₂ at 60 bpm was 11 mL/kg per minute, at 75 bpm was 11.3 mL/kg per minute, and at 90 bpm was 9.5 mL/kg per minute. The exercise tolerance findings may even underestimate the negative effect of the 90 bpm, because one patient who deteriorated clinically was unable to exercise, he said.

Mean ejection fractions at 60 bpm were 33%, at 75 bpm were 30%, and at 90 bpm were 25%. On the 6-minute walk test, the mean distance was 938 feet at 60 bpm, 996 feet at 75 bpm, and 888 feet at 90 bpm.

Chronic use of β-blockers is known to improve cardiac function, though it has not been clear whether the benefits derive from their effects on heart rate or from other actions, he said.

SEATTLE — A heart rate of 90 beats per minute was detrimental in a study of pacemaker-dependent patients with heart failure, Krishnamurti Rao reported at the annual meeting of the Heart Failure Society of America.

Thirteen patients in a crossover study spent 2 months with the heart rate set at 60, 75, or 90 beats per minute (bpm), then were randomized to 2 months at one of the other settings, and then 2 months at the third of the three settings. At 90 bpm, patients had significantly lower ejection fractions and reduced exercise tolerance as measured by maximal oxygen consumption (peak VO₂) and walked significantly shorter distances on 6-minute walk tests, compared with the periods when heart rates were set to 75 or 60 bpm.

“These findings suggest that a mild tachycardia of even 90 [bpm], when chronic, can lead to left ventricular dysfunction,” said Mr. Rao, who conducted the study with associates on the faculty of the University of Maryland, Baltimore, and currently is a student at Boston University. He has no affiliation with the companies that make pacemakers or heart medications.

Patients also fared worse clinically at a setting of 90 bpm, compared with the other two settings. Clinical deterioration caused four patients in the 90-bpm period and one patient in the 60-bpm period to discontinue that setting before the end of the 2 months. Symptoms worsened in some patients immediately upon starting the 90-bpm rate and in others several weeks after changing rates, he noted. Two patients had their rates turned down to 85 or 80 bpm 3–4 weeks into the 90-bpm period.

The study could not determine the optimal heart rate. Based on the data available, the investigators suggest that pacemaker rates should not be set at more than 75 bpm.

Mean peak VO₂ at 60 bpm was 11 mL/kg per minute, at 75 bpm was 11.3 mL/kg per minute, and at 90 bpm was 9.5 mL/kg per minute. The exercise tolerance findings may even underestimate the negative effect of the 90 bpm, because one patient who deteriorated clinically was unable to exercise, he said.

Mean ejection fractions at 60 bpm were 33%, at 75 bpm were 30%, and at 90 bpm were 25%. On the 6-minute walk test, the mean distance was 938 feet at 60 bpm, 996 feet at 75 bpm, and 888 feet at 90 bpm.

Chronic use of β-blockers is known to improve cardiac function, though it has not been clear whether the benefits derive from their effects on heart rate or from other actions, he said.

SEATTLE — A heart rate of 90 beats per minute was detrimental in a study of pacemaker-dependent patients with heart failure, Krishnamurti Rao reported at the annual meeting of the Heart Failure Society of America.

Thirteen patients in a crossover study spent 2 months with the heart rate set at 60, 75, or 90 beats per minute (bpm), then were randomized to 2 months at one of the other settings, and then 2 months at the third of the three settings. At 90 bpm, patients had significantly lower ejection fractions and reduced exercise tolerance as measured by maximal oxygen consumption (peak VO₂) and walked significantly shorter distances on 6-minute walk tests, compared with the periods when heart rates were set to 75 or 60 bpm.

“These findings suggest that a mild tachycardia of even 90 [bpm], when chronic, can lead to left ventricular dysfunction,” said Mr. Rao, who conducted the study with associates on the faculty of the University of Maryland, Baltimore, and currently is a student at Boston University. He has no affiliation with the companies that make pacemakers or heart medications.

Patients also fared worse clinically at a setting of 90 bpm, compared with the other two settings. Clinical deterioration caused four patients in the 90-bpm period and one patient in the 60-bpm period to discontinue that setting before the end of the 2 months. Symptoms worsened in some patients immediately upon starting the 90-bpm rate and in others several weeks after changing rates, he noted. Two patients had their rates turned down to 85 or 80 bpm 3–4 weeks into the 90-bpm period.

The study could not determine the optimal heart rate. Based on the data available, the investigators suggest that pacemaker rates should not be set at more than 75 bpm.

Mean peak VO₂ at 60 bpm was 11 mL/kg per minute, at 75 bpm was 11.3 mL/kg per minute, and at 90 bpm was 9.5 mL/kg per minute. The exercise tolerance findings may even underestimate the negative effect of the 90 bpm, because one patient who deteriorated clinically was unable to exercise, he said.

Mean ejection fractions at 60 bpm were 33%, at 75 bpm were 30%, and at 90 bpm were 25%. On the 6-minute walk test, the mean distance was 938 feet at 60 bpm, 996 feet at 75 bpm, and 888 feet at 90 bpm.

Chronic use of β-blockers is known to improve cardiac function, though it has not been clear whether the benefits derive from their effects on heart rate or from other actions, he said.

SEATTLE — Adding an angiotensin receptor blocker to ACE inhibitor therapy in patients with heart failure significantly increased the risk of hypotension and renal failure, with a trend toward an increased risk for hyperkalemia, compared with ACE inhibitor therapy alone, in a meta-analysis of randomized, controlled trials, Dr. Rachid Lakhdar reported.

A previous meta-analysis of randomized, controlled studies found that combination therapy with an angiotensin receptor blocker (ARB) and an ACE inhibitor reduced hospitalizations in patients with heart failure but provided no survival benefit, he said in poster presentation at the annual meeting of the Heart Failure Society of America. The earlier meta-analysis did not analyze the safety of this drug combination.

Dr. Lakhdar and his coinvestigator, Dr. Mouaz H. Al-Mallah, both of Henry Ford Hospital, Detroit, searched the medical literature and abstracts from medical meetings and analyzed safety data from nine studies including 18,160 patients with heart failure. The incidence of side effects was low but was 25% higher in the combination therapy arms, compared with ACE inhibitor therapy alone, they reported.

Patients on combined therapy were 54% more likely to develop hypotension and twice as likely to develop worsened renal function, compared with patients on an ACE inhibitor alone. A 2.5-fold increase in risk for hyperkalemia was not statistically significant.

“Those side effects—hypotension, hyperkalemia, and renal failure—are related directly or indirectly to reduced angiotensin II formation,” the investigators noted. The rates of cough and angioedema did not differ significantly between groups.

Not all the studies showed a significant increase in side effects with the combination therapy, perhaps owing to small sample size, short follow-up, or the characteristics of different drugs and doses. The longer trials found more side effects than shorter trials did, so it may be that some adverse events associated with the combination therapy would have shown up over time, Dr. Lakhdar and Dr. Al-Mallah suggested. “The presence of this excess risk, lack of a definitive survival benefit of this strategy, and the availability of other agents with proven survival benefit in heart failure in combination with ACE inhibitors suggests that the addition of an ARB to ACE inhibitor therapy should be discouraged,” they said.

The investigators reported that they have no associations with the companies that make the drugs.

SEATTLE — Adding an angiotensin receptor blocker to ACE inhibitor therapy in patients with heart failure significantly increased the risk of hypotension and renal failure, with a trend toward an increased risk for hyperkalemia, compared with ACE inhibitor therapy alone, in a meta-analysis of randomized, controlled trials, Dr. Rachid Lakhdar reported.

A previous meta-analysis of randomized, controlled studies found that combination therapy with an angiotensin receptor blocker (ARB) and an ACE inhibitor reduced hospitalizations in patients with heart failure but provided no survival benefit, he said in poster presentation at the annual meeting of the Heart Failure Society of America. The earlier meta-analysis did not analyze the safety of this drug combination.

Dr. Lakhdar and his coinvestigator, Dr. Mouaz H. Al-Mallah, both of Henry Ford Hospital, Detroit, searched the medical literature and abstracts from medical meetings and analyzed safety data from nine studies including 18,160 patients with heart failure. The incidence of side effects was low but was 25% higher in the combination therapy arms, compared with ACE inhibitor therapy alone, they reported.

Patients on combined therapy were 54% more likely to develop hypotension and twice as likely to develop worsened renal function, compared with patients on an ACE inhibitor alone. A 2.5-fold increase in risk for hyperkalemia was not statistically significant.

“Those side effects—hypotension, hyperkalemia, and renal failure—are related directly or indirectly to reduced angiotensin II formation,” the investigators noted. The rates of cough and angioedema did not differ significantly between groups.

Not all the studies showed a significant increase in side effects with the combination therapy, perhaps owing to small sample size, short follow-up, or the characteristics of different drugs and doses. The longer trials found more side effects than shorter trials did, so it may be that some adverse events associated with the combination therapy would have shown up over time, Dr. Lakhdar and Dr. Al-Mallah suggested. “The presence of this excess risk, lack of a definitive survival benefit of this strategy, and the availability of other agents with proven survival benefit in heart failure in combination with ACE inhibitors suggests that the addition of an ARB to ACE inhibitor therapy should be discouraged,” they said.

The investigators reported that they have no associations with the companies that make the drugs.

SEATTLE — Adding an angiotensin receptor blocker to ACE inhibitor therapy in patients with heart failure significantly increased the risk of hypotension and renal failure, with a trend toward an increased risk for hyperkalemia, compared with ACE inhibitor therapy alone, in a meta-analysis of randomized, controlled trials, Dr. Rachid Lakhdar reported.

A previous meta-analysis of randomized, controlled studies found that combination therapy with an angiotensin receptor blocker (ARB) and an ACE inhibitor reduced hospitalizations in patients with heart failure but provided no survival benefit, he said in poster presentation at the annual meeting of the Heart Failure Society of America. The earlier meta-analysis did not analyze the safety of this drug combination.

Dr. Lakhdar and his coinvestigator, Dr. Mouaz H. Al-Mallah, both of Henry Ford Hospital, Detroit, searched the medical literature and abstracts from medical meetings and analyzed safety data from nine studies including 18,160 patients with heart failure. The incidence of side effects was low but was 25% higher in the combination therapy arms, compared with ACE inhibitor therapy alone, they reported.

Patients on combined therapy were 54% more likely to develop hypotension and twice as likely to develop worsened renal function, compared with patients on an ACE inhibitor alone. A 2.5-fold increase in risk for hyperkalemia was not statistically significant.

“Those side effects—hypotension, hyperkalemia, and renal failure—are related directly or indirectly to reduced angiotensin II formation,” the investigators noted. The rates of cough and angioedema did not differ significantly between groups.

Not all the studies showed a significant increase in side effects with the combination therapy, perhaps owing to small sample size, short follow-up, or the characteristics of different drugs and doses. The longer trials found more side effects than shorter trials did, so it may be that some adverse events associated with the combination therapy would have shown up over time, Dr. Lakhdar and Dr. Al-Mallah suggested. “The presence of this excess risk, lack of a definitive survival benefit of this strategy, and the availability of other agents with proven survival benefit in heart failure in combination with ACE inhibitors suggests that the addition of an ARB to ACE inhibitor therapy should be discouraged,” they said.

The investigators reported that they have no associations with the companies that make the drugs.

BARCELONA — Treatment with the ACE inhibitor perindopril appeared to help elderly patients with left ventricular diastolic dysfunction in a study with about 850 patients.

The study was plagued by underenrollment and by many patients changing medications from their assigned study regimens, and this may explain why the results failed to show a statistically significant difference in favor of perindopril for the primary end point of all-cause death or unplanned hospitalization for heart failure. But post hoc and secondary analyses of the data suggested that treatment with the ACE inhibitor led to improved patient outcomes, including fewer hospitalizations for heart failure, fewer days in the hospital, improved heart failure status, and improved exercise capacity, Dr. John G.F. Cleland reported at a joint meeting of the European Society of Cardiology and the World Heart Federation.

“These data should not be wasted due to methodologic problems; we need to understand what the data are telling us,” commented Dr. Kenneth Dickstein, a cardiologist and professor of medicine at the University of Bergen in Stavanger, Norway. Agreeing with Dr. Cleland's interpretation, Dr. Dickstein concluded that the results “support a role for inhibition of the renin-angiotensin system in patients with heart failure and preserved systolic function.”

This finding is important because although blockade of the renin-angiotensin system with an ACE inhibitor or angiotensin-receptor blocker is standard treatment for LV systolic dysfunction, scant data exist to prove the treatment's value in patients with preserved LV function and diastolic dysfunction. The only study to address this until now was the Candesartan in Heart Failure—Assessment of Reduction in Mortality and Morbidity (CHARM) trial, specifically the CHARM-Preserved part of the study that assessed the efficacy of candesartan in patients with heart failure and a LV ejection fraction of at least 40% (Lancet 2003;362:777–81). The new findings are consistent with the CHARM-Preserved results, Dr. Dickstein said.

The Perindopril in Elderly People With Chronic Heart Failure (PEP-CHF) study enrolled patients aged 70 or older with evidence of diastolic dysfunction. The only background medication that patients had to receive was a diuretic. Patients were randomized to treatment with either 2 mg/day perindopril or placebo. The perindopril dosage was later raised to 4 mg/day if patients had no contraindication to the increased dosage.

The study was sponsored by Servier, which markets perindopril (Acenon). Dr. Cleland and his associates received payments from Servier for working on the study.

The initial statistical calculations called for enrolling about 1,000 patients into the trial, but only 852 entered the study because of slow recruitment. The average age of the enrolled patients was 75, and their average LV ejection fraction was about 65%. About three-quarters of patients had New York Heart Association class I or II heart failure.

Although 90% of patients remained on their assigned therapy after their first year in the study, after 18 months about 40% of patients had stopped their assigned regimen, which Dr. Cleland attributed to the difficulty of keeping older patients on a blinded regimen. Another problem was a much lower than anticipated event rate. The study design anticipated that 50% of patients would have the primary end point of death or heart-failure hospitalization each year. Instead, the actual rate for this end point was 12.7%. Patients were followed for an average of 2.2 years.

For the complete follow-up period, the incidence of the primary end point had a relative rate reduction of 8% in the patients treated with perindopril, a nonsignificant difference. Perindopril treatment also failed to produce a significant reduction in unplanned hospitalizations for heart failure.

But in a post-hoc analysis that focused only on outcomes during the first year of follow-up, when most patients remained on their assigned regimen, the incidence of the primary end point was 10.8% in the perindopril group and 15.3% in the placebo group, a 31% relative reduction that was statistically significant. Also at 1 year, the incidence of unplanned heart failure hospitalizations was reduced by 37% in the perindopril group, compared with the placebo group, also a significant difference.

The 1-year results “are probably the truth and what the study is trying to tell us,” Dr. Dickstein commented.

Additional analysis of data collected in PEP-CHF indicated that patients with a serum level of N-terminal pro-brain natriuretic peptide (NT-proBNP, a marker of cardiac stress) below the median of 400 pg/mL had event rates similar to those in the normal elderly population. In contrast, patients whose level was above the median had event rates that were similar to those in patients with systolic heart failure who benefited when they were treated with perindopril. This finding suggested that NT-proBNP might be a useful marker for predicting the efficacy of ACE inhibitor treatment in patients with diastolic heart failure, Dr. Cleland said in an interview.

BARCELONA — Treatment with the ACE inhibitor perindopril appeared to help elderly patients with left ventricular diastolic dysfunction in a study with about 850 patients.

The study was plagued by underenrollment and by many patients changing medications from their assigned study regimens, and this may explain why the results failed to show a statistically significant difference in favor of perindopril for the primary end point of all-cause death or unplanned hospitalization for heart failure. But post hoc and secondary analyses of the data suggested that treatment with the ACE inhibitor led to improved patient outcomes, including fewer hospitalizations for heart failure, fewer days in the hospital, improved heart failure status, and improved exercise capacity, Dr. John G.F. Cleland reported at a joint meeting of the European Society of Cardiology and the World Heart Federation.

“These data should not be wasted due to methodologic problems; we need to understand what the data are telling us,” commented Dr. Kenneth Dickstein, a cardiologist and professor of medicine at the University of Bergen in Stavanger, Norway. Agreeing with Dr. Cleland's interpretation, Dr. Dickstein concluded that the results “support a role for inhibition of the renin-angiotensin system in patients with heart failure and preserved systolic function.”

This finding is important because although blockade of the renin-angiotensin system with an ACE inhibitor or angiotensin-receptor blocker is standard treatment for LV systolic dysfunction, scant data exist to prove the treatment's value in patients with preserved LV function and diastolic dysfunction. The only study to address this until now was the Candesartan in Heart Failure—Assessment of Reduction in Mortality and Morbidity (CHARM) trial, specifically the CHARM-Preserved part of the study that assessed the efficacy of candesartan in patients with heart failure and a LV ejection fraction of at least 40% (Lancet 2003;362:777–81). The new findings are consistent with the CHARM-Preserved results, Dr. Dickstein said.

The Perindopril in Elderly People With Chronic Heart Failure (PEP-CHF) study enrolled patients aged 70 or older with evidence of diastolic dysfunction. The only background medication that patients had to receive was a diuretic. Patients were randomized to treatment with either 2 mg/day perindopril or placebo. The perindopril dosage was later raised to 4 mg/day if patients had no contraindication to the increased dosage.

The study was sponsored by Servier, which markets perindopril (Acenon). Dr. Cleland and his associates received payments from Servier for working on the study.

The initial statistical calculations called for enrolling about 1,000 patients into the trial, but only 852 entered the study because of slow recruitment. The average age of the enrolled patients was 75, and their average LV ejection fraction was about 65%. About three-quarters of patients had New York Heart Association class I or II heart failure.

Although 90% of patients remained on their assigned therapy after their first year in the study, after 18 months about 40% of patients had stopped their assigned regimen, which Dr. Cleland attributed to the difficulty of keeping older patients on a blinded regimen. Another problem was a much lower than anticipated event rate. The study design anticipated that 50% of patients would have the primary end point of death or heart-failure hospitalization each year. Instead, the actual rate for this end point was 12.7%. Patients were followed for an average of 2.2 years.

For the complete follow-up period, the incidence of the primary end point had a relative rate reduction of 8% in the patients treated with perindopril, a nonsignificant difference. Perindopril treatment also failed to produce a significant reduction in unplanned hospitalizations for heart failure.

But in a post-hoc analysis that focused only on outcomes during the first year of follow-up, when most patients remained on their assigned regimen, the incidence of the primary end point was 10.8% in the perindopril group and 15.3% in the placebo group, a 31% relative reduction that was statistically significant. Also at 1 year, the incidence of unplanned heart failure hospitalizations was reduced by 37% in the perindopril group, compared with the placebo group, also a significant difference.

The 1-year results “are probably the truth and what the study is trying to tell us,” Dr. Dickstein commented.

Additional analysis of data collected in PEP-CHF indicated that patients with a serum level of N-terminal pro-brain natriuretic peptide (NT-proBNP, a marker of cardiac stress) below the median of 400 pg/mL had event rates similar to those in the normal elderly population. In contrast, patients whose level was above the median had event rates that were similar to those in patients with systolic heart failure who benefited when they were treated with perindopril. This finding suggested that NT-proBNP might be a useful marker for predicting the efficacy of ACE inhibitor treatment in patients with diastolic heart failure, Dr. Cleland said in an interview.

BARCELONA — Treatment with the ACE inhibitor perindopril appeared to help elderly patients with left ventricular diastolic dysfunction in a study with about 850 patients.

The study was plagued by underenrollment and by many patients changing medications from their assigned study regimens, and this may explain why the results failed to show a statistically significant difference in favor of perindopril for the primary end point of all-cause death or unplanned hospitalization for heart failure. But post hoc and secondary analyses of the data suggested that treatment with the ACE inhibitor led to improved patient outcomes, including fewer hospitalizations for heart failure, fewer days in the hospital, improved heart failure status, and improved exercise capacity, Dr. John G.F. Cleland reported at a joint meeting of the European Society of Cardiology and the World Heart Federation.

“These data should not be wasted due to methodologic problems; we need to understand what the data are telling us,” commented Dr. Kenneth Dickstein, a cardiologist and professor of medicine at the University of Bergen in Stavanger, Norway. Agreeing with Dr. Cleland's interpretation, Dr. Dickstein concluded that the results “support a role for inhibition of the renin-angiotensin system in patients with heart failure and preserved systolic function.”

This finding is important because although blockade of the renin-angiotensin system with an ACE inhibitor or angiotensin-receptor blocker is standard treatment for LV systolic dysfunction, scant data exist to prove the treatment's value in patients with preserved LV function and diastolic dysfunction. The only study to address this until now was the Candesartan in Heart Failure—Assessment of Reduction in Mortality and Morbidity (CHARM) trial, specifically the CHARM-Preserved part of the study that assessed the efficacy of candesartan in patients with heart failure and a LV ejection fraction of at least 40% (Lancet 2003;362:777–81). The new findings are consistent with the CHARM-Preserved results, Dr. Dickstein said.

The Perindopril in Elderly People With Chronic Heart Failure (PEP-CHF) study enrolled patients aged 70 or older with evidence of diastolic dysfunction. The only background medication that patients had to receive was a diuretic. Patients were randomized to treatment with either 2 mg/day perindopril or placebo. The perindopril dosage was later raised to 4 mg/day if patients had no contraindication to the increased dosage.

The study was sponsored by Servier, which markets perindopril (Acenon). Dr. Cleland and his associates received payments from Servier for working on the study.

The initial statistical calculations called for enrolling about 1,000 patients into the trial, but only 852 entered the study because of slow recruitment. The average age of the enrolled patients was 75, and their average LV ejection fraction was about 65%. About three-quarters of patients had New York Heart Association class I or II heart failure.

Although 90% of patients remained on their assigned therapy after their first year in the study, after 18 months about 40% of patients had stopped their assigned regimen, which Dr. Cleland attributed to the difficulty of keeping older patients on a blinded regimen. Another problem was a much lower than anticipated event rate. The study design anticipated that 50% of patients would have the primary end point of death or heart-failure hospitalization each year. Instead, the actual rate for this end point was 12.7%. Patients were followed for an average of 2.2 years.

For the complete follow-up period, the incidence of the primary end point had a relative rate reduction of 8% in the patients treated with perindopril, a nonsignificant difference. Perindopril treatment also failed to produce a significant reduction in unplanned hospitalizations for heart failure.

But in a post-hoc analysis that focused only on outcomes during the first year of follow-up, when most patients remained on their assigned regimen, the incidence of the primary end point was 10.8% in the perindopril group and 15.3% in the placebo group, a 31% relative reduction that was statistically significant. Also at 1 year, the incidence of unplanned heart failure hospitalizations was reduced by 37% in the perindopril group, compared with the placebo group, also a significant difference.

The 1-year results “are probably the truth and what the study is trying to tell us,” Dr. Dickstein commented.

Additional analysis of data collected in PEP-CHF indicated that patients with a serum level of N-terminal pro-brain natriuretic peptide (NT-proBNP, a marker of cardiac stress) below the median of 400 pg/mL had event rates similar to those in the normal elderly population. In contrast, patients whose level was above the median had event rates that were similar to those in patients with systolic heart failure who benefited when they were treated with perindopril. This finding suggested that NT-proBNP might be a useful marker for predicting the efficacy of ACE inhibitor treatment in patients with diastolic heart failure, Dr. Cleland said in an interview.

SEATTLE — Maximizing heart failure therapy helps treat concomitant sleep apnea, Dr. David P. White said at the annual meeting of the Heart Failure Society of America.

Beyond that, treatment for sleep apnea in patients with heart failure relies mainly on continuous positive airway pressure (CPAP), which can regularize disordered breathing and which may improve ejection fraction and quality of life. There are no randomized trial data, however, showing that treating sleep apnea in patients with heart failure decreases mortality or the need for heart transplant, added Dr. White, professor of medicine at Harvard University, Boston.

The most common type of disordered breathing in heart failure patients is Cheyne-Stokes respiration, a variant of central sleep apnea. A number of short, single-center trials suggested that CPAP in patients with heart failure and either central or obstructive sleep apnea could stabilize respiration, improve cardiac function and quality of life, and perhaps reduce the need for cardiac transplantation.

The only randomized, placebo-controlled trial, however, looked at CPAP for patients with heart failure and Cheyne-Stokes respiration and found no difference in quality of life, mortality, or the need for transplant. In the Canadian Positive Airway Pressure trial, CPAP did produce a mean 3% improvement in ejection fraction (not the 8% found in single-center studies), improved oxygenation, and led to a small increase in 6-minute walk distances (N. Engl. J. Med. 2005;353:2025–41).

“First, always maximize the cardiac medications,” Dr. White urged. Studies show that the severity of heart failure predicts, to some degree, the extent of disordered breathing. The severity of Cheyne-Stokes respiration predicts survival rates independently of the severity of heart failure, he added. Other studies suggest that resynchronization therapy also can reduce the severity of disordered breathing, though not in all patients.

After that, consider CPAP for heart failure patients with central sleep apnea, or possibly one of several new devices designed specifically to relieve Cheyne-Stokes respiration, he said. The devices do regularize breathing but there are no long-term studies of their effects on survival, quality of life, or other parameters.

Dr. White is chief medical officer of a company that makes a variety of devices to treat sleep apnea, and is a consultant to other companies with apnea treatments.

SEATTLE — Maximizing heart failure therapy helps treat concomitant sleep apnea, Dr. David P. White said at the annual meeting of the Heart Failure Society of America.

Beyond that, treatment for sleep apnea in patients with heart failure relies mainly on continuous positive airway pressure (CPAP), which can regularize disordered breathing and which may improve ejection fraction and quality of life. There are no randomized trial data, however, showing that treating sleep apnea in patients with heart failure decreases mortality or the need for heart transplant, added Dr. White, professor of medicine at Harvard University, Boston.

The most common type of disordered breathing in heart failure patients is Cheyne-Stokes respiration, a variant of central sleep apnea. A number of short, single-center trials suggested that CPAP in patients with heart failure and either central or obstructive sleep apnea could stabilize respiration, improve cardiac function and quality of life, and perhaps reduce the need for cardiac transplantation.

The only randomized, placebo-controlled trial, however, looked at CPAP for patients with heart failure and Cheyne-Stokes respiration and found no difference in quality of life, mortality, or the need for transplant. In the Canadian Positive Airway Pressure trial, CPAP did produce a mean 3% improvement in ejection fraction (not the 8% found in single-center studies), improved oxygenation, and led to a small increase in 6-minute walk distances (N. Engl. J. Med. 2005;353:2025–41).

“First, always maximize the cardiac medications,” Dr. White urged. Studies show that the severity of heart failure predicts, to some degree, the extent of disordered breathing. The severity of Cheyne-Stokes respiration predicts survival rates independently of the severity of heart failure, he added. Other studies suggest that resynchronization therapy also can reduce the severity of disordered breathing, though not in all patients.

After that, consider CPAP for heart failure patients with central sleep apnea, or possibly one of several new devices designed specifically to relieve Cheyne-Stokes respiration, he said. The devices do regularize breathing but there are no long-term studies of their effects on survival, quality of life, or other parameters.

Dr. White is chief medical officer of a company that makes a variety of devices to treat sleep apnea, and is a consultant to other companies with apnea treatments.

SEATTLE — Maximizing heart failure therapy helps treat concomitant sleep apnea, Dr. David P. White said at the annual meeting of the Heart Failure Society of America.

Beyond that, treatment for sleep apnea in patients with heart failure relies mainly on continuous positive airway pressure (CPAP), which can regularize disordered breathing and which may improve ejection fraction and quality of life. There are no randomized trial data, however, showing that treating sleep apnea in patients with heart failure decreases mortality or the need for heart transplant, added Dr. White, professor of medicine at Harvard University, Boston.

The most common type of disordered breathing in heart failure patients is Cheyne-Stokes respiration, a variant of central sleep apnea. A number of short, single-center trials suggested that CPAP in patients with heart failure and either central or obstructive sleep apnea could stabilize respiration, improve cardiac function and quality of life, and perhaps reduce the need for cardiac transplantation.

The only randomized, placebo-controlled trial, however, looked at CPAP for patients with heart failure and Cheyne-Stokes respiration and found no difference in quality of life, mortality, or the need for transplant. In the Canadian Positive Airway Pressure trial, CPAP did produce a mean 3% improvement in ejection fraction (not the 8% found in single-center studies), improved oxygenation, and led to a small increase in 6-minute walk distances (N. Engl. J. Med. 2005;353:2025–41).

“First, always maximize the cardiac medications,” Dr. White urged. Studies show that the severity of heart failure predicts, to some degree, the extent of disordered breathing. The severity of Cheyne-Stokes respiration predicts survival rates independently of the severity of heart failure, he added. Other studies suggest that resynchronization therapy also can reduce the severity of disordered breathing, though not in all patients.

After that, consider CPAP for heart failure patients with central sleep apnea, or possibly one of several new devices designed specifically to relieve Cheyne-Stokes respiration, he said. The devices do regularize breathing but there are no long-term studies of their effects on survival, quality of life, or other parameters.

Dr. White is chief medical officer of a company that makes a variety of devices to treat sleep apnea, and is a consultant to other companies with apnea treatments.

SEATTLE — Patients with heart failure or hypertension who answered “Yes” to at least two of three questions had a high likelihood of having obstructive sleep apnea, Cheryl L. Bartone reported in a poster presentation at the annual meeting of the Heart Failure Society of America.

She and associates compared responses to the screening questionnaire with polysomnography results in 70 outpatients with heart failure or hypertension seen at a cardiology office.

The three-question screening tool was 90% sensitive and 45% specific in detecting obstructive sleep apnea, said Ms. Bartone of the Ohio Heart and Vascular Center, Cincinnati.

The tool had a positive predictive value of 67% and a negative predictive value of 78%.

Patients were asked:

▸ Do you snore loudly?

▸ Do you wake up more than once a night?

▸ Do you have morning fatigue?

Polysomnograms showed that 67 patients had some degree of obstructive sleep apnea, defined as an apnea-hypopnea index of 5 or greater. The obstructive sleep apnea was considered significant in 39 patients who had moderate or severe obstructive sleep apnea, defined as an apnea-hypopnea index of 20 or greater.

Of the 52 patients who answered “Yes” to at least two questions, 32 had significant obstructive sleep apnea. Among the 18 patients who answered “Yes” to only one or none of the questions, 4 had significant obstructive sleep apnea.

Patients with significant obstructive sleep apnea were more likely to be on β-blockers than were those without significant obstructive sleep apnea (82% vs. 74%) and less likely to be on an ACE inhibitor or angiotensin receptor blocker (74% vs. 77%).

Obstructive sleep apnea is a significant contributor to morbidity and mortality in patients with heart failure or hypertension, the investigators said.

There is no other easily applicable screening tool for effective detection of obstructive sleep apnea in these patients, they added. The investigators have no financial conflicts of interest in the study.

The groups with and without significant obstructive sleep apnea did not differ by age, sex, left ventricular ejection fraction, weight, body mass index, or morning fatigue.

SEATTLE — Patients with heart failure or hypertension who answered “Yes” to at least two of three questions had a high likelihood of having obstructive sleep apnea, Cheryl L. Bartone reported in a poster presentation at the annual meeting of the Heart Failure Society of America.

She and associates compared responses to the screening questionnaire with polysomnography results in 70 outpatients with heart failure or hypertension seen at a cardiology office.

The three-question screening tool was 90% sensitive and 45% specific in detecting obstructive sleep apnea, said Ms. Bartone of the Ohio Heart and Vascular Center, Cincinnati.

The tool had a positive predictive value of 67% and a negative predictive value of 78%.

Patients were asked:

▸ Do you snore loudly?

▸ Do you wake up more than once a night?

▸ Do you have morning fatigue?

Polysomnograms showed that 67 patients had some degree of obstructive sleep apnea, defined as an apnea-hypopnea index of 5 or greater. The obstructive sleep apnea was considered significant in 39 patients who had moderate or severe obstructive sleep apnea, defined as an apnea-hypopnea index of 20 or greater.

Of the 52 patients who answered “Yes” to at least two questions, 32 had significant obstructive sleep apnea. Among the 18 patients who answered “Yes” to only one or none of the questions, 4 had significant obstructive sleep apnea.

Patients with significant obstructive sleep apnea were more likely to be on β-blockers than were those without significant obstructive sleep apnea (82% vs. 74%) and less likely to be on an ACE inhibitor or angiotensin receptor blocker (74% vs. 77%).

Obstructive sleep apnea is a significant contributor to morbidity and mortality in patients with heart failure or hypertension, the investigators said.

There is no other easily applicable screening tool for effective detection of obstructive sleep apnea in these patients, they added. The investigators have no financial conflicts of interest in the study.

The groups with and without significant obstructive sleep apnea did not differ by age, sex, left ventricular ejection fraction, weight, body mass index, or morning fatigue.

SEATTLE — Patients with heart failure or hypertension who answered “Yes” to at least two of three questions had a high likelihood of having obstructive sleep apnea, Cheryl L. Bartone reported in a poster presentation at the annual meeting of the Heart Failure Society of America.

She and associates compared responses to the screening questionnaire with polysomnography results in 70 outpatients with heart failure or hypertension seen at a cardiology office.

The three-question screening tool was 90% sensitive and 45% specific in detecting obstructive sleep apnea, said Ms. Bartone of the Ohio Heart and Vascular Center, Cincinnati.

The tool had a positive predictive value of 67% and a negative predictive value of 78%.

Patients were asked:

▸ Do you snore loudly?

▸ Do you wake up more than once a night?

▸ Do you have morning fatigue?

Polysomnograms showed that 67 patients had some degree of obstructive sleep apnea, defined as an apnea-hypopnea index of 5 or greater. The obstructive sleep apnea was considered significant in 39 patients who had moderate or severe obstructive sleep apnea, defined as an apnea-hypopnea index of 20 or greater.

Of the 52 patients who answered “Yes” to at least two questions, 32 had significant obstructive sleep apnea. Among the 18 patients who answered “Yes” to only one or none of the questions, 4 had significant obstructive sleep apnea.

Patients with significant obstructive sleep apnea were more likely to be on β-blockers than were those without significant obstructive sleep apnea (82% vs. 74%) and less likely to be on an ACE inhibitor or angiotensin receptor blocker (74% vs. 77%).

Obstructive sleep apnea is a significant contributor to morbidity and mortality in patients with heart failure or hypertension, the investigators said.

There is no other easily applicable screening tool for effective detection of obstructive sleep apnea in these patients, they added. The investigators have no financial conflicts of interest in the study.

The groups with and without significant obstructive sleep apnea did not differ by age, sex, left ventricular ejection fraction, weight, body mass index, or morning fatigue.

SEATTLE — There is no standard way to screen for sleep apnea in patients with heart failure, but there are several screening models to choose from, Dr. Steven M. Scharf said at the annual meeting of the Heart Failure Society of America.

Sleep apnea commonly accompanies heart failure, and can be treated, though there's little high-quality evidence that treatment alters mortality or quality of life. Still, “I think you certainly should screen all your heart failure patients,” said Dr. Scharf, professor of medicine and director of the sleep disorders lab at the University of Maryland, Baltimore.

One good screening tool is the Berlin Questionnaire, which asks about symptoms in three categories: excessive sleepiness or sleepiness while driving; wild, disturbing snoring or gasping; and either obesity or heart failure (Ann. Intern. Med. 1999;131:485–91). Primary care patients with symptoms in two of the three categories are at high risk of obstructive sleep apnea, but the sensitivity and specificity of the questionnaire in patients with heart failure are unknown, he said.

Other screening schemes stratify patients by neck circumference, with larger necks increasing sleep apnea risk (N. Engl. J. Med. 2002;347:498–91). Other scoring systems combine clinical findings such as male gender, body mass index, a snoring index, and a choking index to rate the likelihood of sleep apnea. Many of these screening models may be useful, Dr. Scharf suggested. (See article at right for another screening tool).

If a heart failure patient seems to have a high probability of sleep apnea (perhaps based on the Berlin Questionnaire and neck circumference), schedule a full polysomnograph evaluation, he advised. Consider doing overnight pulse oximetry testing in heart failure patients who don't meet your threshold for high risk of apnea, he added. A recent metaanalysis of 79 studies that used pulse oximetry for screening suggests that if you have a strong clinical suspicion for obstructive sleep apnea and testing shows fewer than 15 desaturations per hour, diagnostic polysomnography may be warranted (Chest 2001;120:625–33). With more than 15 desaturations per hour, a full evaluation for sleep apnea or treatment with titrated continuous positive airway pressure may be reasonable.

Two articles suggest that an algorithm assessing heart rate variability might help screen for apnea in heart failure patients, but practice parameters don't exist and would need to be developed, he said (Eur. Respir. J. 2006;27:571–7). One small study suggests the PAT100 Watch, which measures peripheral arterial tone, also might help screen for sleep apnea.

Dr. Scharf has no affiliation with companies that sell the tools he discussed.

Patients with symptoms in two of the three Berlin Questionnaire categories are at high risk for apnea. DR. SCHARF

SEATTLE — There is no standard way to screen for sleep apnea in patients with heart failure, but there are several screening models to choose from, Dr. Steven M. Scharf said at the annual meeting of the Heart Failure Society of America.

Sleep apnea commonly accompanies heart failure, and can be treated, though there's little high-quality evidence that treatment alters mortality or quality of life. Still, “I think you certainly should screen all your heart failure patients,” said Dr. Scharf, professor of medicine and director of the sleep disorders lab at the University of Maryland, Baltimore.

One good screening tool is the Berlin Questionnaire, which asks about symptoms in three categories: excessive sleepiness or sleepiness while driving; wild, disturbing snoring or gasping; and either obesity or heart failure (Ann. Intern. Med. 1999;131:485–91). Primary care patients with symptoms in two of the three categories are at high risk of obstructive sleep apnea, but the sensitivity and specificity of the questionnaire in patients with heart failure are unknown, he said.

Other screening schemes stratify patients by neck circumference, with larger necks increasing sleep apnea risk (N. Engl. J. Med. 2002;347:498–91). Other scoring systems combine clinical findings such as male gender, body mass index, a snoring index, and a choking index to rate the likelihood of sleep apnea. Many of these screening models may be useful, Dr. Scharf suggested. (See article at right for another screening tool).

If a heart failure patient seems to have a high probability of sleep apnea (perhaps based on the Berlin Questionnaire and neck circumference), schedule a full polysomnograph evaluation, he advised. Consider doing overnight pulse oximetry testing in heart failure patients who don't meet your threshold for high risk of apnea, he added. A recent metaanalysis of 79 studies that used pulse oximetry for screening suggests that if you have a strong clinical suspicion for obstructive sleep apnea and testing shows fewer than 15 desaturations per hour, diagnostic polysomnography may be warranted (Chest 2001;120:625–33). With more than 15 desaturations per hour, a full evaluation for sleep apnea or treatment with titrated continuous positive airway pressure may be reasonable.

Two articles suggest that an algorithm assessing heart rate variability might help screen for apnea in heart failure patients, but practice parameters don't exist and would need to be developed, he said (Eur. Respir. J. 2006;27:571–7). One small study suggests the PAT100 Watch, which measures peripheral arterial tone, also might help screen for sleep apnea.

Dr. Scharf has no affiliation with companies that sell the tools he discussed.

Patients with symptoms in two of the three Berlin Questionnaire categories are at high risk for apnea. DR. SCHARF

SEATTLE — There is no standard way to screen for sleep apnea in patients with heart failure, but there are several screening models to choose from, Dr. Steven M. Scharf said at the annual meeting of the Heart Failure Society of America.

Sleep apnea commonly accompanies heart failure, and can be treated, though there's little high-quality evidence that treatment alters mortality or quality of life. Still, “I think you certainly should screen all your heart failure patients,” said Dr. Scharf, professor of medicine and director of the sleep disorders lab at the University of Maryland, Baltimore.

One good screening tool is the Berlin Questionnaire, which asks about symptoms in three categories: excessive sleepiness or sleepiness while driving; wild, disturbing snoring or gasping; and either obesity or heart failure (Ann. Intern. Med. 1999;131:485–91). Primary care patients with symptoms in two of the three categories are at high risk of obstructive sleep apnea, but the sensitivity and specificity of the questionnaire in patients with heart failure are unknown, he said.

Other screening schemes stratify patients by neck circumference, with larger necks increasing sleep apnea risk (N. Engl. J. Med. 2002;347:498–91). Other scoring systems combine clinical findings such as male gender, body mass index, a snoring index, and a choking index to rate the likelihood of sleep apnea. Many of these screening models may be useful, Dr. Scharf suggested. (See article at right for another screening tool).

If a heart failure patient seems to have a high probability of sleep apnea (perhaps based on the Berlin Questionnaire and neck circumference), schedule a full polysomnograph evaluation, he advised. Consider doing overnight pulse oximetry testing in heart failure patients who don't meet your threshold for high risk of apnea, he added. A recent metaanalysis of 79 studies that used pulse oximetry for screening suggests that if you have a strong clinical suspicion for obstructive sleep apnea and testing shows fewer than 15 desaturations per hour, diagnostic polysomnography may be warranted (Chest 2001;120:625–33). With more than 15 desaturations per hour, a full evaluation for sleep apnea or treatment with titrated continuous positive airway pressure may be reasonable.

Two articles suggest that an algorithm assessing heart rate variability might help screen for apnea in heart failure patients, but practice parameters don't exist and would need to be developed, he said (Eur. Respir. J. 2006;27:571–7). One small study suggests the PAT100 Watch, which measures peripheral arterial tone, also might help screen for sleep apnea.

Dr. Scharf has no affiliation with companies that sell the tools he discussed.

Patients with symptoms in two of the three Berlin Questionnaire categories are at high risk for apnea. DR. SCHARF

SEATTLE — Cardiologists outperformed internists, family physicians, and other specialists in meeting the measures of care for hospitalized patients with heart failure prescribed by the Joint Commission on Accreditation of Healthcare Organizations, Kismet D. Rasmusson reported.

A study of care within the 20-hospital Intermountain Healthcare system, which handled 2,000 admissions for a primary diagnosis of heart failure in 2005, assessed documentation of three aspects of care mandated by the Joint Commission (JCAHO) for evidence-based care of heart failure. Intermountain Healthcare employs about 400 physicians, mainly in primary care, and is affiliated with 2,500 more physicians, mainly specialists.

Results showed that internists cared for 31% of patients admitted for the first time with a primary diagnosis of heart failure during 2002–2006. Family physicians handled 19%, cardiologists or thoracic surgeons provided 22% of care, and other specialists handled the remainder of care for heart failure, she and her associates reported in a poster presentation.

Overall, 62% of cardiologists documented compliance with all three measures of heart failure care, compared with 43% of noncardiologists, said Ms. Rasmusson, a family nurse practitioner at LDS Hospital, Salt Lake City.

Noncardiologists were more likely to comply with only one, two, or none of the measures, documentation suggested.

The JCAHO requires documentation of four steps in caring for hospitalized heart failure patients:

1. Measurement of left ventricular function in the past, or planned measurement after discharge.

2. Prescription of an ACE inhibitor or an angiotensin receptor blocker when the left ventricular ejection fraction is 40% or lower, unless the drugs are contraindicated.

3. Providing self-management education to patients.

4. Providing smoking cessation counseling (the study did not include this measure because of the low numbers of smokers).

Previous studies have shown that compliance with these measures is associated with improved patient outcomes. “Health systems need to either increase the numbers of cardiologists providing heart failure care or improve care provided by noncardiologists,” the investigators concluded.

SEATTLE — Cardiologists outperformed internists, family physicians, and other specialists in meeting the measures of care for hospitalized patients with heart failure prescribed by the Joint Commission on Accreditation of Healthcare Organizations, Kismet D. Rasmusson reported.

A study of care within the 20-hospital Intermountain Healthcare system, which handled 2,000 admissions for a primary diagnosis of heart failure in 2005, assessed documentation of three aspects of care mandated by the Joint Commission (JCAHO) for evidence-based care of heart failure. Intermountain Healthcare employs about 400 physicians, mainly in primary care, and is affiliated with 2,500 more physicians, mainly specialists.

Results showed that internists cared for 31% of patients admitted for the first time with a primary diagnosis of heart failure during 2002–2006. Family physicians handled 19%, cardiologists or thoracic surgeons provided 22% of care, and other specialists handled the remainder of care for heart failure, she and her associates reported in a poster presentation.

Overall, 62% of cardiologists documented compliance with all three measures of heart failure care, compared with 43% of noncardiologists, said Ms. Rasmusson, a family nurse practitioner at LDS Hospital, Salt Lake City.

Noncardiologists were more likely to comply with only one, two, or none of the measures, documentation suggested.

The JCAHO requires documentation of four steps in caring for hospitalized heart failure patients:

1. Measurement of left ventricular function in the past, or planned measurement after discharge.

2. Prescription of an ACE inhibitor or an angiotensin receptor blocker when the left ventricular ejection fraction is 40% or lower, unless the drugs are contraindicated.

3. Providing self-management education to patients.

4. Providing smoking cessation counseling (the study did not include this measure because of the low numbers of smokers).

Previous studies have shown that compliance with these measures is associated with improved patient outcomes. “Health systems need to either increase the numbers of cardiologists providing heart failure care or improve care provided by noncardiologists,” the investigators concluded.

SEATTLE — Cardiologists outperformed internists, family physicians, and other specialists in meeting the measures of care for hospitalized patients with heart failure prescribed by the Joint Commission on Accreditation of Healthcare Organizations, Kismet D. Rasmusson reported.

A study of care within the 20-hospital Intermountain Healthcare system, which handled 2,000 admissions for a primary diagnosis of heart failure in 2005, assessed documentation of three aspects of care mandated by the Joint Commission (JCAHO) for evidence-based care of heart failure. Intermountain Healthcare employs about 400 physicians, mainly in primary care, and is affiliated with 2,500 more physicians, mainly specialists.

Results showed that internists cared for 31% of patients admitted for the first time with a primary diagnosis of heart failure during 2002–2006. Family physicians handled 19%, cardiologists or thoracic surgeons provided 22% of care, and other specialists handled the remainder of care for heart failure, she and her associates reported in a poster presentation.

Overall, 62% of cardiologists documented compliance with all three measures of heart failure care, compared with 43% of noncardiologists, said Ms. Rasmusson, a family nurse practitioner at LDS Hospital, Salt Lake City.

Noncardiologists were more likely to comply with only one, two, or none of the measures, documentation suggested.

The JCAHO requires documentation of four steps in caring for hospitalized heart failure patients:

1. Measurement of left ventricular function in the past, or planned measurement after discharge.

2. Prescription of an ACE inhibitor or an angiotensin receptor blocker when the left ventricular ejection fraction is 40% or lower, unless the drugs are contraindicated.

3. Providing self-management education to patients.

4. Providing smoking cessation counseling (the study did not include this measure because of the low numbers of smokers).

Previous studies have shown that compliance with these measures is associated with improved patient outcomes. “Health systems need to either increase the numbers of cardiologists providing heart failure care or improve care provided by noncardiologists,” the investigators concluded.