Heart Failure

CHICAGO — As in outpatients, cystatin C levels appear to offer additional prognostic information in patients admitted with heart failure exacerbations, according to an analysis of 240 consecutive inpatients.

Although there was no significant association between the serum protein levels on admission and the study's primary end point of length of hospitalization, cystatin C was more predictive of all-cause mortality and the combined end point of readmission or death than was creatinine, Dr. Daniel J. Brotman and his colleagues reported in a poster at the annual meeting of the Society of Hospital Medicine.

Patients in the highest quartile of cystatin C (mean 2.44 mg/L) were at significantly increased risk of death (hazard ratio 2.07) and of readmission or death (HR 1.61) during the first year after admission, compared with those in the lower three cystatin C quartiles (mean 0.66-1.43 mg/L).

The association between cystatin C and the risk of readmission or death remained significant on multivariate analysis after adjustment for age, race, gender, and creatinine level (HR 1.65), according to Dr. Brotman, director of the hospitalists program at Johns Hopkins Hospital in Baltimore. The relationship also remained significant when ejection fraction was included in the model.

Cystatin C level has been shown to be a stronger predictor of the risk of death and cardiovascular events in elderly patients, compared with creatinine level (N. Engl. J. Med. 2005;352:2049-60). Accumulating evidence also supports its use as an alternative and more sensitive endogenous marker, compared with serum creatinine, for the estimation of glomerular filtration rate.

In the current analysis, there was a trend toward increased risk of readmission or death (HR 1.44) for patients in the top quartile of creatinine (mean 2.0 mg/dL), compared with those in the lower three creatinine quartiles (1.0-1.3 mg/dL), but this difference did not reach statistical significance.

The combination of cystatin C and creatinine, however, was significantly more predictive of the combined end point of readmission or death than was either variable alone (HR 1.81).

“We are looking into whether serial changes in this biomarker during the course of hospitalization will have any potential clinical utility,” Dr. Brotman said in an interview. Clinical application is currently limited, as most labs do not routinely test for cystatin C.

Dr. Brotman disclosed receiving research funding from Siemens Healthcare Diagnostics Inc., serving on the hospitalist leadership panel for Quantia Communications LLC, and being on the advisory boards of several pharmaceutical companies.

The combination of cystatin C and creatinine was more predictive of readmission or death than was either one alone.

Source DR. BROTMAN

CHICAGO — As in outpatients, cystatin C levels appear to offer additional prognostic information in patients admitted with heart failure exacerbations, according to an analysis of 240 consecutive inpatients.

Although there was no significant association between the serum protein levels on admission and the study's primary end point of length of hospitalization, cystatin C was more predictive of all-cause mortality and the combined end point of readmission or death than was creatinine, Dr. Daniel J. Brotman and his colleagues reported in a poster at the annual meeting of the Society of Hospital Medicine.

Patients in the highest quartile of cystatin C (mean 2.44 mg/L) were at significantly increased risk of death (hazard ratio 2.07) and of readmission or death (HR 1.61) during the first year after admission, compared with those in the lower three cystatin C quartiles (mean 0.66-1.43 mg/L).

The association between cystatin C and the risk of readmission or death remained significant on multivariate analysis after adjustment for age, race, gender, and creatinine level (HR 1.65), according to Dr. Brotman, director of the hospitalists program at Johns Hopkins Hospital in Baltimore. The relationship also remained significant when ejection fraction was included in the model.

Cystatin C level has been shown to be a stronger predictor of the risk of death and cardiovascular events in elderly patients, compared with creatinine level (N. Engl. J. Med. 2005;352:2049-60). Accumulating evidence also supports its use as an alternative and more sensitive endogenous marker, compared with serum creatinine, for the estimation of glomerular filtration rate.

In the current analysis, there was a trend toward increased risk of readmission or death (HR 1.44) for patients in the top quartile of creatinine (mean 2.0 mg/dL), compared with those in the lower three creatinine quartiles (1.0-1.3 mg/dL), but this difference did not reach statistical significance.

The combination of cystatin C and creatinine, however, was significantly more predictive of the combined end point of readmission or death than was either variable alone (HR 1.81).

“We are looking into whether serial changes in this biomarker during the course of hospitalization will have any potential clinical utility,” Dr. Brotman said in an interview. Clinical application is currently limited, as most labs do not routinely test for cystatin C.

Dr. Brotman disclosed receiving research funding from Siemens Healthcare Diagnostics Inc., serving on the hospitalist leadership panel for Quantia Communications LLC, and being on the advisory boards of several pharmaceutical companies.

The combination of cystatin C and creatinine was more predictive of readmission or death than was either one alone.

Source DR. BROTMAN

CHICAGO — As in outpatients, cystatin C levels appear to offer additional prognostic information in patients admitted with heart failure exacerbations, according to an analysis of 240 consecutive inpatients.

Although there was no significant association between the serum protein levels on admission and the study's primary end point of length of hospitalization, cystatin C was more predictive of all-cause mortality and the combined end point of readmission or death than was creatinine, Dr. Daniel J. Brotman and his colleagues reported in a poster at the annual meeting of the Society of Hospital Medicine.

Patients in the highest quartile of cystatin C (mean 2.44 mg/L) were at significantly increased risk of death (hazard ratio 2.07) and of readmission or death (HR 1.61) during the first year after admission, compared with those in the lower three cystatin C quartiles (mean 0.66-1.43 mg/L).

The association between cystatin C and the risk of readmission or death remained significant on multivariate analysis after adjustment for age, race, gender, and creatinine level (HR 1.65), according to Dr. Brotman, director of the hospitalists program at Johns Hopkins Hospital in Baltimore. The relationship also remained significant when ejection fraction was included in the model.

Cystatin C level has been shown to be a stronger predictor of the risk of death and cardiovascular events in elderly patients, compared with creatinine level (N. Engl. J. Med. 2005;352:2049-60). Accumulating evidence also supports its use as an alternative and more sensitive endogenous marker, compared with serum creatinine, for the estimation of glomerular filtration rate.

In the current analysis, there was a trend toward increased risk of readmission or death (HR 1.44) for patients in the top quartile of creatinine (mean 2.0 mg/dL), compared with those in the lower three creatinine quartiles (1.0-1.3 mg/dL), but this difference did not reach statistical significance.

The combination of cystatin C and creatinine, however, was significantly more predictive of the combined end point of readmission or death than was either variable alone (HR 1.81).

“We are looking into whether serial changes in this biomarker during the course of hospitalization will have any potential clinical utility,” Dr. Brotman said in an interview. Clinical application is currently limited, as most labs do not routinely test for cystatin C.

Dr. Brotman disclosed receiving research funding from Siemens Healthcare Diagnostics Inc., serving on the hospitalist leadership panel for Quantia Communications LLC, and being on the advisory boards of several pharmaceutical companies.

The combination of cystatin C and creatinine was more predictive of readmission or death than was either one alone.

Source DR. BROTMAN

ORLANDO — Chronic vagus nerve stimulation delivered by an implantable device resulted in significant functional and quality of life improvements in patients with advanced heart failure in a first-in-man study.

The 32-patient trial documented significant reductions in heart rate, New York Heart Association functional class, and Minnesota Living With Heart Failure scores along with increased left ventricular ejection fraction and improved 6-minute walk distance at assessment after 3 months of treatment, Dr. Gaetano M. De Ferrari reported at the annual meeting of the American College of Cardiology.

All of these benefits were maintained at the 6-month mark (see box).

“We believe that a large controlled study is now warranted,” said Dr. De Ferrari, head of cardiac intensive care at San Matteo Polyclinic in Pavia, Italy.

Vagus nerve stimulation (VNS) is approved for drug-refractory epilepsy and drug-refractory depression. Dr. De Ferrari presented the first-ever experience with the therapy in heart failure patients.

The rationale for VNS as a novel therapy for heart failure lies in the observation that reduced vagal activity and increased sympathetic tone are associated with increased mortality following acute MI as well as in heart failure. Moreover, additional vagal withdrawal often precedes episodes of acute decompensated heart failure.

Animal studies conducted by Dr. De Ferrari and coworkers at the University of Pavia 2 decades ago showed that chronic VNS markedly reduced mortality in the setting of post-MI heart failure, the cardiologist reported.

In the new clinical trial, 32 participants with NYHA class II-III heart failure each had an investigational CardioFit stimulator made by BioControl, an Israeli company, implanted in the right upper chest under the clavicle. The device was connected to a cuff electrode wrapped around the right cervical vagus nerve. The system is capable of sensing the R wave and delivering one or more pulse-synchronous stimuli of 0.5-msec duration. The stimulatory pulses were delivered at an average amplitude of 4.1 mAmp. The device was on an average of 21% of the time.

In this study, intended to establish safety, six patients experienced minor treatment-related adverse events such as cough, pain at stimulation site, or voice difficulties, all of which resolved with device tuning or adaptation. In addition, there were two serious device-related adverse events: a case of postoperative pulmonary edema, and a surgical revision after device implantation.

While there was no control group in this early study, Dr. De Ferrari dismissed the notion that the observed benefits might be due to the placebo effect.

“Most often the placebo effect lasts a few months. It's unlikely to continue for a 6-month period,” he said.

He and his coworkers are now trying to pin down which patients with advanced heart failure are most likely to respond to VNS. The five diabetic patients in the study did not benefit. The best responders were patients with a slightly higher baseline heart rate and those who could tolerate more intensive vagal stimulation.

Discussant Marvin A. Konstam called chronic VNS an intriguing and promising new therapeutic approach.

“The opportunity for benefit from increasing vagal tone is multifactorial. In the very simplest of terms, just the reduction in heart rate may be beneficial. I think to this day we don't know for sure how much of the benefit of beta-blockade in heart failure may simply be heart rate reduction, so on that ground alone I think there's potential benefit. Also, there's a potential antiarrhythmic effect from increasing vagal tone,” said Dr. Konstam, professor of medicine at Tufts University, Boston.

Dr. De Ferrari replied that there are several additional plausible mechanisms of benefit for chronic VNS, including anti-apoptotic and anti-inflammatory effects.

He disclosed having received research grants from, and serving as a paid consultant to, BioControl.

VNS benefits were maintained after 6 months. 'We believe that a large controlled study is now warranted.' DR. DE FERRARI

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Chronic vagus nerve stimulation delivered by an implantable device resulted in significant functional and quality of life improvements in patients with advanced heart failure in a first-in-man study.

The 32-patient trial documented significant reductions in heart rate, New York Heart Association functional class, and Minnesota Living With Heart Failure scores along with increased left ventricular ejection fraction and improved 6-minute walk distance at assessment after 3 months of treatment, Dr. Gaetano M. De Ferrari reported at the annual meeting of the American College of Cardiology.

All of these benefits were maintained at the 6-month mark (see box).

“We believe that a large controlled study is now warranted,” said Dr. De Ferrari, head of cardiac intensive care at San Matteo Polyclinic in Pavia, Italy.

Vagus nerve stimulation (VNS) is approved for drug-refractory epilepsy and drug-refractory depression. Dr. De Ferrari presented the first-ever experience with the therapy in heart failure patients.

The rationale for VNS as a novel therapy for heart failure lies in the observation that reduced vagal activity and increased sympathetic tone are associated with increased mortality following acute MI as well as in heart failure. Moreover, additional vagal withdrawal often precedes episodes of acute decompensated heart failure.

Animal studies conducted by Dr. De Ferrari and coworkers at the University of Pavia 2 decades ago showed that chronic VNS markedly reduced mortality in the setting of post-MI heart failure, the cardiologist reported.

In the new clinical trial, 32 participants with NYHA class II-III heart failure each had an investigational CardioFit stimulator made by BioControl, an Israeli company, implanted in the right upper chest under the clavicle. The device was connected to a cuff electrode wrapped around the right cervical vagus nerve. The system is capable of sensing the R wave and delivering one or more pulse-synchronous stimuli of 0.5-msec duration. The stimulatory pulses were delivered at an average amplitude of 4.1 mAmp. The device was on an average of 21% of the time.

In this study, intended to establish safety, six patients experienced minor treatment-related adverse events such as cough, pain at stimulation site, or voice difficulties, all of which resolved with device tuning or adaptation. In addition, there were two serious device-related adverse events: a case of postoperative pulmonary edema, and a surgical revision after device implantation.

While there was no control group in this early study, Dr. De Ferrari dismissed the notion that the observed benefits might be due to the placebo effect.

“Most often the placebo effect lasts a few months. It's unlikely to continue for a 6-month period,” he said.

He and his coworkers are now trying to pin down which patients with advanced heart failure are most likely to respond to VNS. The five diabetic patients in the study did not benefit. The best responders were patients with a slightly higher baseline heart rate and those who could tolerate more intensive vagal stimulation.

Discussant Marvin A. Konstam called chronic VNS an intriguing and promising new therapeutic approach.

“The opportunity for benefit from increasing vagal tone is multifactorial. In the very simplest of terms, just the reduction in heart rate may be beneficial. I think to this day we don't know for sure how much of the benefit of beta-blockade in heart failure may simply be heart rate reduction, so on that ground alone I think there's potential benefit. Also, there's a potential antiarrhythmic effect from increasing vagal tone,” said Dr. Konstam, professor of medicine at Tufts University, Boston.

Dr. De Ferrari replied that there are several additional plausible mechanisms of benefit for chronic VNS, including anti-apoptotic and anti-inflammatory effects.

He disclosed having received research grants from, and serving as a paid consultant to, BioControl.

VNS benefits were maintained after 6 months. 'We believe that a large controlled study is now warranted.' DR. DE FERRARI

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Chronic vagus nerve stimulation delivered by an implantable device resulted in significant functional and quality of life improvements in patients with advanced heart failure in a first-in-man study.

The 32-patient trial documented significant reductions in heart rate, New York Heart Association functional class, and Minnesota Living With Heart Failure scores along with increased left ventricular ejection fraction and improved 6-minute walk distance at assessment after 3 months of treatment, Dr. Gaetano M. De Ferrari reported at the annual meeting of the American College of Cardiology.

All of these benefits were maintained at the 6-month mark (see box).

“We believe that a large controlled study is now warranted,” said Dr. De Ferrari, head of cardiac intensive care at San Matteo Polyclinic in Pavia, Italy.

Vagus nerve stimulation (VNS) is approved for drug-refractory epilepsy and drug-refractory depression. Dr. De Ferrari presented the first-ever experience with the therapy in heart failure patients.

The rationale for VNS as a novel therapy for heart failure lies in the observation that reduced vagal activity and increased sympathetic tone are associated with increased mortality following acute MI as well as in heart failure. Moreover, additional vagal withdrawal often precedes episodes of acute decompensated heart failure.

Animal studies conducted by Dr. De Ferrari and coworkers at the University of Pavia 2 decades ago showed that chronic VNS markedly reduced mortality in the setting of post-MI heart failure, the cardiologist reported.

In the new clinical trial, 32 participants with NYHA class II-III heart failure each had an investigational CardioFit stimulator made by BioControl, an Israeli company, implanted in the right upper chest under the clavicle. The device was connected to a cuff electrode wrapped around the right cervical vagus nerve. The system is capable of sensing the R wave and delivering one or more pulse-synchronous stimuli of 0.5-msec duration. The stimulatory pulses were delivered at an average amplitude of 4.1 mAmp. The device was on an average of 21% of the time.

In this study, intended to establish safety, six patients experienced minor treatment-related adverse events such as cough, pain at stimulation site, or voice difficulties, all of which resolved with device tuning or adaptation. In addition, there were two serious device-related adverse events: a case of postoperative pulmonary edema, and a surgical revision after device implantation.

While there was no control group in this early study, Dr. De Ferrari dismissed the notion that the observed benefits might be due to the placebo effect.

“Most often the placebo effect lasts a few months. It's unlikely to continue for a 6-month period,” he said.

He and his coworkers are now trying to pin down which patients with advanced heart failure are most likely to respond to VNS. The five diabetic patients in the study did not benefit. The best responders were patients with a slightly higher baseline heart rate and those who could tolerate more intensive vagal stimulation.

Discussant Marvin A. Konstam called chronic VNS an intriguing and promising new therapeutic approach.

“The opportunity for benefit from increasing vagal tone is multifactorial. In the very simplest of terms, just the reduction in heart rate may be beneficial. I think to this day we don't know for sure how much of the benefit of beta-blockade in heart failure may simply be heart rate reduction, so on that ground alone I think there's potential benefit. Also, there's a potential antiarrhythmic effect from increasing vagal tone,” said Dr. Konstam, professor of medicine at Tufts University, Boston.

Dr. De Ferrari replied that there are several additional plausible mechanisms of benefit for chronic VNS, including anti-apoptotic and anti-inflammatory effects.

He disclosed having received research grants from, and serving as a paid consultant to, BioControl.

VNS benefits were maintained after 6 months. 'We believe that a large controlled study is now warranted.' DR. DE FERRARI

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Cardiac contractility modulation, an innovative device therapy for advanced heart failure, significantly improved peak VO2, quality of life scores, and New York Heart Association functional class in the randomized 50-center FIX-HF-5 trial.

“I'm extremely encouraged by the results of this study, and I think there's a future for cardiac contractility modulation. It has the potential to be a real breakthrough,” Dr. William T. Abraham said at the annual meeting of the American College of Cardiology.

There's a hitch, however. The FIX-HF-5 trial did not meet its primary efficacy end point, which was achievement of at least a 20% improvement in anaerobic threshold on metabolic exercise testing. That end point, imposed by the Food and Drug Administration, has never been used as a pivotal outcome in a heart failure study, and in hindsight it was a poor choice, according to Dr. Abraham, professor of medicine, physiology, and cell biology, and director of cardiovascular medicine, at Ohio State University, Columbus.

“In other trials of metabolic exercise testing and heart failure there seems to be a disconnect between peak VO2 and anaerobic threshold. Peak VO2 may improve significantly with little or no change in anaerobic threshold. I just don't think it's the right measure of exercise capacity in heart failure. We'll look to use a different primary end point in our confirmatory study,” he explained.

Cardiac contractility monitoring (CCM) involves implantation of a pacemaker-like device with leads to the right heart. The device, known as the Optimizer III, delivers an electrical signal during the absolute refractory period of the cardiac cycle; thus, unlike a pacemaker, the Optimizer III signal does not initiate a heartbeat. Instead, it upregulates genes involved in cardiac calcium channels to boost cardiac contractility at a lower work level, thus improving overall cardiac efficiency. The system relies on a transcutaneously charged battery, promoting long device life.

FIT-HF-5 was an unblinded study in which 428 patients with advanced heart failure were placed on optimal medical therapy and randomized to receive the Optimizer III or not. Roughly 90% of participants were NYHA class III, the rest were class IV. The average QRS duration was 101 ms. The Optimizer III operated for 5 hours per day during the 12 months of follow-up.

A 20% or greater improvement in anaerobic threshold occurred in 17.6% of the CCM group and 11.7% of controls, a nonsignificant difference.

The real action involved the prespecified secondary end points—which in other heart failure trials with metabolic exercise testing have been the primary end points. Peak VO2 worsened over the course of the year in controls but improved in the CCM group, with a highly significant mean difference of 0.65 mL/kg per min between the two groups.

There was also a mean 10-point difference favoring the CCM group in quality of life as measured by the Minnesota Living With Heart Failure Questionnaire. “That meets or exceeds the benefit seen with other device or drug therapies,” Dr. Abraham noted.

More than 44% of the CCM group experienced at least a 1-grade improvement in NYHA functional class, which was nearly twice the rate in controls.

Roughly half of FIX-HF-5 participants were NYHA class III with a left ventricular ejection fraction of 25% or more. The magnitude of benefit with CCM seen in this subgroup exceeded that in other participants. For example, they had a mean 1.3 mL/kg per min advantage in peak VO2 compared with controls, which is better than that seen in the controlled trials of cardiac resynchronization therapy. These are the type of patients to be enrolled in the pivotal trial now being planned, according to the cardiologist.

Discussant Clyde W. Yancy, president-elect of the American Heart Association, observed that new therapies with novel mechanisms of action are desperately needed in the field of heart failure, and said he is pleased that further studies of CCM are planned. But he sounded a note of caution.

“This is a very provocative study, but by the same token there is something about CCM that bespeaks of an inotropic effect, so we have to continue to be very thoughtful and circumspect and follow up larger populations for a longer period of time,” said Dr. Yancy, medical director of the Baylor Heart and Vascular Institute, Dallas.

Dr. Abraham has received research grants and consulting fees from Impulse Dynamics, sponsor of FIT-HF-5.

ORLANDO — Cardiac contractility modulation, an innovative device therapy for advanced heart failure, significantly improved peak VO2, quality of life scores, and New York Heart Association functional class in the randomized 50-center FIX-HF-5 trial.

“I'm extremely encouraged by the results of this study, and I think there's a future for cardiac contractility modulation. It has the potential to be a real breakthrough,” Dr. William T. Abraham said at the annual meeting of the American College of Cardiology.

There's a hitch, however. The FIX-HF-5 trial did not meet its primary efficacy end point, which was achievement of at least a 20% improvement in anaerobic threshold on metabolic exercise testing. That end point, imposed by the Food and Drug Administration, has never been used as a pivotal outcome in a heart failure study, and in hindsight it was a poor choice, according to Dr. Abraham, professor of medicine, physiology, and cell biology, and director of cardiovascular medicine, at Ohio State University, Columbus.

“In other trials of metabolic exercise testing and heart failure there seems to be a disconnect between peak VO2 and anaerobic threshold. Peak VO2 may improve significantly with little or no change in anaerobic threshold. I just don't think it's the right measure of exercise capacity in heart failure. We'll look to use a different primary end point in our confirmatory study,” he explained.

Cardiac contractility monitoring (CCM) involves implantation of a pacemaker-like device with leads to the right heart. The device, known as the Optimizer III, delivers an electrical signal during the absolute refractory period of the cardiac cycle; thus, unlike a pacemaker, the Optimizer III signal does not initiate a heartbeat. Instead, it upregulates genes involved in cardiac calcium channels to boost cardiac contractility at a lower work level, thus improving overall cardiac efficiency. The system relies on a transcutaneously charged battery, promoting long device life.

FIT-HF-5 was an unblinded study in which 428 patients with advanced heart failure were placed on optimal medical therapy and randomized to receive the Optimizer III or not. Roughly 90% of participants were NYHA class III, the rest were class IV. The average QRS duration was 101 ms. The Optimizer III operated for 5 hours per day during the 12 months of follow-up.

A 20% or greater improvement in anaerobic threshold occurred in 17.6% of the CCM group and 11.7% of controls, a nonsignificant difference.

The real action involved the prespecified secondary end points—which in other heart failure trials with metabolic exercise testing have been the primary end points. Peak VO2 worsened over the course of the year in controls but improved in the CCM group, with a highly significant mean difference of 0.65 mL/kg per min between the two groups.

There was also a mean 10-point difference favoring the CCM group in quality of life as measured by the Minnesota Living With Heart Failure Questionnaire. “That meets or exceeds the benefit seen with other device or drug therapies,” Dr. Abraham noted.

More than 44% of the CCM group experienced at least a 1-grade improvement in NYHA functional class, which was nearly twice the rate in controls.

Roughly half of FIX-HF-5 participants were NYHA class III with a left ventricular ejection fraction of 25% or more. The magnitude of benefit with CCM seen in this subgroup exceeded that in other participants. For example, they had a mean 1.3 mL/kg per min advantage in peak VO2 compared with controls, which is better than that seen in the controlled trials of cardiac resynchronization therapy. These are the type of patients to be enrolled in the pivotal trial now being planned, according to the cardiologist.

Discussant Clyde W. Yancy, president-elect of the American Heart Association, observed that new therapies with novel mechanisms of action are desperately needed in the field of heart failure, and said he is pleased that further studies of CCM are planned. But he sounded a note of caution.

“This is a very provocative study, but by the same token there is something about CCM that bespeaks of an inotropic effect, so we have to continue to be very thoughtful and circumspect and follow up larger populations for a longer period of time,” said Dr. Yancy, medical director of the Baylor Heart and Vascular Institute, Dallas.

Dr. Abraham has received research grants and consulting fees from Impulse Dynamics, sponsor of FIT-HF-5.

ORLANDO — Cardiac contractility modulation, an innovative device therapy for advanced heart failure, significantly improved peak VO2, quality of life scores, and New York Heart Association functional class in the randomized 50-center FIX-HF-5 trial.

“I'm extremely encouraged by the results of this study, and I think there's a future for cardiac contractility modulation. It has the potential to be a real breakthrough,” Dr. William T. Abraham said at the annual meeting of the American College of Cardiology.

There's a hitch, however. The FIX-HF-5 trial did not meet its primary efficacy end point, which was achievement of at least a 20% improvement in anaerobic threshold on metabolic exercise testing. That end point, imposed by the Food and Drug Administration, has never been used as a pivotal outcome in a heart failure study, and in hindsight it was a poor choice, according to Dr. Abraham, professor of medicine, physiology, and cell biology, and director of cardiovascular medicine, at Ohio State University, Columbus.

“In other trials of metabolic exercise testing and heart failure there seems to be a disconnect between peak VO2 and anaerobic threshold. Peak VO2 may improve significantly with little or no change in anaerobic threshold. I just don't think it's the right measure of exercise capacity in heart failure. We'll look to use a different primary end point in our confirmatory study,” he explained.

Cardiac contractility monitoring (CCM) involves implantation of a pacemaker-like device with leads to the right heart. The device, known as the Optimizer III, delivers an electrical signal during the absolute refractory period of the cardiac cycle; thus, unlike a pacemaker, the Optimizer III signal does not initiate a heartbeat. Instead, it upregulates genes involved in cardiac calcium channels to boost cardiac contractility at a lower work level, thus improving overall cardiac efficiency. The system relies on a transcutaneously charged battery, promoting long device life.

FIT-HF-5 was an unblinded study in which 428 patients with advanced heart failure were placed on optimal medical therapy and randomized to receive the Optimizer III or not. Roughly 90% of participants were NYHA class III, the rest were class IV. The average QRS duration was 101 ms. The Optimizer III operated for 5 hours per day during the 12 months of follow-up.

A 20% or greater improvement in anaerobic threshold occurred in 17.6% of the CCM group and 11.7% of controls, a nonsignificant difference.

The real action involved the prespecified secondary end points—which in other heart failure trials with metabolic exercise testing have been the primary end points. Peak VO2 worsened over the course of the year in controls but improved in the CCM group, with a highly significant mean difference of 0.65 mL/kg per min between the two groups.

There was also a mean 10-point difference favoring the CCM group in quality of life as measured by the Minnesota Living With Heart Failure Questionnaire. “That meets or exceeds the benefit seen with other device or drug therapies,” Dr. Abraham noted.

More than 44% of the CCM group experienced at least a 1-grade improvement in NYHA functional class, which was nearly twice the rate in controls.

Roughly half of FIX-HF-5 participants were NYHA class III with a left ventricular ejection fraction of 25% or more. The magnitude of benefit with CCM seen in this subgroup exceeded that in other participants. For example, they had a mean 1.3 mL/kg per min advantage in peak VO2 compared with controls, which is better than that seen in the controlled trials of cardiac resynchronization therapy. These are the type of patients to be enrolled in the pivotal trial now being planned, according to the cardiologist.

Discussant Clyde W. Yancy, president-elect of the American Heart Association, observed that new therapies with novel mechanisms of action are desperately needed in the field of heart failure, and said he is pleased that further studies of CCM are planned. But he sounded a note of caution.

“This is a very provocative study, but by the same token there is something about CCM that bespeaks of an inotropic effect, so we have to continue to be very thoughtful and circumspect and follow up larger populations for a longer period of time,” said Dr. Yancy, medical director of the Baylor Heart and Vascular Institute, Dallas.

Dr. Abraham has received research grants and consulting fees from Impulse Dynamics, sponsor of FIT-HF-5.

ORLANDO — Cardiac resynchronization therapy improves key clinical outcomes in patients with mild heart failure, a randomized trial has shown.

In the European cohort of the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) trial, patients with cardiac synchronization therapy switched on had a 62% relative risk reduction in the combined end point of heart failure hospitalization or death compared with those assigned to CRT-off, at 24 months' follow-up, Dr. Cecilia Linde said at the annual meeting of the American College of Cardiology.

Patients with the CRT device turned on also had significantly improved left ventricular function, as reflected in their ejection fraction and end-diastolic and end-systolic volumes (see box). All these outcomes combined suggest that reverse ventricular remodeling had occurred, added Dr. Linde, professor of cardiology at Karolinska Hospital, Stockholm.

The European follow-up analysis, prespecified in the double-blind prospective REVERSE study, involved 262 patients who underwent implantation of a biventricular pacemaker and were then randomized 2:1 to have CRT switched on or off.

All subjects had New York Heart Association class II or previously symptomatic class I heart failure, a left ventricular ejection fraction of 40% or less, and a wide QRS interval of at least 120 ms. All were on optimal guideline-recommended medical therapy.

The goal of REVERSE was to learn whether heart failure patients who improved with medications to the point of being asymptomatic or mildly symptomatic could maintain that status with CRT. The answer, Dr. Linde said, is yes.

There was a 10% major complication rate related to the CRT devices in REVERSE. Lead dislocation, perforation of the coronary sinus, and other complications were concentrated in the left ventricular lead during the first year and the right lead in year 2.

The 12-month REVERSE results, presented last year, showed only a nonsignificant trend favoring better outcomes in the CRT-on group. Why the difference a year later?

“It takes time to have an effect in patients with asymptomatic or mildly symptomatic heart failure, so of course when you follow patients for 24 months you're going to find more than if you follow them for 12 months,” she observed.

Today CRT is indicated for patients with class III or ambulatory class IV heart failure. Dr. Linde predicted that if the new REVERSE findings are confirmed in the Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy (MADIT-CRT) trial and Rythmol SR Atrial Fibrillation Trial (RAFT), the indications for CRT will broaden to incorporate the large population of patients with class I and II heart failure along with a low ejection fraction and wide QRS interval.

Discussant Richard L. Page said he found it difficult to reconcile the enhanced LV function and improved clinical outcomes seen with CRT in REVERSE with the observed lack of functional and symptomatic improvement. The CRT on and off groups did not differ significantly at 24 months in the 6-minute walk test, Minnesota Living With Heart Failure Questionnaire, or NYHA class, noted Dr. Page, professor of medicine at the University of Washington, Seattle.

Dr. Jean-Claude Daubert of the REVERSE steering committee replied that since most patients were asymptomatic or mildly symptomatic at entry, there was little room for functional or symptomatic improvement.

“We suspect that to show functional benefit we'll need a much longer follow-up,” said Dr. Daubert, professor of cardiology at Central University Hospital, Rennes, France.

REVERSE was sponsored by Medtronic. Dr. Linde and Dr. Daubert are consultants to, and are on the speakers bureaus for, Medtronic and St. Jude Medical.

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Cardiac resynchronization therapy improves key clinical outcomes in patients with mild heart failure, a randomized trial has shown.

In the European cohort of the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) trial, patients with cardiac synchronization therapy switched on had a 62% relative risk reduction in the combined end point of heart failure hospitalization or death compared with those assigned to CRT-off, at 24 months' follow-up, Dr. Cecilia Linde said at the annual meeting of the American College of Cardiology.

Patients with the CRT device turned on also had significantly improved left ventricular function, as reflected in their ejection fraction and end-diastolic and end-systolic volumes (see box). All these outcomes combined suggest that reverse ventricular remodeling had occurred, added Dr. Linde, professor of cardiology at Karolinska Hospital, Stockholm.

The European follow-up analysis, prespecified in the double-blind prospective REVERSE study, involved 262 patients who underwent implantation of a biventricular pacemaker and were then randomized 2:1 to have CRT switched on or off.

All subjects had New York Heart Association class II or previously symptomatic class I heart failure, a left ventricular ejection fraction of 40% or less, and a wide QRS interval of at least 120 ms. All were on optimal guideline-recommended medical therapy.

The goal of REVERSE was to learn whether heart failure patients who improved with medications to the point of being asymptomatic or mildly symptomatic could maintain that status with CRT. The answer, Dr. Linde said, is yes.

There was a 10% major complication rate related to the CRT devices in REVERSE. Lead dislocation, perforation of the coronary sinus, and other complications were concentrated in the left ventricular lead during the first year and the right lead in year 2.

The 12-month REVERSE results, presented last year, showed only a nonsignificant trend favoring better outcomes in the CRT-on group. Why the difference a year later?

“It takes time to have an effect in patients with asymptomatic or mildly symptomatic heart failure, so of course when you follow patients for 24 months you're going to find more than if you follow them for 12 months,” she observed.

Today CRT is indicated for patients with class III or ambulatory class IV heart failure. Dr. Linde predicted that if the new REVERSE findings are confirmed in the Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy (MADIT-CRT) trial and Rythmol SR Atrial Fibrillation Trial (RAFT), the indications for CRT will broaden to incorporate the large population of patients with class I and II heart failure along with a low ejection fraction and wide QRS interval.

Discussant Richard L. Page said he found it difficult to reconcile the enhanced LV function and improved clinical outcomes seen with CRT in REVERSE with the observed lack of functional and symptomatic improvement. The CRT on and off groups did not differ significantly at 24 months in the 6-minute walk test, Minnesota Living With Heart Failure Questionnaire, or NYHA class, noted Dr. Page, professor of medicine at the University of Washington, Seattle.

Dr. Jean-Claude Daubert of the REVERSE steering committee replied that since most patients were asymptomatic or mildly symptomatic at entry, there was little room for functional or symptomatic improvement.

“We suspect that to show functional benefit we'll need a much longer follow-up,” said Dr. Daubert, professor of cardiology at Central University Hospital, Rennes, France.

REVERSE was sponsored by Medtronic. Dr. Linde and Dr. Daubert are consultants to, and are on the speakers bureaus for, Medtronic and St. Jude Medical.

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Cardiac resynchronization therapy improves key clinical outcomes in patients with mild heart failure, a randomized trial has shown.

In the European cohort of the Resynchronization Reverses Remodeling in Systolic Left Ventricular Dysfunction (REVERSE) trial, patients with cardiac synchronization therapy switched on had a 62% relative risk reduction in the combined end point of heart failure hospitalization or death compared with those assigned to CRT-off, at 24 months' follow-up, Dr. Cecilia Linde said at the annual meeting of the American College of Cardiology.

Patients with the CRT device turned on also had significantly improved left ventricular function, as reflected in their ejection fraction and end-diastolic and end-systolic volumes (see box). All these outcomes combined suggest that reverse ventricular remodeling had occurred, added Dr. Linde, professor of cardiology at Karolinska Hospital, Stockholm.

The European follow-up analysis, prespecified in the double-blind prospective REVERSE study, involved 262 patients who underwent implantation of a biventricular pacemaker and were then randomized 2:1 to have CRT switched on or off.

All subjects had New York Heart Association class II or previously symptomatic class I heart failure, a left ventricular ejection fraction of 40% or less, and a wide QRS interval of at least 120 ms. All were on optimal guideline-recommended medical therapy.

The goal of REVERSE was to learn whether heart failure patients who improved with medications to the point of being asymptomatic or mildly symptomatic could maintain that status with CRT. The answer, Dr. Linde said, is yes.

There was a 10% major complication rate related to the CRT devices in REVERSE. Lead dislocation, perforation of the coronary sinus, and other complications were concentrated in the left ventricular lead during the first year and the right lead in year 2.

The 12-month REVERSE results, presented last year, showed only a nonsignificant trend favoring better outcomes in the CRT-on group. Why the difference a year later?

“It takes time to have an effect in patients with asymptomatic or mildly symptomatic heart failure, so of course when you follow patients for 24 months you're going to find more than if you follow them for 12 months,” she observed.

Today CRT is indicated for patients with class III or ambulatory class IV heart failure. Dr. Linde predicted that if the new REVERSE findings are confirmed in the Automatic Defibrillator Implantation With Cardiac Resynchronization Therapy (MADIT-CRT) trial and Rythmol SR Atrial Fibrillation Trial (RAFT), the indications for CRT will broaden to incorporate the large population of patients with class I and II heart failure along with a low ejection fraction and wide QRS interval.

Discussant Richard L. Page said he found it difficult to reconcile the enhanced LV function and improved clinical outcomes seen with CRT in REVERSE with the observed lack of functional and symptomatic improvement. The CRT on and off groups did not differ significantly at 24 months in the 6-minute walk test, Minnesota Living With Heart Failure Questionnaire, or NYHA class, noted Dr. Page, professor of medicine at the University of Washington, Seattle.

Dr. Jean-Claude Daubert of the REVERSE steering committee replied that since most patients were asymptomatic or mildly symptomatic at entry, there was little room for functional or symptomatic improvement.

“We suspect that to show functional benefit we'll need a much longer follow-up,” said Dr. Daubert, professor of cardiology at Central University Hospital, Rennes, France.

REVERSE was sponsored by Medtronic. Dr. Linde and Dr. Daubert are consultants to, and are on the speakers bureaus for, Medtronic and St. Jude Medical.

ELSEVIER GLOBAL MEDICAL NEWS

ORLANDO — Coupling surgical ventricular reconstruction with coronary artery bypass grafting in patients with severe ischemic heart failure provided no survival or quality of life benefits over surgery alone in the largest randomized trial in cardiac surgery.

“These are definitive findings, and we have to conclude from them that there is no justification to offer [surgical ventricular reconstruction] to these patients, Dr. Robert H. Jones said in presenting the Surgical Treatment for Ischemic Heart Failure (STICH) trial results at the annual meeting of the American College of Cardiology.

STICH, funded by the National Heart, Lung, and Blood Institute, randomized 1,000 patients with left ventricular heart failure, an ejection fraction of 35% or less, and coronary artery disease suitable for coronary artery bypass grafting to CABG alone or CABG plus surgical ventricular reconstruction (SVR), an operation designed to reduce the size of the dilated ventricle and normalize the damaged heart's shape.

During the past decade, SVR has generated excitement among cardiac surgeons, based on the fact that beta-blockers, ACE inhibitors, and other highly effective medications for heart failure make the hypertrophic heart smaller and more normal-shaped. Surgeons reasoned that mechanically reshaping and downsizing the hypertrophic heart might similarly improve clinical outcomes.

“Now we know that it does not,” said Dr. Jones, professor of surgery at Duke University, Durham, N.C. Dr. Jones was the principal investigator for the STICH trial (N. Engl. J. Med. 2009;360:1705-16).

During a median follow-up of 48 months, the primary study end point of all-cause mortality or cardiac hospitalization occurred in 58% of the CABG-plus- SVR group and 59% of those who underwent CABG alone.

The STICH trial included an in-depth quality of life assessment led by Dr. Daniel Mark, director of outcomes research at the Duke Clinical Research Institute.

“We looked at a variety of different ways of assessing quality of life, including heart failure-specific quality of life, and found no evidence that the patients who received SVR on top of their bypass operation did any better or were in any way different in their long-term outcome out to 3 years compared to patients who got bypass surgery alone,” he said.

Hospital costs averaged more than $14,500 higher in the SVR-plus-bypass group, mostly because they spent more time in intensive care, Dr. Mark added.

STICH is a milestone study not only because of its size and clarity, but also because it's the first major comparative effectiveness study examining two different cardiac surgical strategies, he said.

” The tendency of cardiac surgery and, I think, other forms of surgery has been to evolve in an anecdotal fashion,” Dr. Mark said.

Discussant Marvin A. Konstam said that the amount of reduction in end systolic volume achieved in the SVR recipients clearly indicates the STICH surgeons did an effective job of decreasing ventricular wall stress. It is noteworthy that this did not translate into improved outcomes, considering the abundant evidence that doing so pharmacologically does, he said.

This suggests that pharmacologic reduction of end systolic volume by reducing the amount of pathologic myocyte hypertrophy is a very good thing, but when a reduction in end systolic volume is achieved simply structurally it might not have the same benefit, said Dr. Konstam, chief of cardiology at Tufts Medical Center, Boston.

The STICH trial continues, with another 1,212 ischemic heart failure patients who have been randomized to intensive medical therapy alone or in conjunction with CABG. They will be followed for another 2 years. This study has potentially far-reaching impact for all of cardiovascular medicine, Dr. Jones stressed.

“If we find in another 2 years that intensive medical therapy has gotten so good that there's not much room for surgery to further improve outcomes, it's going to change a whole lot of cardiology,” from noninvasive testing to how many cardiac caths get done, he said.

Surgical ventricular reconstruction methods shown here are Dor (A), Jatene (B), McCarthy (C), and Mickleborough (D). ©Elsevier; Reprinted from J. Thorac. Cardiovasc. Surg.; Semin. Thorac. Cardiovasc. Surg.; Ann. Thorac. Surg.

ORLANDO — Coupling surgical ventricular reconstruction with coronary artery bypass grafting in patients with severe ischemic heart failure provided no survival or quality of life benefits over surgery alone in the largest randomized trial in cardiac surgery.

“These are definitive findings, and we have to conclude from them that there is no justification to offer [surgical ventricular reconstruction] to these patients, Dr. Robert H. Jones said in presenting the Surgical Treatment for Ischemic Heart Failure (STICH) trial results at the annual meeting of the American College of Cardiology.

STICH, funded by the National Heart, Lung, and Blood Institute, randomized 1,000 patients with left ventricular heart failure, an ejection fraction of 35% or less, and coronary artery disease suitable for coronary artery bypass grafting to CABG alone or CABG plus surgical ventricular reconstruction (SVR), an operation designed to reduce the size of the dilated ventricle and normalize the damaged heart's shape.

During the past decade, SVR has generated excitement among cardiac surgeons, based on the fact that beta-blockers, ACE inhibitors, and other highly effective medications for heart failure make the hypertrophic heart smaller and more normal-shaped. Surgeons reasoned that mechanically reshaping and downsizing the hypertrophic heart might similarly improve clinical outcomes.

“Now we know that it does not,” said Dr. Jones, professor of surgery at Duke University, Durham, N.C. Dr. Jones was the principal investigator for the STICH trial (N. Engl. J. Med. 2009;360:1705-16).

During a median follow-up of 48 months, the primary study end point of all-cause mortality or cardiac hospitalization occurred in 58% of the CABG-plus- SVR group and 59% of those who underwent CABG alone.

The STICH trial included an in-depth quality of life assessment led by Dr. Daniel Mark, director of outcomes research at the Duke Clinical Research Institute.

“We looked at a variety of different ways of assessing quality of life, including heart failure-specific quality of life, and found no evidence that the patients who received SVR on top of their bypass operation did any better or were in any way different in their long-term outcome out to 3 years compared to patients who got bypass surgery alone,” he said.

Hospital costs averaged more than $14,500 higher in the SVR-plus-bypass group, mostly because they spent more time in intensive care, Dr. Mark added.

STICH is a milestone study not only because of its size and clarity, but also because it's the first major comparative effectiveness study examining two different cardiac surgical strategies, he said.

” The tendency of cardiac surgery and, I think, other forms of surgery has been to evolve in an anecdotal fashion,” Dr. Mark said.

Discussant Marvin A. Konstam said that the amount of reduction in end systolic volume achieved in the SVR recipients clearly indicates the STICH surgeons did an effective job of decreasing ventricular wall stress. It is noteworthy that this did not translate into improved outcomes, considering the abundant evidence that doing so pharmacologically does, he said.

This suggests that pharmacologic reduction of end systolic volume by reducing the amount of pathologic myocyte hypertrophy is a very good thing, but when a reduction in end systolic volume is achieved simply structurally it might not have the same benefit, said Dr. Konstam, chief of cardiology at Tufts Medical Center, Boston.

The STICH trial continues, with another 1,212 ischemic heart failure patients who have been randomized to intensive medical therapy alone or in conjunction with CABG. They will be followed for another 2 years. This study has potentially far-reaching impact for all of cardiovascular medicine, Dr. Jones stressed.

“If we find in another 2 years that intensive medical therapy has gotten so good that there's not much room for surgery to further improve outcomes, it's going to change a whole lot of cardiology,” from noninvasive testing to how many cardiac caths get done, he said.

Surgical ventricular reconstruction methods shown here are Dor (A), Jatene (B), McCarthy (C), and Mickleborough (D). ©Elsevier; Reprinted from J. Thorac. Cardiovasc. Surg.; Semin. Thorac. Cardiovasc. Surg.; Ann. Thorac. Surg.

ORLANDO — Coupling surgical ventricular reconstruction with coronary artery bypass grafting in patients with severe ischemic heart failure provided no survival or quality of life benefits over surgery alone in the largest randomized trial in cardiac surgery.

“These are definitive findings, and we have to conclude from them that there is no justification to offer [surgical ventricular reconstruction] to these patients, Dr. Robert H. Jones said in presenting the Surgical Treatment for Ischemic Heart Failure (STICH) trial results at the annual meeting of the American College of Cardiology.

STICH, funded by the National Heart, Lung, and Blood Institute, randomized 1,000 patients with left ventricular heart failure, an ejection fraction of 35% or less, and coronary artery disease suitable for coronary artery bypass grafting to CABG alone or CABG plus surgical ventricular reconstruction (SVR), an operation designed to reduce the size of the dilated ventricle and normalize the damaged heart's shape.

During the past decade, SVR has generated excitement among cardiac surgeons, based on the fact that beta-blockers, ACE inhibitors, and other highly effective medications for heart failure make the hypertrophic heart smaller and more normal-shaped. Surgeons reasoned that mechanically reshaping and downsizing the hypertrophic heart might similarly improve clinical outcomes.

“Now we know that it does not,” said Dr. Jones, professor of surgery at Duke University, Durham, N.C. Dr. Jones was the principal investigator for the STICH trial (N. Engl. J. Med. 2009;360:1705-16).

During a median follow-up of 48 months, the primary study end point of all-cause mortality or cardiac hospitalization occurred in 58% of the CABG-plus- SVR group and 59% of those who underwent CABG alone.

The STICH trial included an in-depth quality of life assessment led by Dr. Daniel Mark, director of outcomes research at the Duke Clinical Research Institute.

“We looked at a variety of different ways of assessing quality of life, including heart failure-specific quality of life, and found no evidence that the patients who received SVR on top of their bypass operation did any better or were in any way different in their long-term outcome out to 3 years compared to patients who got bypass surgery alone,” he said.

Hospital costs averaged more than $14,500 higher in the SVR-plus-bypass group, mostly because they spent more time in intensive care, Dr. Mark added.

STICH is a milestone study not only because of its size and clarity, but also because it's the first major comparative effectiveness study examining two different cardiac surgical strategies, he said.

” The tendency of cardiac surgery and, I think, other forms of surgery has been to evolve in an anecdotal fashion,” Dr. Mark said.

Discussant Marvin A. Konstam said that the amount of reduction in end systolic volume achieved in the SVR recipients clearly indicates the STICH surgeons did an effective job of decreasing ventricular wall stress. It is noteworthy that this did not translate into improved outcomes, considering the abundant evidence that doing so pharmacologically does, he said.

This suggests that pharmacologic reduction of end systolic volume by reducing the amount of pathologic myocyte hypertrophy is a very good thing, but when a reduction in end systolic volume is achieved simply structurally it might not have the same benefit, said Dr. Konstam, chief of cardiology at Tufts Medical Center, Boston.

The STICH trial continues, with another 1,212 ischemic heart failure patients who have been randomized to intensive medical therapy alone or in conjunction with CABG. They will be followed for another 2 years. This study has potentially far-reaching impact for all of cardiovascular medicine, Dr. Jones stressed.

“If we find in another 2 years that intensive medical therapy has gotten so good that there's not much room for surgery to further improve outcomes, it's going to change a whole lot of cardiology,” from noninvasive testing to how many cardiac caths get done, he said.

Surgical ventricular reconstruction methods shown here are Dor (A), Jatene (B), McCarthy (C), and Mickleborough (D). ©Elsevier; Reprinted from J. Thorac. Cardiovasc. Surg.; Semin. Thorac. Cardiovasc. Surg.; Ann. Thorac. Surg.

The use of brain natriuretic peptide levels to guide heart failure therapy did not reduce hospitalizations or improve quality of life in a study comparing that intensified approach against standard symptom-guided treatment.

In the Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIMECHF), researchers found that contrary to their hypothesis, the new strategy was not helpful overall and was actually harmful in the subgroup of the oldest patients.

The findings indicate that despite the “undisputed diagnostic and prognostic importance” of brain natriuretic peptide (BNP) levels, they are no better than clinical symptom-based judgment for managing heart failure, said Dr. Matthias Pfisterer of University Hospital Basel (Switzerland) and his associates.

The investigators compared the two treatment approaches in 622 outpatients aged 60 and older who were followed for 18 months at 15 medical centers in Switzerland and Germany. Compared with symptom-guided treatment, intensified therapy guided by centrally obtained BNP levels did not improve survival free of hospitalization, the primary end point of the study. The rates of hospitalization-free survival were 41% and 40%, respectively.

Overall survival also did not differ significantly between patients who received BNP-guided therapy (84%) and those who received standard treatment (78%).

Patients aged 60–74 years showed some benefit with the intensified treatment approach, while those aged 75 and older did not (JAMA 2009;301:383–92).

BNP levels are no better than clinical symptom-based judgment for managing heart failure. DR. PFISTERER

The use of brain natriuretic peptide levels to guide heart failure therapy did not reduce hospitalizations or improve quality of life in a study comparing that intensified approach against standard symptom-guided treatment.

In the Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIMECHF), researchers found that contrary to their hypothesis, the new strategy was not helpful overall and was actually harmful in the subgroup of the oldest patients.

The findings indicate that despite the “undisputed diagnostic and prognostic importance” of brain natriuretic peptide (BNP) levels, they are no better than clinical symptom-based judgment for managing heart failure, said Dr. Matthias Pfisterer of University Hospital Basel (Switzerland) and his associates.

The investigators compared the two treatment approaches in 622 outpatients aged 60 and older who were followed for 18 months at 15 medical centers in Switzerland and Germany. Compared with symptom-guided treatment, intensified therapy guided by centrally obtained BNP levels did not improve survival free of hospitalization, the primary end point of the study. The rates of hospitalization-free survival were 41% and 40%, respectively.

Overall survival also did not differ significantly between patients who received BNP-guided therapy (84%) and those who received standard treatment (78%).

Patients aged 60–74 years showed some benefit with the intensified treatment approach, while those aged 75 and older did not (JAMA 2009;301:383–92).

BNP levels are no better than clinical symptom-based judgment for managing heart failure. DR. PFISTERER

The use of brain natriuretic peptide levels to guide heart failure therapy did not reduce hospitalizations or improve quality of life in a study comparing that intensified approach against standard symptom-guided treatment.

In the Trial of Intensified vs. Standard Medical Therapy in Elderly Patients With Congestive Heart Failure (TIMECHF), researchers found that contrary to their hypothesis, the new strategy was not helpful overall and was actually harmful in the subgroup of the oldest patients.

The findings indicate that despite the “undisputed diagnostic and prognostic importance” of brain natriuretic peptide (BNP) levels, they are no better than clinical symptom-based judgment for managing heart failure, said Dr. Matthias Pfisterer of University Hospital Basel (Switzerland) and his associates.

The investigators compared the two treatment approaches in 622 outpatients aged 60 and older who were followed for 18 months at 15 medical centers in Switzerland and Germany. Compared with symptom-guided treatment, intensified therapy guided by centrally obtained BNP levels did not improve survival free of hospitalization, the primary end point of the study. The rates of hospitalization-free survival were 41% and 40%, respectively.

Overall survival also did not differ significantly between patients who received BNP-guided therapy (84%) and those who received standard treatment (78%).

Patients aged 60–74 years showed some benefit with the intensified treatment approach, while those aged 75 and older did not (JAMA 2009;301:383–92).

BNP levels are no better than clinical symptom-based judgment for managing heart failure. DR. PFISTERER

SAN FRANCISCO — Heart transplant recipients who were bridged to transplant with an implantable left ventricular assist device showed similar survival to patients who were treated with inotrope-only support, in a retrospective study.

From 1994 to 2007, 173 status 1 patients received orthotopic heart transplants after inotrope-only (IO) support, and 86 patients received transplants after support with an LVAD used as a bridge to transplant, Dr. Jay D. Pal reported at the annual meeting of the Society of Thoracic Surgeons.

Baseline characteristics were similar between the IO and the LVAD patients at the time of transplant. But prior to LVAD implantation, this group of patients had significantly worse hemodynamics. “During the period of LVAD support, cardiopulmonary status improved to become equivalent to the inotropic-bridged patients,” noted Dr. Pal and his colleagues at Duke University, Durham, N.C.

Survival at 1 year after transplant was similar in both groups (88% in the IO patients vs. 85% in the LVAD group) and at 5 years (76% of IO vs. 73% of LVAD). Infectious complications after transplant were also similar in both groups.

The likelihood of a rejection episode during the first year post transplant was also similar (44% IO vs. 52% LVAD).

“Bridge to transplant with an implantable LVAD device provides comparable outcomes to status 1 patients who were stabilized on inotrope infusion only,” the researchers said. This is despite the fact that patients bridged to transplant with an LVAD represent a subset of patients who deteriorated on maximal medical therapy, according to Dr. Pal, who had no disclosures to report.

SAN FRANCISCO — Heart transplant recipients who were bridged to transplant with an implantable left ventricular assist device showed similar survival to patients who were treated with inotrope-only support, in a retrospective study.

From 1994 to 2007, 173 status 1 patients received orthotopic heart transplants after inotrope-only (IO) support, and 86 patients received transplants after support with an LVAD used as a bridge to transplant, Dr. Jay D. Pal reported at the annual meeting of the Society of Thoracic Surgeons.

Baseline characteristics were similar between the IO and the LVAD patients at the time of transplant. But prior to LVAD implantation, this group of patients had significantly worse hemodynamics. “During the period of LVAD support, cardiopulmonary status improved to become equivalent to the inotropic-bridged patients,” noted Dr. Pal and his colleagues at Duke University, Durham, N.C.

Survival at 1 year after transplant was similar in both groups (88% in the IO patients vs. 85% in the LVAD group) and at 5 years (76% of IO vs. 73% of LVAD). Infectious complications after transplant were also similar in both groups.

The likelihood of a rejection episode during the first year post transplant was also similar (44% IO vs. 52% LVAD).

“Bridge to transplant with an implantable LVAD device provides comparable outcomes to status 1 patients who were stabilized on inotrope infusion only,” the researchers said. This is despite the fact that patients bridged to transplant with an LVAD represent a subset of patients who deteriorated on maximal medical therapy, according to Dr. Pal, who had no disclosures to report.

SAN FRANCISCO — Heart transplant recipients who were bridged to transplant with an implantable left ventricular assist device showed similar survival to patients who were treated with inotrope-only support, in a retrospective study.

From 1994 to 2007, 173 status 1 patients received orthotopic heart transplants after inotrope-only (IO) support, and 86 patients received transplants after support with an LVAD used as a bridge to transplant, Dr. Jay D. Pal reported at the annual meeting of the Society of Thoracic Surgeons.

Baseline characteristics were similar between the IO and the LVAD patients at the time of transplant. But prior to LVAD implantation, this group of patients had significantly worse hemodynamics. “During the period of LVAD support, cardiopulmonary status improved to become equivalent to the inotropic-bridged patients,” noted Dr. Pal and his colleagues at Duke University, Durham, N.C.

Survival at 1 year after transplant was similar in both groups (88% in the IO patients vs. 85% in the LVAD group) and at 5 years (76% of IO vs. 73% of LVAD). Infectious complications after transplant were also similar in both groups.

The likelihood of a rejection episode during the first year post transplant was also similar (44% IO vs. 52% LVAD).

“Bridge to transplant with an implantable LVAD device provides comparable outcomes to status 1 patients who were stabilized on inotrope infusion only,” the researchers said. This is despite the fact that patients bridged to transplant with an LVAD represent a subset of patients who deteriorated on maximal medical therapy, according to Dr. Pal, who had no disclosures to report.

NEW ORLEANS — The annual number of Americans aged 65 or older hospitalized for heart failure jumped more than 230% between 1980 and 2006.

“Heart failure has reached epidemic levels. The prevention and treatment of heart failure have become an urgent public health need with national implications,” Dr. Longjian Liu declared in presenting his analysis of 27 years' worth of National Hospital Discharge Surveys.

And the peak of the epidemic has yet to come.

As steep as the rise in heart failure cases has been since 1980, the rate of increase will become even more pronounced in the near future, Dr. Liu said at the annual scientific sessions of the American Heart Association.

This trend is due to a combination of factors, including the explosive growth in the prevalences of diabetes, obesity, and chronic kidney disease; improved survival after myocardial infarction; and the graying of America.

Indeed, the aging of the baby boomers will have an enormous impact on the heart failure epidemic. In Dr. Liu's study of the 1980–2006 U.S. experience, which included more than 2.2 million hospitalized patients over age 65 years, individuals aged 75–84 had an adjusted 2.3-fold greater rate of hospitalization for heart failure than those aged 65–69. Those aged 85 and up had a 4.1-fold greater rate than the 65- to 69-year-olds, and these oldest of the elderly constitute the fastest-growing segment of the U.S. population.

“The reality about heart failure is that the burden of disease will definitely increase for the next 1, 2, and 3 decades,” observed Dr. Liu of the Drexel University School of Public Health, Philadelphia.

For men aged 65 and older, the rate of hospitalization for heart failure rose from 16.6 hospitalizations per 1,000 in 1980 to 22.9 in 2006. Among women, the rate was 13.9 per 1,000 in 1980 and 19.6 in 2006. The age-adjusted rate of hospitalization for heart failure increased by an average of 1.2% annually in men and 1.55% per year in women.

Men were an adjusted 16% more likely than women to be hospitalized for heart failure. But because women have a longer life expectancy and hence a greater opportunity to develop heart failure, the absolute number of women hospitalized for the disease in any given year was substantially greater, the physician explained.

The relative risk of being hospitalized for heart failure among seniors alive during the last 5 years of the study period was 37% greater than for those living in 1980–1984.

The American Heart Association estimates that at present 660,000 new cases of heart failure are diagnosed per year, and 5.3 million Americans are living with the disease. Heart failure is the number one cause of hospitalization in the Medicare population.

NEW ORLEANS — The annual number of Americans aged 65 or older hospitalized for heart failure jumped more than 230% between 1980 and 2006.

“Heart failure has reached epidemic levels. The prevention and treatment of heart failure have become an urgent public health need with national implications,” Dr. Longjian Liu declared in presenting his analysis of 27 years' worth of National Hospital Discharge Surveys.

And the peak of the epidemic has yet to come.

As steep as the rise in heart failure cases has been since 1980, the rate of increase will become even more pronounced in the near future, Dr. Liu said at the annual scientific sessions of the American Heart Association.

This trend is due to a combination of factors, including the explosive growth in the prevalences of diabetes, obesity, and chronic kidney disease; improved survival after myocardial infarction; and the graying of America.

Indeed, the aging of the baby boomers will have an enormous impact on the heart failure epidemic. In Dr. Liu's study of the 1980–2006 U.S. experience, which included more than 2.2 million hospitalized patients over age 65 years, individuals aged 75–84 had an adjusted 2.3-fold greater rate of hospitalization for heart failure than those aged 65–69. Those aged 85 and up had a 4.1-fold greater rate than the 65- to 69-year-olds, and these oldest of the elderly constitute the fastest-growing segment of the U.S. population.

“The reality about heart failure is that the burden of disease will definitely increase for the next 1, 2, and 3 decades,” observed Dr. Liu of the Drexel University School of Public Health, Philadelphia.

For men aged 65 and older, the rate of hospitalization for heart failure rose from 16.6 hospitalizations per 1,000 in 1980 to 22.9 in 2006. Among women, the rate was 13.9 per 1,000 in 1980 and 19.6 in 2006. The age-adjusted rate of hospitalization for heart failure increased by an average of 1.2% annually in men and 1.55% per year in women.

Men were an adjusted 16% more likely than women to be hospitalized for heart failure. But because women have a longer life expectancy and hence a greater opportunity to develop heart failure, the absolute number of women hospitalized for the disease in any given year was substantially greater, the physician explained.

The relative risk of being hospitalized for heart failure among seniors alive during the last 5 years of the study period was 37% greater than for those living in 1980–1984.

The American Heart Association estimates that at present 660,000 new cases of heart failure are diagnosed per year, and 5.3 million Americans are living with the disease. Heart failure is the number one cause of hospitalization in the Medicare population.

NEW ORLEANS — The annual number of Americans aged 65 or older hospitalized for heart failure jumped more than 230% between 1980 and 2006.

“Heart failure has reached epidemic levels. The prevention and treatment of heart failure have become an urgent public health need with national implications,” Dr. Longjian Liu declared in presenting his analysis of 27 years' worth of National Hospital Discharge Surveys.

And the peak of the epidemic has yet to come.

As steep as the rise in heart failure cases has been since 1980, the rate of increase will become even more pronounced in the near future, Dr. Liu said at the annual scientific sessions of the American Heart Association.

This trend is due to a combination of factors, including the explosive growth in the prevalences of diabetes, obesity, and chronic kidney disease; improved survival after myocardial infarction; and the graying of America.

Indeed, the aging of the baby boomers will have an enormous impact on the heart failure epidemic. In Dr. Liu's study of the 1980–2006 U.S. experience, which included more than 2.2 million hospitalized patients over age 65 years, individuals aged 75–84 had an adjusted 2.3-fold greater rate of hospitalization for heart failure than those aged 65–69. Those aged 85 and up had a 4.1-fold greater rate than the 65- to 69-year-olds, and these oldest of the elderly constitute the fastest-growing segment of the U.S. population.

“The reality about heart failure is that the burden of disease will definitely increase for the next 1, 2, and 3 decades,” observed Dr. Liu of the Drexel University School of Public Health, Philadelphia.

For men aged 65 and older, the rate of hospitalization for heart failure rose from 16.6 hospitalizations per 1,000 in 1980 to 22.9 in 2006. Among women, the rate was 13.9 per 1,000 in 1980 and 19.6 in 2006. The age-adjusted rate of hospitalization for heart failure increased by an average of 1.2% annually in men and 1.55% per year in women.

Men were an adjusted 16% more likely than women to be hospitalized for heart failure. But because women have a longer life expectancy and hence a greater opportunity to develop heart failure, the absolute number of women hospitalized for the disease in any given year was substantially greater, the physician explained.

The relative risk of being hospitalized for heart failure among seniors alive during the last 5 years of the study period was 37% greater than for those living in 1980–1984.

The American Heart Association estimates that at present 660,000 new cases of heart failure are diagnosed per year, and 5.3 million Americans are living with the disease. Heart failure is the number one cause of hospitalization in the Medicare population.

NEW ORLEANS — Preclinical diastolic dysfunction was highly prevalent among patients with diabetes, occurring in 24% of more than 1,700 largely unselected patients in a retrospective study.

Diastolic dysfunction without any clinical manifestations in patients with either type 1 or type 2 diabetes also had substantial clinical consequences, leading to a significantly increased rate of both heart failure and all-cause mortality during up to 5 years of follow-up, Dr. Aaron M. From reported at the annual scientific sessions of the American Heart Association.

Because the increased risk for heart failure in patients with diabetes and diastolic dysfunction was independent of both hypertension and coronary artery disease, “we suspect that the cardiomyopathy may be a direct consequence of diabetes itself,” said Dr. From, a cardiologist at the Mayo Clinic in Rochester, Minn.

He and his associates studied the natural history of preclinical diastolic dysfunction in diabetes patients by reviewing the records of 2,770 patients with type 1 or type 2 diabetes who were residents of Olmsted County, Minn., and who had an echocardiographic exam at the Mayo Clinic during 1996–2006. The analysis excluded 975 patients who were diagnosed with heart failure within 30 days of their echo exam, and 1 patient with severe heart-valve regurgitation, leaving 1,794 in the analysis. The patients' average age was 60, about half were women, their average body mass index was 33 kg/m

Diastolic dysfunction was identified by calculating the ratio of a patient's early mitral filling velocity—the E wave—and the mitral annulus velocity—the e: wave—obtained from the echo results. If the E/e: ratio was more than 15, the patient was deemed to have diastolic dysfunction. Using this criterion, 431 (24%) of the 1,784 patients with diabetes had diastolic dysfunction at the time of their echo exam. Subsequent development of heart failure was identified by finding ICD-9 code 428 in the patient's record.

Clinical follow-up data were available for an average of 2.7 years following the echo exam, and for periods as long as 5 years. During follow-up, the rate of new-onset heart failure was 37% in patients with diastolic dysfunction at baseline and 17% in those without diastolic dysfunction, a statistically significant difference, said Dr. From, who reported that he and his coauthors had no conflicts of interest related to the study.

In a multivariate analysis controlling for baseline differences in age, sex, body mass index, hypertension, coronary disease, ejection fraction, left atrial volume, and deceleration time, diabetes patients with diastolic dysfunction were 67% more likely to develop heart failure.

During up to 5 years of follow-up, the rate of death from any cause was 33% in patients with diastolic dysfunction at baseline and 13% in those without dysfunction, also a significant difference. In a multivariate analysis that controlled for the same baseline variables, patients with diastolic dysfunction had an 88% higher risk of dying from any cause than did patients without dysfunction at the time of their echo exam.

NEW ORLEANS — Preclinical diastolic dysfunction was highly prevalent among patients with diabetes, occurring in 24% of more than 1,700 largely unselected patients in a retrospective study.

Diastolic dysfunction without any clinical manifestations in patients with either type 1 or type 2 diabetes also had substantial clinical consequences, leading to a significantly increased rate of both heart failure and all-cause mortality during up to 5 years of follow-up, Dr. Aaron M. From reported at the annual scientific sessions of the American Heart Association.

Because the increased risk for heart failure in patients with diabetes and diastolic dysfunction was independent of both hypertension and coronary artery disease, “we suspect that the cardiomyopathy may be a direct consequence of diabetes itself,” said Dr. From, a cardiologist at the Mayo Clinic in Rochester, Minn.

He and his associates studied the natural history of preclinical diastolic dysfunction in diabetes patients by reviewing the records of 2,770 patients with type 1 or type 2 diabetes who were residents of Olmsted County, Minn., and who had an echocardiographic exam at the Mayo Clinic during 1996–2006. The analysis excluded 975 patients who were diagnosed with heart failure within 30 days of their echo exam, and 1 patient with severe heart-valve regurgitation, leaving 1,794 in the analysis. The patients' average age was 60, about half were women, their average body mass index was 33 kg/m

Diastolic dysfunction was identified by calculating the ratio of a patient's early mitral filling velocity—the E wave—and the mitral annulus velocity—the e: wave—obtained from the echo results. If the E/e: ratio was more than 15, the patient was deemed to have diastolic dysfunction. Using this criterion, 431 (24%) of the 1,784 patients with diabetes had diastolic dysfunction at the time of their echo exam. Subsequent development of heart failure was identified by finding ICD-9 code 428 in the patient's record.

Clinical follow-up data were available for an average of 2.7 years following the echo exam, and for periods as long as 5 years. During follow-up, the rate of new-onset heart failure was 37% in patients with diastolic dysfunction at baseline and 17% in those without diastolic dysfunction, a statistically significant difference, said Dr. From, who reported that he and his coauthors had no conflicts of interest related to the study.

In a multivariate analysis controlling for baseline differences in age, sex, body mass index, hypertension, coronary disease, ejection fraction, left atrial volume, and deceleration time, diabetes patients with diastolic dysfunction were 67% more likely to develop heart failure.

During up to 5 years of follow-up, the rate of death from any cause was 33% in patients with diastolic dysfunction at baseline and 13% in those without dysfunction, also a significant difference. In a multivariate analysis that controlled for the same baseline variables, patients with diastolic dysfunction had an 88% higher risk of dying from any cause than did patients without dysfunction at the time of their echo exam.

NEW ORLEANS — Preclinical diastolic dysfunction was highly prevalent among patients with diabetes, occurring in 24% of more than 1,700 largely unselected patients in a retrospective study.

Diastolic dysfunction without any clinical manifestations in patients with either type 1 or type 2 diabetes also had substantial clinical consequences, leading to a significantly increased rate of both heart failure and all-cause mortality during up to 5 years of follow-up, Dr. Aaron M. From reported at the annual scientific sessions of the American Heart Association.

Because the increased risk for heart failure in patients with diabetes and diastolic dysfunction was independent of both hypertension and coronary artery disease, “we suspect that the cardiomyopathy may be a direct consequence of diabetes itself,” said Dr. From, a cardiologist at the Mayo Clinic in Rochester, Minn.

He and his associates studied the natural history of preclinical diastolic dysfunction in diabetes patients by reviewing the records of 2,770 patients with type 1 or type 2 diabetes who were residents of Olmsted County, Minn., and who had an echocardiographic exam at the Mayo Clinic during 1996–2006. The analysis excluded 975 patients who were diagnosed with heart failure within 30 days of their echo exam, and 1 patient with severe heart-valve regurgitation, leaving 1,794 in the analysis. The patients' average age was 60, about half were women, their average body mass index was 33 kg/m

Diastolic dysfunction was identified by calculating the ratio of a patient's early mitral filling velocity—the E wave—and the mitral annulus velocity—the e: wave—obtained from the echo results. If the E/e: ratio was more than 15, the patient was deemed to have diastolic dysfunction. Using this criterion, 431 (24%) of the 1,784 patients with diabetes had diastolic dysfunction at the time of their echo exam. Subsequent development of heart failure was identified by finding ICD-9 code 428 in the patient's record.

Clinical follow-up data were available for an average of 2.7 years following the echo exam, and for periods as long as 5 years. During follow-up, the rate of new-onset heart failure was 37% in patients with diastolic dysfunction at baseline and 17% in those without diastolic dysfunction, a statistically significant difference, said Dr. From, who reported that he and his coauthors had no conflicts of interest related to the study.

In a multivariate analysis controlling for baseline differences in age, sex, body mass index, hypertension, coronary disease, ejection fraction, left atrial volume, and deceleration time, diabetes patients with diastolic dysfunction were 67% more likely to develop heart failure.

During up to 5 years of follow-up, the rate of death from any cause was 33% in patients with diastolic dysfunction at baseline and 13% in those without dysfunction, also a significant difference. In a multivariate analysis that controlled for the same baseline variables, patients with diastolic dysfunction had an 88% higher risk of dying from any cause than did patients without dysfunction at the time of their echo exam.

NEW ORLEANS — Medicare beneficiaries with heart failure see an average of 16–23 different physicians annually, depending upon the severity of their heart failure.

This finding, based on extrapolation from fiscal year 2005 data on a representative sample of more than 1.7 million Medicare beneficiaries, underscores the need to develop systems and processes of coordinated care for the nation's more than 5 million heart failure patients, Robert L. Page II, Pharm.D., said at the annual scientific sessions of the American Heart Association.

Better-coordinated care is the key to avoiding duplication of services, improving care, and reining in health care costs in the heart failure population. In 2005, patients with heart failure accounted for 37% of all Medicare spending and nearly 50% of all inpatient costs, added Dr. Page of the University of Colorado, Denver.

The overall Medicare population, more than 34 million strong, saw an average of 7.9 different physicians in 2005. In contrast, Medicare beneficiaries with mild heart failure saw an average of 15.9 physicians that year. Those with moderate heart failure saw an average of 18.6 different physicians, while the more than 537,000 patients with severe heart failure saw an average of 23. The average number of physicians who ordered care for these patients ranged from 8.3 to 11.2, depending on heart failure severity.

Heart failure patients saw an average of 5.8–11 different physicians in the inpatient setting over the course of the year. Only 10% of all outpatient physician visits by patients with mild heart failure were specifically for their heart failure. Among patients with moderate or severe heart failure, this figure was 20%. The other 80%-90% of outpatient visits were driven largely by the numerous comorbidities present in the heart failure population. (See box.)

Close to half of all outpatient care for Medicare beneficiaries with heart failure was provided by internists and family physicians. Cardiologists handled 16%-20% of all outpatient visits, with the proportion climbing as severity of heart failure increased.

As severity of heart failure increased, so did total costs of care and the proportion of those costs devoted to inpatient or emergency department care. There were significant racial and sex differences in this spending. For example, total 2005 costs of care in black men with mild, moderate, and severe heart failure averaged $35,106, $43,536, and $55,457, respectively, compared with $26,433, $30,536, and $44,433 in white men. Costs in black women with heart failure were lower than in black men but higher than in white men. Costs in white women were lowest of all.

ELESEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Medicare beneficiaries with heart failure see an average of 16–23 different physicians annually, depending upon the severity of their heart failure.

This finding, based on extrapolation from fiscal year 2005 data on a representative sample of more than 1.7 million Medicare beneficiaries, underscores the need to develop systems and processes of coordinated care for the nation's more than 5 million heart failure patients, Robert L. Page II, Pharm.D., said at the annual scientific sessions of the American Heart Association.

Better-coordinated care is the key to avoiding duplication of services, improving care, and reining in health care costs in the heart failure population. In 2005, patients with heart failure accounted for 37% of all Medicare spending and nearly 50% of all inpatient costs, added Dr. Page of the University of Colorado, Denver.

The overall Medicare population, more than 34 million strong, saw an average of 7.9 different physicians in 2005. In contrast, Medicare beneficiaries with mild heart failure saw an average of 15.9 physicians that year. Those with moderate heart failure saw an average of 18.6 different physicians, while the more than 537,000 patients with severe heart failure saw an average of 23. The average number of physicians who ordered care for these patients ranged from 8.3 to 11.2, depending on heart failure severity.

Heart failure patients saw an average of 5.8–11 different physicians in the inpatient setting over the course of the year. Only 10% of all outpatient physician visits by patients with mild heart failure were specifically for their heart failure. Among patients with moderate or severe heart failure, this figure was 20%. The other 80%-90% of outpatient visits were driven largely by the numerous comorbidities present in the heart failure population. (See box.)

Close to half of all outpatient care for Medicare beneficiaries with heart failure was provided by internists and family physicians. Cardiologists handled 16%-20% of all outpatient visits, with the proportion climbing as severity of heart failure increased.

As severity of heart failure increased, so did total costs of care and the proportion of those costs devoted to inpatient or emergency department care. There were significant racial and sex differences in this spending. For example, total 2005 costs of care in black men with mild, moderate, and severe heart failure averaged $35,106, $43,536, and $55,457, respectively, compared with $26,433, $30,536, and $44,433 in white men. Costs in black women with heart failure were lower than in black men but higher than in white men. Costs in white women were lowest of all.

ELESEVIER GLOBAL MEDICAL NEWS

NEW ORLEANS — Medicare beneficiaries with heart failure see an average of 16–23 different physicians annually, depending upon the severity of their heart failure.

This finding, based on extrapolation from fiscal year 2005 data on a representative sample of more than 1.7 million Medicare beneficiaries, underscores the need to develop systems and processes of coordinated care for the nation's more than 5 million heart failure patients, Robert L. Page II, Pharm.D., said at the annual scientific sessions of the American Heart Association.

Better-coordinated care is the key to avoiding duplication of services, improving care, and reining in health care costs in the heart failure population. In 2005, patients with heart failure accounted for 37% of all Medicare spending and nearly 50% of all inpatient costs, added Dr. Page of the University of Colorado, Denver.

The overall Medicare population, more than 34 million strong, saw an average of 7.9 different physicians in 2005. In contrast, Medicare beneficiaries with mild heart failure saw an average of 15.9 physicians that year. Those with moderate heart failure saw an average of 18.6 different physicians, while the more than 537,000 patients with severe heart failure saw an average of 23. The average number of physicians who ordered care for these patients ranged from 8.3 to 11.2, depending on heart failure severity.

Heart failure patients saw an average of 5.8–11 different physicians in the inpatient setting over the course of the year. Only 10% of all outpatient physician visits by patients with mild heart failure were specifically for their heart failure. Among patients with moderate or severe heart failure, this figure was 20%. The other 80%-90% of outpatient visits were driven largely by the numerous comorbidities present in the heart failure population. (See box.)

Close to half of all outpatient care for Medicare beneficiaries with heart failure was provided by internists and family physicians. Cardiologists handled 16%-20% of all outpatient visits, with the proportion climbing as severity of heart failure increased.

As severity of heart failure increased, so did total costs of care and the proportion of those costs devoted to inpatient or emergency department care. There were significant racial and sex differences in this spending. For example, total 2005 costs of care in black men with mild, moderate, and severe heart failure averaged $35,106, $43,536, and $55,457, respectively, compared with $26,433, $30,536, and $44,433 in white men. Costs in black women with heart failure were lower than in black men but higher than in white men. Costs in white women were lowest of all.

ELESEVIER GLOBAL MEDICAL NEWS