Heart Failure

ORLANDO, FLA. — Starting heart failure patients on a β-blocker and an ACE inhibitor before hospital discharge increases the likelihood of adherence at follow-up 60-90 days later, Gregg C. Fonarow, M.D., reported at the annual meeting of the American College of Cardiology.

This tells us “that hospitalization can serve as a teachable moment for patients and clinicians regarding heart failure medications, that patients can be effectively initiated on these evidence-based therapies, and if they're started in the hospital they're much more likely to be on treatment during long-term follow-up,” he said.

“We need to provide for all patients hospitalized with heart failure a systematic approach to ensure that the evidence-based therapies are started prior to discharge,” said Dr. Fonarow, professor of cardiovascular medicine at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.

He presented data on 4,434 patients with systolic heart failure (HF) treated at 86 hospitals participating in the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry, a national quality-improvement project.

None of the patients in this subset of the larger OPTIMIZE-HF database had contraindications to β-blockers or ACE inhibitors/angiotensin receptor blockers (ARBs). Of the 86% discharged on a β-blocker, 95% remained on β-blocker therapy at follow-up 60-90 days post discharge, compared with 32% of patients who were not yet on a β-blocker at discharge.

“That means two-thirds of these eligible patients [discharged without β-blocker] remained untreated with what is our single most important life-saving therapy in heart failure: β-blocker treatment,” said Dr. Fonarow, director of OPTIMIZE-HF.

The same was true for ACE inhibitors/ARBs: 84% of eligible patients were on one of these drugs at discharge, and 74% of this group remained on the medication at 60-90 days. Only 19% of patients not discharged on one of these drugs were taking one at follow-up.

“Many clinicians have kind of had the view, 'Well, we don't need to worry about starting treatment in the hospital, we'll get around to it on an outpatient basis.' There hasn't necessarily been a consensus that each of these therapies needs to be started prior to hospital discharge,” Dr. Fonarow said.

But that's changing fast, in large part because of the evidence gathered in OPTIMIZE-HF. At the ACC meeting, the American Heart Association launched a new nationwide, hospital-based, quality-improvement project called Get With The Guidelines-Heart Failure (GWTG-HF).

The program, aimed at accelerating adherence to ACC/AHA treatment guidelines, uses techniques similar to those in the OPTIMIZE-HF registry, including decision-support tools, customized patient education materials, real-time performance benchmarking, and collaborative workshops. Dr. Fonarow is chairman of the GWTG Science Subcommittee. “We hope that hospitals across the country will sign up and participate.” Get With The Guidelines-Coronary Artery Disease has been in place for 2 years and “has shown remarkable improvements in care and is currently in more than 300 U.S. hospitals.”

With 5 million Americans currently diagnosed with HF, and the ranks expected to swell further as baby boomers age, this type of systems approach is badly needed, according to John S. Rumsfeld, M.D., who chaired a session on quality-improvement programs at the ACC meeting.

“We can have all sorts of late-breaking clinical trials telling us about better care, but if we don't apply them, we won't actually be improving our population outcomes,” noted Dr. Rumsfeld of the University of Colorado, Denver.

Dr. Fonarow is a consultant to and member of the speakers' bureau for GlaxoSmithKline Inc., which funds bothGWTG-HF and OPTIMIZE-HF.

ORLANDO, FLA. — Starting heart failure patients on a β-blocker and an ACE inhibitor before hospital discharge increases the likelihood of adherence at follow-up 60-90 days later, Gregg C. Fonarow, M.D., reported at the annual meeting of the American College of Cardiology.

This tells us “that hospitalization can serve as a teachable moment for patients and clinicians regarding heart failure medications, that patients can be effectively initiated on these evidence-based therapies, and if they're started in the hospital they're much more likely to be on treatment during long-term follow-up,” he said.

“We need to provide for all patients hospitalized with heart failure a systematic approach to ensure that the evidence-based therapies are started prior to discharge,” said Dr. Fonarow, professor of cardiovascular medicine at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.

He presented data on 4,434 patients with systolic heart failure (HF) treated at 86 hospitals participating in the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry, a national quality-improvement project.

None of the patients in this subset of the larger OPTIMIZE-HF database had contraindications to β-blockers or ACE inhibitors/angiotensin receptor blockers (ARBs). Of the 86% discharged on a β-blocker, 95% remained on β-blocker therapy at follow-up 60-90 days post discharge, compared with 32% of patients who were not yet on a β-blocker at discharge.

“That means two-thirds of these eligible patients [discharged without β-blocker] remained untreated with what is our single most important life-saving therapy in heart failure: β-blocker treatment,” said Dr. Fonarow, director of OPTIMIZE-HF.

The same was true for ACE inhibitors/ARBs: 84% of eligible patients were on one of these drugs at discharge, and 74% of this group remained on the medication at 60-90 days. Only 19% of patients not discharged on one of these drugs were taking one at follow-up.

“Many clinicians have kind of had the view, 'Well, we don't need to worry about starting treatment in the hospital, we'll get around to it on an outpatient basis.' There hasn't necessarily been a consensus that each of these therapies needs to be started prior to hospital discharge,” Dr. Fonarow said.

But that's changing fast, in large part because of the evidence gathered in OPTIMIZE-HF. At the ACC meeting, the American Heart Association launched a new nationwide, hospital-based, quality-improvement project called Get With The Guidelines-Heart Failure (GWTG-HF).

The program, aimed at accelerating adherence to ACC/AHA treatment guidelines, uses techniques similar to those in the OPTIMIZE-HF registry, including decision-support tools, customized patient education materials, real-time performance benchmarking, and collaborative workshops. Dr. Fonarow is chairman of the GWTG Science Subcommittee. “We hope that hospitals across the country will sign up and participate.” Get With The Guidelines-Coronary Artery Disease has been in place for 2 years and “has shown remarkable improvements in care and is currently in more than 300 U.S. hospitals.”

With 5 million Americans currently diagnosed with HF, and the ranks expected to swell further as baby boomers age, this type of systems approach is badly needed, according to John S. Rumsfeld, M.D., who chaired a session on quality-improvement programs at the ACC meeting.

“We can have all sorts of late-breaking clinical trials telling us about better care, but if we don't apply them, we won't actually be improving our population outcomes,” noted Dr. Rumsfeld of the University of Colorado, Denver.

Dr. Fonarow is a consultant to and member of the speakers' bureau for GlaxoSmithKline Inc., which funds bothGWTG-HF and OPTIMIZE-HF.

ORLANDO, FLA. — Starting heart failure patients on a β-blocker and an ACE inhibitor before hospital discharge increases the likelihood of adherence at follow-up 60-90 days later, Gregg C. Fonarow, M.D., reported at the annual meeting of the American College of Cardiology.

This tells us “that hospitalization can serve as a teachable moment for patients and clinicians regarding heart failure medications, that patients can be effectively initiated on these evidence-based therapies, and if they're started in the hospital they're much more likely to be on treatment during long-term follow-up,” he said.

“We need to provide for all patients hospitalized with heart failure a systematic approach to ensure that the evidence-based therapies are started prior to discharge,” said Dr. Fonarow, professor of cardiovascular medicine at the University of California, Los Angeles, and director of the Ahmanson-UCLA Cardiomyopathy Center.

He presented data on 4,434 patients with systolic heart failure (HF) treated at 86 hospitals participating in the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) registry, a national quality-improvement project.

None of the patients in this subset of the larger OPTIMIZE-HF database had contraindications to β-blockers or ACE inhibitors/angiotensin receptor blockers (ARBs). Of the 86% discharged on a β-blocker, 95% remained on β-blocker therapy at follow-up 60-90 days post discharge, compared with 32% of patients who were not yet on a β-blocker at discharge.

“That means two-thirds of these eligible patients [discharged without β-blocker] remained untreated with what is our single most important life-saving therapy in heart failure: β-blocker treatment,” said Dr. Fonarow, director of OPTIMIZE-HF.

The same was true for ACE inhibitors/ARBs: 84% of eligible patients were on one of these drugs at discharge, and 74% of this group remained on the medication at 60-90 days. Only 19% of patients not discharged on one of these drugs were taking one at follow-up.

“Many clinicians have kind of had the view, 'Well, we don't need to worry about starting treatment in the hospital, we'll get around to it on an outpatient basis.' There hasn't necessarily been a consensus that each of these therapies needs to be started prior to hospital discharge,” Dr. Fonarow said.

But that's changing fast, in large part because of the evidence gathered in OPTIMIZE-HF. At the ACC meeting, the American Heart Association launched a new nationwide, hospital-based, quality-improvement project called Get With The Guidelines-Heart Failure (GWTG-HF).

The program, aimed at accelerating adherence to ACC/AHA treatment guidelines, uses techniques similar to those in the OPTIMIZE-HF registry, including decision-support tools, customized patient education materials, real-time performance benchmarking, and collaborative workshops. Dr. Fonarow is chairman of the GWTG Science Subcommittee. “We hope that hospitals across the country will sign up and participate.” Get With The Guidelines-Coronary Artery Disease has been in place for 2 years and “has shown remarkable improvements in care and is currently in more than 300 U.S. hospitals.”

With 5 million Americans currently diagnosed with HF, and the ranks expected to swell further as baby boomers age, this type of systems approach is badly needed, according to John S. Rumsfeld, M.D., who chaired a session on quality-improvement programs at the ACC meeting.

“We can have all sorts of late-breaking clinical trials telling us about better care, but if we don't apply them, we won't actually be improving our population outcomes,” noted Dr. Rumsfeld of the University of Colorado, Denver.

Dr. Fonarow is a consultant to and member of the speakers' bureau for GlaxoSmithKline Inc., which funds bothGWTG-HF and OPTIMIZE-HF.

TORONTO — Intracoronary transfer of autologous bone marrow cells led to improved left ventricular function after acute MI in a randomized trial.

After 6 months, there was a highly significant increase in mean left ventricular ejection fractions (LVEFs) in acute MI patients after intracoronary injection of bone marrow cells, according to data from the Bone Marrow Transfer to Enhance ST-Elevation Infarct Regeneration (BOOST) study. But treatment did not appear to affect left ventricular remodeling.

“The results from the BOOST trial indicate that intracoronary transfer of autologous bone marrow cells is safe, and enhances left ventricular function” after an MI, Kai Wollert, M.D., said at the annual meeting of the Heart Failure Society of America.

Emerging evidence suggests that direct injection of stem cells and progenitor cells derived from bone marrow can improve cardiac function in patients after acute MI. Although only 30 patients were treated with bone marrow cells in the BOOST trial, the results are promising, said Dr. Wollert of Hannover (Germany) Medical School.

“Subgroup analysis must be viewed with caution, considering the size of our study population,” Dr. Wollert said. “However, it was encouraging to see that the effects of bone marrow transfer were observable in all investigated subgroups—men and women, older people, younger people—regardless of the prevalence of risk factors, the time from symptoms to PCI [percutaneous coronary intervention], the infarct localization, and the baseline ejection fraction, or baseline infarct size.”

In the BOOST trial, 60 patients (42 men, 18 women) were evenly randomized after successful PCI to receive optimal medical treatment or optimal medical treatment plus intracoronary transfer of autologous bone-marrow cells 5 days after PCI or 6 days after symptom onset.

There were no significant differences between groups in regard to age, major cardiovascular risk factors, time from symptoms to PCI, infarct size, or treatment with thrombolytics or ACE inhibitors during the primary intervention. More than 90% of patients received aspirin, ACE inhibitors, β-blockers, and statins—both at discharge and at 6 month follow-up.

Investigators harvested 128 mL of bone marrow from the posterior iliac crest, which was reduced to an average volume of 26 mL. The final preparation contained 25 × 10

Dr. Wollert said the study's institutional review board would not allow sham catheterizations, but MRI investigators were blinded to the treatment assignment. The primary end point was change in global LVEF from baseline to 6 months' follow-up, as determined by cardiac MRI.

After 6 months, mean global LVEF had increased by 6.7% in the bone-marrow-cell group vs. 0.7% in the control group, a highly significant difference. LVEFs in the treatment group were 50% at baseline and 56.7% at 6 months vs. 51.3% and 52.0%, respectively, in the control group.

There was no significant difference between groups in regional wall motion from baseline to follow-up. However, transfer of bone marrow cells enhanced left ventricular systolic function primarily in the border zones of the infarct.

The secondary end point of left ventricular end-diastolic volume index (LVEDVI) increased for both groups during the 6-month follow-up. But the difference in LVEDVI change was not significantly different between the two groups, suggesting that bone marrow cell transfer does not affect left ventricular remodeling after MI, Dr. Wollert said.

Cell transfer did not increase the risk of adverse events, in-stent restenosis, or proarrhythmic effects. There was no significant difference in extrasystole between groups, although there was a trend toward fewer ventricular extrasystole in the bone marrow cell transfer group.

Dr. Wollert said that future studies should utilize a double-blind design with sham catheterizations, and ultimately address the impact of bone marrow transfer on clinical end points in a large patient population.

TORONTO — Intracoronary transfer of autologous bone marrow cells led to improved left ventricular function after acute MI in a randomized trial.

After 6 months, there was a highly significant increase in mean left ventricular ejection fractions (LVEFs) in acute MI patients after intracoronary injection of bone marrow cells, according to data from the Bone Marrow Transfer to Enhance ST-Elevation Infarct Regeneration (BOOST) study. But treatment did not appear to affect left ventricular remodeling.

“The results from the BOOST trial indicate that intracoronary transfer of autologous bone marrow cells is safe, and enhances left ventricular function” after an MI, Kai Wollert, M.D., said at the annual meeting of the Heart Failure Society of America.

Emerging evidence suggests that direct injection of stem cells and progenitor cells derived from bone marrow can improve cardiac function in patients after acute MI. Although only 30 patients were treated with bone marrow cells in the BOOST trial, the results are promising, said Dr. Wollert of Hannover (Germany) Medical School.

“Subgroup analysis must be viewed with caution, considering the size of our study population,” Dr. Wollert said. “However, it was encouraging to see that the effects of bone marrow transfer were observable in all investigated subgroups—men and women, older people, younger people—regardless of the prevalence of risk factors, the time from symptoms to PCI [percutaneous coronary intervention], the infarct localization, and the baseline ejection fraction, or baseline infarct size.”

In the BOOST trial, 60 patients (42 men, 18 women) were evenly randomized after successful PCI to receive optimal medical treatment or optimal medical treatment plus intracoronary transfer of autologous bone-marrow cells 5 days after PCI or 6 days after symptom onset.

There were no significant differences between groups in regard to age, major cardiovascular risk factors, time from symptoms to PCI, infarct size, or treatment with thrombolytics or ACE inhibitors during the primary intervention. More than 90% of patients received aspirin, ACE inhibitors, β-blockers, and statins—both at discharge and at 6 month follow-up.

Investigators harvested 128 mL of bone marrow from the posterior iliac crest, which was reduced to an average volume of 26 mL. The final preparation contained 25 × 10

Dr. Wollert said the study's institutional review board would not allow sham catheterizations, but MRI investigators were blinded to the treatment assignment. The primary end point was change in global LVEF from baseline to 6 months' follow-up, as determined by cardiac MRI.

After 6 months, mean global LVEF had increased by 6.7% in the bone-marrow-cell group vs. 0.7% in the control group, a highly significant difference. LVEFs in the treatment group were 50% at baseline and 56.7% at 6 months vs. 51.3% and 52.0%, respectively, in the control group.

There was no significant difference between groups in regional wall motion from baseline to follow-up. However, transfer of bone marrow cells enhanced left ventricular systolic function primarily in the border zones of the infarct.

The secondary end point of left ventricular end-diastolic volume index (LVEDVI) increased for both groups during the 6-month follow-up. But the difference in LVEDVI change was not significantly different between the two groups, suggesting that bone marrow cell transfer does not affect left ventricular remodeling after MI, Dr. Wollert said.

Cell transfer did not increase the risk of adverse events, in-stent restenosis, or proarrhythmic effects. There was no significant difference in extrasystole between groups, although there was a trend toward fewer ventricular extrasystole in the bone marrow cell transfer group.

Dr. Wollert said that future studies should utilize a double-blind design with sham catheterizations, and ultimately address the impact of bone marrow transfer on clinical end points in a large patient population.

TORONTO — Intracoronary transfer of autologous bone marrow cells led to improved left ventricular function after acute MI in a randomized trial.

After 6 months, there was a highly significant increase in mean left ventricular ejection fractions (LVEFs) in acute MI patients after intracoronary injection of bone marrow cells, according to data from the Bone Marrow Transfer to Enhance ST-Elevation Infarct Regeneration (BOOST) study. But treatment did not appear to affect left ventricular remodeling.

“The results from the BOOST trial indicate that intracoronary transfer of autologous bone marrow cells is safe, and enhances left ventricular function” after an MI, Kai Wollert, M.D., said at the annual meeting of the Heart Failure Society of America.

Emerging evidence suggests that direct injection of stem cells and progenitor cells derived from bone marrow can improve cardiac function in patients after acute MI. Although only 30 patients were treated with bone marrow cells in the BOOST trial, the results are promising, said Dr. Wollert of Hannover (Germany) Medical School.

“Subgroup analysis must be viewed with caution, considering the size of our study population,” Dr. Wollert said. “However, it was encouraging to see that the effects of bone marrow transfer were observable in all investigated subgroups—men and women, older people, younger people—regardless of the prevalence of risk factors, the time from symptoms to PCI [percutaneous coronary intervention], the infarct localization, and the baseline ejection fraction, or baseline infarct size.”

In the BOOST trial, 60 patients (42 men, 18 women) were evenly randomized after successful PCI to receive optimal medical treatment or optimal medical treatment plus intracoronary transfer of autologous bone-marrow cells 5 days after PCI or 6 days after symptom onset.

There were no significant differences between groups in regard to age, major cardiovascular risk factors, time from symptoms to PCI, infarct size, or treatment with thrombolytics or ACE inhibitors during the primary intervention. More than 90% of patients received aspirin, ACE inhibitors, β-blockers, and statins—both at discharge and at 6 month follow-up.

Investigators harvested 128 mL of bone marrow from the posterior iliac crest, which was reduced to an average volume of 26 mL. The final preparation contained 25 × 10

Dr. Wollert said the study's institutional review board would not allow sham catheterizations, but MRI investigators were blinded to the treatment assignment. The primary end point was change in global LVEF from baseline to 6 months' follow-up, as determined by cardiac MRI.

After 6 months, mean global LVEF had increased by 6.7% in the bone-marrow-cell group vs. 0.7% in the control group, a highly significant difference. LVEFs in the treatment group were 50% at baseline and 56.7% at 6 months vs. 51.3% and 52.0%, respectively, in the control group.

There was no significant difference between groups in regional wall motion from baseline to follow-up. However, transfer of bone marrow cells enhanced left ventricular systolic function primarily in the border zones of the infarct.

The secondary end point of left ventricular end-diastolic volume index (LVEDVI) increased for both groups during the 6-month follow-up. But the difference in LVEDVI change was not significantly different between the two groups, suggesting that bone marrow cell transfer does not affect left ventricular remodeling after MI, Dr. Wollert said.

Cell transfer did not increase the risk of adverse events, in-stent restenosis, or proarrhythmic effects. There was no significant difference in extrasystole between groups, although there was a trend toward fewer ventricular extrasystole in the bone marrow cell transfer group.

Dr. Wollert said that future studies should utilize a double-blind design with sham catheterizations, and ultimately address the impact of bone marrow transfer on clinical end points in a large patient population.

NEW ORLEANS — Poor kidney function is the strongest indicator for anemia in heart failure patients, according to the results of a large study in HMO patients.

A reduced glomerular filtration rate emerged as the strongest risk factor for developing anemia in 41,754 heart failure (HF) patients free of anemia at baseline, Alan S. Go, M.D., reported at the annual scientific sessions of the American Heart Association.

Anemia was a common occurrence in this HMO population with HF, with an incidence of 9% per year, according to Dr. Go of Kaiser Permanente of Northern California, Oakland. The study featured nearly 83,000 person-years of follow-up.

Chronic renal impairment is extremely common among HF patients. Roughly 40% of patients had a baseline glomerular filtration rate of less than 60 mL/min per 1.73 m

Among those patients with a baseline GFR less than 15 mL/min per 1.73 m

Other independent predictors of the development of anemia in a multivariate analysis included cirrhosis, with an adjusted 2.3-fold relative risk, compared with noncirrhotic patients, and HIV infection, which conferred an 80% increase in risk. African descent and age greater than 70 years were each associated with a 40% increased risk of becoming anemic, he said.

NEW ORLEANS — Poor kidney function is the strongest indicator for anemia in heart failure patients, according to the results of a large study in HMO patients.

A reduced glomerular filtration rate emerged as the strongest risk factor for developing anemia in 41,754 heart failure (HF) patients free of anemia at baseline, Alan S. Go, M.D., reported at the annual scientific sessions of the American Heart Association.

Anemia was a common occurrence in this HMO population with HF, with an incidence of 9% per year, according to Dr. Go of Kaiser Permanente of Northern California, Oakland. The study featured nearly 83,000 person-years of follow-up.

Chronic renal impairment is extremely common among HF patients. Roughly 40% of patients had a baseline glomerular filtration rate of less than 60 mL/min per 1.73 m

Among those patients with a baseline GFR less than 15 mL/min per 1.73 m

Other independent predictors of the development of anemia in a multivariate analysis included cirrhosis, with an adjusted 2.3-fold relative risk, compared with noncirrhotic patients, and HIV infection, which conferred an 80% increase in risk. African descent and age greater than 70 years were each associated with a 40% increased risk of becoming anemic, he said.

NEW ORLEANS — Poor kidney function is the strongest indicator for anemia in heart failure patients, according to the results of a large study in HMO patients.

A reduced glomerular filtration rate emerged as the strongest risk factor for developing anemia in 41,754 heart failure (HF) patients free of anemia at baseline, Alan S. Go, M.D., reported at the annual scientific sessions of the American Heart Association.

Anemia was a common occurrence in this HMO population with HF, with an incidence of 9% per year, according to Dr. Go of Kaiser Permanente of Northern California, Oakland. The study featured nearly 83,000 person-years of follow-up.

Chronic renal impairment is extremely common among HF patients. Roughly 40% of patients had a baseline glomerular filtration rate of less than 60 mL/min per 1.73 m

Among those patients with a baseline GFR less than 15 mL/min per 1.73 m

Other independent predictors of the development of anemia in a multivariate analysis included cirrhosis, with an adjusted 2.3-fold relative risk, compared with noncirrhotic patients, and HIV infection, which conferred an 80% increase in risk. African descent and age greater than 70 years were each associated with a 40% increased risk of becoming anemic, he said.

ROCKVILLE, MD. — The angiotensin receptor blocker candesartan should be approved as a treatment for heart failure in patients who are on an ACE inhibitor, a Food and Drug Administration advisory panel has unanimously recommended.

The FDA's cardiovascular and renal drugs advisory committee backed the approval on the basis of results of one of the three Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) trials.

In CHARM-Added, candesartan (titrated to a target dose of 32 mg/day) was compared with placebo in 2,548 patients with New York Heart Association (NYHA) class II-IV heart failure (HF) and a left ventricular ejection fraction (LVEF) at or below 40% who were on an ACE inhibitor and standard therapy. The results showed that adding an ARB to standard treatment that included an ACE inhibitor added an incremental benefit in this population: The relative risk of cardiovascular mortality or HF hospitalization—the primary end point—was reduced by 15% in those on candesartan during a median follow-up of 41 months. The benefits were also seen in patients treated with β-blockers, which suggested no adverse interactions among β-blockers, candesartan, and ACE inhibitors, as was noted in the Valsartan Heart Failure Trial (Val-HeFT), in which HF morbidity was worse in patients on an ACE inhibitor, β-blocker, and valsartan, according to the FDA.

The purpose of the panel meeting was to determine, according to the FDA's agenda, “whether CHARM-Added provides compelling evidence that candesartan should, under some circumstances, be recommended for use in patients on an ACE inhibitor.”

But a large portion of the meeting was spent discussing whether patients in the trial were on optimal ACE inhibitor doses and whether the same benefits might have been achieved by increasing the dose of the ACE inhibitor.

Although panelists said a forced titration of ACE inhibitor therapy in the study protocol would have been ideal, they said they felt comfortable that the ACE inhibitor doses used fell into the ranges considered adequate or optimal. The “final doses of ACE inhibitor achieved were quite substantial” and in line with the doses seen in other trials of ACE inhibitor therapy, said Blasé Carabello, M.D., professor of medicine at Baylor University, Houston. In addition, an analysis of a subset of patients on high doses of ACE inhibitors “all go in the same direction” favoring the benefit.

The FDA usually follows the recommendations of its advisory panels, which are made up of outside experts. If approved, candesartan (marketed as Atacand by AstraZeneca Pharmaceuticals LP) will be the first ARB approved for use with an ACE inhibitor. Shortly before the panel meeting, the agency approved candesartan for patients with NYHA class II-IV heart failure, and an LVEF at or below 40%, who are not on an ACE inhibitor, to reduce the risk of death from cardiovascular causes and reduce HF hospitalization based on the CHARM-Alternative trial.

Speaking for AstraZeneca at the meeting, John McMurray, M.D., the principal investigator of CHARM-Added, said that 96% of the patients in the trial were taking an “individualized, optimum” dose of an ACE inhibitor at baseline, and about 80% of patients were on one of five ACE inhibitors that were considered preferred because of randomized controlled outcome studies of these drugs, said Dr. McMurray, professor of medical cardiology, Western Infirmary, Glasgow, Scotland.

Speaking on the study's efficacy for AstraZeneca, Marc Pfeffer, M.D., interim chair of medicine at Brigham and Women's Hospital, Boston, and cochair of the CHARM executive committee, said that in CHARM-Added, there was there was no evidence that the beneficial effect of candesartan on cardiovascular death or HF hospitalization, was modified “based on ACE inhibitor dose or choice of ACE inhibitor.”

James Hainer, M.D., senior director of clinical research at AstraZeneca, said that as expected, due to a greater degree of renin-angiotensin-aldosterone system inhibition, rates of hypotension, abnormal renal function, and hyperkalemia were greater with candesartan. However, these adverse events did not translate into any increases in all-cause hospitalization and/or mortality, sudden death, renal failure, or ventricular fibrillation, he said.

These risks will be addressed on the label in warnings and precautions about hypotension, renal dysfunction, and hyperkalemia and recommendations for monitoring and reducing risk, and through interactions with major societies and treatment guidelines committees, he said.

Dr. McMurray said that on balance, the risk was “substantially” in favor of candesartan: A cost analysis found that for every 1,000 patients treated with candesartan, there were 1,900 fewer days spent in the hospital for worsening heart failure, he told the panel.

ROCKVILLE, MD. — The angiotensin receptor blocker candesartan should be approved as a treatment for heart failure in patients who are on an ACE inhibitor, a Food and Drug Administration advisory panel has unanimously recommended.

The FDA's cardiovascular and renal drugs advisory committee backed the approval on the basis of results of one of the three Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) trials.

In CHARM-Added, candesartan (titrated to a target dose of 32 mg/day) was compared with placebo in 2,548 patients with New York Heart Association (NYHA) class II-IV heart failure (HF) and a left ventricular ejection fraction (LVEF) at or below 40% who were on an ACE inhibitor and standard therapy. The results showed that adding an ARB to standard treatment that included an ACE inhibitor added an incremental benefit in this population: The relative risk of cardiovascular mortality or HF hospitalization—the primary end point—was reduced by 15% in those on candesartan during a median follow-up of 41 months. The benefits were also seen in patients treated with β-blockers, which suggested no adverse interactions among β-blockers, candesartan, and ACE inhibitors, as was noted in the Valsartan Heart Failure Trial (Val-HeFT), in which HF morbidity was worse in patients on an ACE inhibitor, β-blocker, and valsartan, according to the FDA.

The purpose of the panel meeting was to determine, according to the FDA's agenda, “whether CHARM-Added provides compelling evidence that candesartan should, under some circumstances, be recommended for use in patients on an ACE inhibitor.”

But a large portion of the meeting was spent discussing whether patients in the trial were on optimal ACE inhibitor doses and whether the same benefits might have been achieved by increasing the dose of the ACE inhibitor.

Although panelists said a forced titration of ACE inhibitor therapy in the study protocol would have been ideal, they said they felt comfortable that the ACE inhibitor doses used fell into the ranges considered adequate or optimal. The “final doses of ACE inhibitor achieved were quite substantial” and in line with the doses seen in other trials of ACE inhibitor therapy, said Blasé Carabello, M.D., professor of medicine at Baylor University, Houston. In addition, an analysis of a subset of patients on high doses of ACE inhibitors “all go in the same direction” favoring the benefit.

The FDA usually follows the recommendations of its advisory panels, which are made up of outside experts. If approved, candesartan (marketed as Atacand by AstraZeneca Pharmaceuticals LP) will be the first ARB approved for use with an ACE inhibitor. Shortly before the panel meeting, the agency approved candesartan for patients with NYHA class II-IV heart failure, and an LVEF at or below 40%, who are not on an ACE inhibitor, to reduce the risk of death from cardiovascular causes and reduce HF hospitalization based on the CHARM-Alternative trial.

Speaking for AstraZeneca at the meeting, John McMurray, M.D., the principal investigator of CHARM-Added, said that 96% of the patients in the trial were taking an “individualized, optimum” dose of an ACE inhibitor at baseline, and about 80% of patients were on one of five ACE inhibitors that were considered preferred because of randomized controlled outcome studies of these drugs, said Dr. McMurray, professor of medical cardiology, Western Infirmary, Glasgow, Scotland.

Speaking on the study's efficacy for AstraZeneca, Marc Pfeffer, M.D., interim chair of medicine at Brigham and Women's Hospital, Boston, and cochair of the CHARM executive committee, said that in CHARM-Added, there was there was no evidence that the beneficial effect of candesartan on cardiovascular death or HF hospitalization, was modified “based on ACE inhibitor dose or choice of ACE inhibitor.”

James Hainer, M.D., senior director of clinical research at AstraZeneca, said that as expected, due to a greater degree of renin-angiotensin-aldosterone system inhibition, rates of hypotension, abnormal renal function, and hyperkalemia were greater with candesartan. However, these adverse events did not translate into any increases in all-cause hospitalization and/or mortality, sudden death, renal failure, or ventricular fibrillation, he said.

These risks will be addressed on the label in warnings and precautions about hypotension, renal dysfunction, and hyperkalemia and recommendations for monitoring and reducing risk, and through interactions with major societies and treatment guidelines committees, he said.

Dr. McMurray said that on balance, the risk was “substantially” in favor of candesartan: A cost analysis found that for every 1,000 patients treated with candesartan, there were 1,900 fewer days spent in the hospital for worsening heart failure, he told the panel.

ROCKVILLE, MD. — The angiotensin receptor blocker candesartan should be approved as a treatment for heart failure in patients who are on an ACE inhibitor, a Food and Drug Administration advisory panel has unanimously recommended.

The FDA's cardiovascular and renal drugs advisory committee backed the approval on the basis of results of one of the three Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) trials.

In CHARM-Added, candesartan (titrated to a target dose of 32 mg/day) was compared with placebo in 2,548 patients with New York Heart Association (NYHA) class II-IV heart failure (HF) and a left ventricular ejection fraction (LVEF) at or below 40% who were on an ACE inhibitor and standard therapy. The results showed that adding an ARB to standard treatment that included an ACE inhibitor added an incremental benefit in this population: The relative risk of cardiovascular mortality or HF hospitalization—the primary end point—was reduced by 15% in those on candesartan during a median follow-up of 41 months. The benefits were also seen in patients treated with β-blockers, which suggested no adverse interactions among β-blockers, candesartan, and ACE inhibitors, as was noted in the Valsartan Heart Failure Trial (Val-HeFT), in which HF morbidity was worse in patients on an ACE inhibitor, β-blocker, and valsartan, according to the FDA.

The purpose of the panel meeting was to determine, according to the FDA's agenda, “whether CHARM-Added provides compelling evidence that candesartan should, under some circumstances, be recommended for use in patients on an ACE inhibitor.”

But a large portion of the meeting was spent discussing whether patients in the trial were on optimal ACE inhibitor doses and whether the same benefits might have been achieved by increasing the dose of the ACE inhibitor.

Although panelists said a forced titration of ACE inhibitor therapy in the study protocol would have been ideal, they said they felt comfortable that the ACE inhibitor doses used fell into the ranges considered adequate or optimal. The “final doses of ACE inhibitor achieved were quite substantial” and in line with the doses seen in other trials of ACE inhibitor therapy, said Blasé Carabello, M.D., professor of medicine at Baylor University, Houston. In addition, an analysis of a subset of patients on high doses of ACE inhibitors “all go in the same direction” favoring the benefit.

The FDA usually follows the recommendations of its advisory panels, which are made up of outside experts. If approved, candesartan (marketed as Atacand by AstraZeneca Pharmaceuticals LP) will be the first ARB approved for use with an ACE inhibitor. Shortly before the panel meeting, the agency approved candesartan for patients with NYHA class II-IV heart failure, and an LVEF at or below 40%, who are not on an ACE inhibitor, to reduce the risk of death from cardiovascular causes and reduce HF hospitalization based on the CHARM-Alternative trial.

Speaking for AstraZeneca at the meeting, John McMurray, M.D., the principal investigator of CHARM-Added, said that 96% of the patients in the trial were taking an “individualized, optimum” dose of an ACE inhibitor at baseline, and about 80% of patients were on one of five ACE inhibitors that were considered preferred because of randomized controlled outcome studies of these drugs, said Dr. McMurray, professor of medical cardiology, Western Infirmary, Glasgow, Scotland.

Speaking on the study's efficacy for AstraZeneca, Marc Pfeffer, M.D., interim chair of medicine at Brigham and Women's Hospital, Boston, and cochair of the CHARM executive committee, said that in CHARM-Added, there was there was no evidence that the beneficial effect of candesartan on cardiovascular death or HF hospitalization, was modified “based on ACE inhibitor dose or choice of ACE inhibitor.”

James Hainer, M.D., senior director of clinical research at AstraZeneca, said that as expected, due to a greater degree of renin-angiotensin-aldosterone system inhibition, rates of hypotension, abnormal renal function, and hyperkalemia were greater with candesartan. However, these adverse events did not translate into any increases in all-cause hospitalization and/or mortality, sudden death, renal failure, or ventricular fibrillation, he said.

These risks will be addressed on the label in warnings and precautions about hypotension, renal dysfunction, and hyperkalemia and recommendations for monitoring and reducing risk, and through interactions with major societies and treatment guidelines committees, he said.

Dr. McMurray said that on balance, the risk was “substantially” in favor of candesartan: A cost analysis found that for every 1,000 patients treated with candesartan, there were 1,900 fewer days spent in the hospital for worsening heart failure, he told the panel.

The recent approval of candesartan for a heart failure indication reflects the key findings of one of the three international trials comparing candesartan with placebo in patients with heart failure.

In February, the Food and Drug Administration approved the angiotensin receptor blocker (ARB) for treating patients with heart failure (New York Heart Association class II or IV and a left ventricular ejection fraction [LVEF] of 40% or less), “to reduce the risk of death from cardiovascular causes and to reduce hospitalizations for heart failure.” In the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM)-Alternative trial, the risk of cardiovascular death or hospitalization for heart failure, the primary end point, was reduced by 23% among those on candesartan after a median follow-up of 34 months, compared with those on placebo—a highly statistically significant effect.

This trial, one of three in the CHARM program, enrolled 2,028 patients with symptomatic heart failure and an LVEF less than or equal to 40%, who were on standard heart failure treatments but were intolerant of ACE inhibitors. At baseline, 85% were on diuretics, 46% on digoxin, 55% on β-blockers, and 24% on spironolactone. There were 334 events in the 1,013 patients on candesartan, vs. 406 events in the 1,015 on placebo.

Supporting the approval of this indication, according to the FDA, were the results of CHARM-Added, which enrolled more than 2,500 patients with NYHA class II-IV heart failure and LVEFs at or below 40% who were on an ACE inhibitor. In this trial, adding candesartan to standard treatment, including a β-blocker, reduced the risk of cardiovascular mortality by 15%, compared with placebo, and significantly improved in heart failure symptoms, as assessed by NYHA functional class.

An approval for use in heart failure patients on ACE inhibitors is likely to follow. (See accompanying story.)

Candesartan, marketed as Atacand by AstraZeneca Pharmaceuticals LP, is the second ARB approved for heart failure; the first was Diovan (valsartan), approved in 2002 for a narrower indication, NYHA class II-IV heart failure in people who cannot tolerate ACE inhibitors. Candesartan was approved for hypertension in 1998.

Using candesartan for these indications will provide an important new tool for treating heart failure, said Christopher Granger, M.D., CHARM-Alternative's principal investigator, in an interview.

In the CHARM program, 4% of those on candesartan had to stop treatment with the drug because of hypotension, versus 2% of those on placebo. Hyperkalemia leading to discontinuation occurred in 2.4% of those on candesartan, versus 0.6% of those on placebo.

The recommended starting dosage is 4 mg/day, with a target dosage of 32 mg once daily, achieved by doubling the dose approximately every 2 weeks, as tolerated, according to the package insert.

Patients need to be monitored closely when the drug is being titrated because some will develop renal insufficiency, hyperkalemia, or hypotension during titration, side effects expected with any drug that affects the renal angiotensin system, said Dr. Granger, who is director of the cardiac care unit at Duke University, Durham, N.C. In the CHARM trials, it was recommended that investigators check serum potassium and creatinine approximately 2 weeks after dose titration.

Dr. Granger was on the executive committee for CHARM and was a consultant to AstraZeneca for this FDA approval and for the meeting of the FDA's cardiovascular and renal drugs advisory committee.

The recent approval of candesartan for a heart failure indication reflects the key findings of one of the three international trials comparing candesartan with placebo in patients with heart failure.

In February, the Food and Drug Administration approved the angiotensin receptor blocker (ARB) for treating patients with heart failure (New York Heart Association class II or IV and a left ventricular ejection fraction [LVEF] of 40% or less), “to reduce the risk of death from cardiovascular causes and to reduce hospitalizations for heart failure.” In the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM)-Alternative trial, the risk of cardiovascular death or hospitalization for heart failure, the primary end point, was reduced by 23% among those on candesartan after a median follow-up of 34 months, compared with those on placebo—a highly statistically significant effect.

This trial, one of three in the CHARM program, enrolled 2,028 patients with symptomatic heart failure and an LVEF less than or equal to 40%, who were on standard heart failure treatments but were intolerant of ACE inhibitors. At baseline, 85% were on diuretics, 46% on digoxin, 55% on β-blockers, and 24% on spironolactone. There were 334 events in the 1,013 patients on candesartan, vs. 406 events in the 1,015 on placebo.

Supporting the approval of this indication, according to the FDA, were the results of CHARM-Added, which enrolled more than 2,500 patients with NYHA class II-IV heart failure and LVEFs at or below 40% who were on an ACE inhibitor. In this trial, adding candesartan to standard treatment, including a β-blocker, reduced the risk of cardiovascular mortality by 15%, compared with placebo, and significantly improved in heart failure symptoms, as assessed by NYHA functional class.

An approval for use in heart failure patients on ACE inhibitors is likely to follow. (See accompanying story.)

Candesartan, marketed as Atacand by AstraZeneca Pharmaceuticals LP, is the second ARB approved for heart failure; the first was Diovan (valsartan), approved in 2002 for a narrower indication, NYHA class II-IV heart failure in people who cannot tolerate ACE inhibitors. Candesartan was approved for hypertension in 1998.

Using candesartan for these indications will provide an important new tool for treating heart failure, said Christopher Granger, M.D., CHARM-Alternative's principal investigator, in an interview.

In the CHARM program, 4% of those on candesartan had to stop treatment with the drug because of hypotension, versus 2% of those on placebo. Hyperkalemia leading to discontinuation occurred in 2.4% of those on candesartan, versus 0.6% of those on placebo.

The recommended starting dosage is 4 mg/day, with a target dosage of 32 mg once daily, achieved by doubling the dose approximately every 2 weeks, as tolerated, according to the package insert.

Patients need to be monitored closely when the drug is being titrated because some will develop renal insufficiency, hyperkalemia, or hypotension during titration, side effects expected with any drug that affects the renal angiotensin system, said Dr. Granger, who is director of the cardiac care unit at Duke University, Durham, N.C. In the CHARM trials, it was recommended that investigators check serum potassium and creatinine approximately 2 weeks after dose titration.

Dr. Granger was on the executive committee for CHARM and was a consultant to AstraZeneca for this FDA approval and for the meeting of the FDA's cardiovascular and renal drugs advisory committee.

The recent approval of candesartan for a heart failure indication reflects the key findings of one of the three international trials comparing candesartan with placebo in patients with heart failure.

In February, the Food and Drug Administration approved the angiotensin receptor blocker (ARB) for treating patients with heart failure (New York Heart Association class II or IV and a left ventricular ejection fraction [LVEF] of 40% or less), “to reduce the risk of death from cardiovascular causes and to reduce hospitalizations for heart failure.” In the Candesartan in Heart Failure: Assessment of Reduction in Mortality and Morbidity (CHARM)-Alternative trial, the risk of cardiovascular death or hospitalization for heart failure, the primary end point, was reduced by 23% among those on candesartan after a median follow-up of 34 months, compared with those on placebo—a highly statistically significant effect.

This trial, one of three in the CHARM program, enrolled 2,028 patients with symptomatic heart failure and an LVEF less than or equal to 40%, who were on standard heart failure treatments but were intolerant of ACE inhibitors. At baseline, 85% were on diuretics, 46% on digoxin, 55% on β-blockers, and 24% on spironolactone. There were 334 events in the 1,013 patients on candesartan, vs. 406 events in the 1,015 on placebo.

Supporting the approval of this indication, according to the FDA, were the results of CHARM-Added, which enrolled more than 2,500 patients with NYHA class II-IV heart failure and LVEFs at or below 40% who were on an ACE inhibitor. In this trial, adding candesartan to standard treatment, including a β-blocker, reduced the risk of cardiovascular mortality by 15%, compared with placebo, and significantly improved in heart failure symptoms, as assessed by NYHA functional class.

An approval for use in heart failure patients on ACE inhibitors is likely to follow. (See accompanying story.)

Candesartan, marketed as Atacand by AstraZeneca Pharmaceuticals LP, is the second ARB approved for heart failure; the first was Diovan (valsartan), approved in 2002 for a narrower indication, NYHA class II-IV heart failure in people who cannot tolerate ACE inhibitors. Candesartan was approved for hypertension in 1998.

Using candesartan for these indications will provide an important new tool for treating heart failure, said Christopher Granger, M.D., CHARM-Alternative's principal investigator, in an interview.

In the CHARM program, 4% of those on candesartan had to stop treatment with the drug because of hypotension, versus 2% of those on placebo. Hyperkalemia leading to discontinuation occurred in 2.4% of those on candesartan, versus 0.6% of those on placebo.

The recommended starting dosage is 4 mg/day, with a target dosage of 32 mg once daily, achieved by doubling the dose approximately every 2 weeks, as tolerated, according to the package insert.

Patients need to be monitored closely when the drug is being titrated because some will develop renal insufficiency, hyperkalemia, or hypotension during titration, side effects expected with any drug that affects the renal angiotensin system, said Dr. Granger, who is director of the cardiac care unit at Duke University, Durham, N.C. In the CHARM trials, it was recommended that investigators check serum potassium and creatinine approximately 2 weeks after dose titration.

Dr. Granger was on the executive committee for CHARM and was a consultant to AstraZeneca for this FDA approval and for the meeting of the FDA's cardiovascular and renal drugs advisory committee.

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see box), according to Dr. Havranek of Denver Health Medical Center.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk. In addition, the risk of depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year. The incidence of depression rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less.

The impetus for developing the social/health risk factor checklist as a tool for predicting onset of depression stems from prior studies that established depression in patients with HF is quite common and is associated in this population with decline in health status, more frequent hospitalization, and increased mortality.

“Routine screening of high-risk patients with heart failure followed by psychosocial intervention to reduce the incidence of depression is a strategy that deserves study,” Dr. Havranek observed. “This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events.”

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see box), according to Dr. Havranek of Denver Health Medical Center.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk. In addition, the risk of depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year. The incidence of depression rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less.

The impetus for developing the social/health risk factor checklist as a tool for predicting onset of depression stems from prior studies that established depression in patients with HF is quite common and is associated in this population with decline in health status, more frequent hospitalization, and increased mortality.

“Routine screening of high-risk patients with heart failure followed by psychosocial intervention to reduce the incidence of depression is a strategy that deserves study,” Dr. Havranek observed. “This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events.”

The four-item checklist consists of living alone, alcohol abuse, poor health status as measured by the Kansas City Cardiomyopathy Questionnaire (KCCQ), and the patient's perception that his or her medical care poses a substantial economic burden. A heart failure patient's risk of developing depression within 1 year rises in stepwise fashion as the number of applicable risk factors increases (see box), according to Dr. Havranek of Denver Health Medical Center.

The checklist was developed as part of a multicenter prospective cohort study involving 245 outpatients with heart failure (HF) and a left ventricular ejection fraction less than 40% who were free of depression at baseline. During 1 year of follow-up, 21.5% of patients developed clinically significant symptoms of depression as defined by a score above 0.06 on the widely used Medical Outcomes Study Depression Scale.

Multivariate analysis identified four independent predictors of onset of depression in this HF population. Alcohol abuse was associated with a 3-fold elevated risk, living alone conferred a 2.8-fold risk, and medical care being seen by the patient as a substantial economic burden carried a 2.9-fold increased risk. In addition, the risk of depression rose by 22% for each 10-point decrement on the KCCQ. The study results were published in December (J. Am. Coll. Cardiol. 2004;44:2333-8).

The KCCQ is a self-administered 23-item multiple-choice instrument that inquires about the impact of HF upon a patient's life. For example, the KCCQ asks patients how much swelling in their feet, ankles, or legs has bothered them in the last 2 weeks, how many times during that period they have been forced by shortness of breath to sleep sitting in a chair propped up by at least three pillows, and how much HF has limited their enjoyment of life during the last 2 weeks.

The range of possible scores on the KCCQ is 0-100. Higher scores indicate less disease impact. Study participants with a baseline score greater than 75 had a 13% incidence of depression onset within 1 year. The incidence of depression rose to 20% among those with a baseline score of 51-75, 42% in those who scored 26-50, and 44% with a score of 25 or less.

The impetus for developing the social/health risk factor checklist as a tool for predicting onset of depression stems from prior studies that established depression in patients with HF is quite common and is associated in this population with decline in health status, more frequent hospitalization, and increased mortality.

“Routine screening of high-risk patients with heart failure followed by psychosocial intervention to reduce the incidence of depression is a strategy that deserves study,” Dr. Havranek observed. “This would be consistent with the Institute of Medicine position that one of the changes necessary for American health care is for the system to anticipate patient needs rather than simply to react to events.”

NEW ORLEANS — Chronic use of methamphetamine can lead to nonischemic, dilated cardiomyopathy and profound left-ventricular dysfunction, according to a study of 53 methamphetamine users seen at a single medical center in California.

“To our knowledge, this is the first study of its type to examine the relationship between chronic methamphetamine use and its effect on the heart,” Melissa R. Robinson, M.D., reported in a poster at the annual scientific sessions of the American Heart Association.

“In contrast with cocaine, long-term methamphetamine use seems to have a direct, cardiotoxic effect, and promotes the development of severe, nonischemic, dilated cardiomyopathy,” said Dr. Robinson of the department of internal medicine at the University of California, Davis. Although the number of chronic users of methamphetamine is not known, a 2001 survey estimated that more than 5 million people in the United States had tried the drug, she said.

Her review started with 226 patients who were either hospitalized at the UC Davis Medical Center or seen in its emergency department during 1993-2002 and reported using methamphetamine and were diagnosed with either cardiomyopathy or heart failure. This list of patients was then pared to exclude those with another possible explanation for their heart disease, including a history of significant alcohol use (at least four drinks per day for at least 5 years), alcoholic cirrhosis, cocaine use, or severe coronary artery disease.

These exclusions left 53 patients who were methamphetamine users and had no clear etiology for their cardiomyopathy or heart failure. The average duration of drug use among these 53 patients was 5 years.

Their average age was 46 years, and 43% were younger than 45. Their average left-ventricular end-diastolic dimension was 66.3 mm, and 87% had an end-diastolic dimension of more than 55 mm, indicating severe dilated cardiomyopathy. Echocardiography was done on 46 patients, who had an average left-ventricular ejection fraction of 25%; 35 of the 46 patients (76%) had an ejection fraction of less than 30%.

Several of the patients had severe complications while they were followed at UC Davis. Five patients had strokes, another five had recurrent ventricular arrhythmias that required implantation of a cardioverter defibrillator, and six had sudden deaths. “These clinical findings were unusual given the relatively young age of these patients,” Dr. Robinson said.

Four patients had resolution of their cardiomyopathy after they stopped using methamphetamine.

Methamphetamine probably triggers cardiomyopathy by causing a chronic excess of catecholamines, similar to what happens in patients with a pheochromocytoma, an adrenal gland tumor, Dr. Robinson told this newspaper. The effects of methamphetamine are exacerbated by its relatively long half-life, 8-12 hours. In contrast, the half-life of cocaine is 30-60 minutes.

NEW ORLEANS — Chronic use of methamphetamine can lead to nonischemic, dilated cardiomyopathy and profound left-ventricular dysfunction, according to a study of 53 methamphetamine users seen at a single medical center in California.

“To our knowledge, this is the first study of its type to examine the relationship between chronic methamphetamine use and its effect on the heart,” Melissa R. Robinson, M.D., reported in a poster at the annual scientific sessions of the American Heart Association.

“In contrast with cocaine, long-term methamphetamine use seems to have a direct, cardiotoxic effect, and promotes the development of severe, nonischemic, dilated cardiomyopathy,” said Dr. Robinson of the department of internal medicine at the University of California, Davis. Although the number of chronic users of methamphetamine is not known, a 2001 survey estimated that more than 5 million people in the United States had tried the drug, she said.

Her review started with 226 patients who were either hospitalized at the UC Davis Medical Center or seen in its emergency department during 1993-2002 and reported using methamphetamine and were diagnosed with either cardiomyopathy or heart failure. This list of patients was then pared to exclude those with another possible explanation for their heart disease, including a history of significant alcohol use (at least four drinks per day for at least 5 years), alcoholic cirrhosis, cocaine use, or severe coronary artery disease.

These exclusions left 53 patients who were methamphetamine users and had no clear etiology for their cardiomyopathy or heart failure. The average duration of drug use among these 53 patients was 5 years.

Their average age was 46 years, and 43% were younger than 45. Their average left-ventricular end-diastolic dimension was 66.3 mm, and 87% had an end-diastolic dimension of more than 55 mm, indicating severe dilated cardiomyopathy. Echocardiography was done on 46 patients, who had an average left-ventricular ejection fraction of 25%; 35 of the 46 patients (76%) had an ejection fraction of less than 30%.

Several of the patients had severe complications while they were followed at UC Davis. Five patients had strokes, another five had recurrent ventricular arrhythmias that required implantation of a cardioverter defibrillator, and six had sudden deaths. “These clinical findings were unusual given the relatively young age of these patients,” Dr. Robinson said.

Four patients had resolution of their cardiomyopathy after they stopped using methamphetamine.

Methamphetamine probably triggers cardiomyopathy by causing a chronic excess of catecholamines, similar to what happens in patients with a pheochromocytoma, an adrenal gland tumor, Dr. Robinson told this newspaper. The effects of methamphetamine are exacerbated by its relatively long half-life, 8-12 hours. In contrast, the half-life of cocaine is 30-60 minutes.

NEW ORLEANS — Chronic use of methamphetamine can lead to nonischemic, dilated cardiomyopathy and profound left-ventricular dysfunction, according to a study of 53 methamphetamine users seen at a single medical center in California.

“To our knowledge, this is the first study of its type to examine the relationship between chronic methamphetamine use and its effect on the heart,” Melissa R. Robinson, M.D., reported in a poster at the annual scientific sessions of the American Heart Association.

“In contrast with cocaine, long-term methamphetamine use seems to have a direct, cardiotoxic effect, and promotes the development of severe, nonischemic, dilated cardiomyopathy,” said Dr. Robinson of the department of internal medicine at the University of California, Davis. Although the number of chronic users of methamphetamine is not known, a 2001 survey estimated that more than 5 million people in the United States had tried the drug, she said.

Her review started with 226 patients who were either hospitalized at the UC Davis Medical Center or seen in its emergency department during 1993-2002 and reported using methamphetamine and were diagnosed with either cardiomyopathy or heart failure. This list of patients was then pared to exclude those with another possible explanation for their heart disease, including a history of significant alcohol use (at least four drinks per day for at least 5 years), alcoholic cirrhosis, cocaine use, or severe coronary artery disease.

These exclusions left 53 patients who were methamphetamine users and had no clear etiology for their cardiomyopathy or heart failure. The average duration of drug use among these 53 patients was 5 years.

Their average age was 46 years, and 43% were younger than 45. Their average left-ventricular end-diastolic dimension was 66.3 mm, and 87% had an end-diastolic dimension of more than 55 mm, indicating severe dilated cardiomyopathy. Echocardiography was done on 46 patients, who had an average left-ventricular ejection fraction of 25%; 35 of the 46 patients (76%) had an ejection fraction of less than 30%.

Several of the patients had severe complications while they were followed at UC Davis. Five patients had strokes, another five had recurrent ventricular arrhythmias that required implantation of a cardioverter defibrillator, and six had sudden deaths. “These clinical findings were unusual given the relatively young age of these patients,” Dr. Robinson said.

Four patients had resolution of their cardiomyopathy after they stopped using methamphetamine.

Methamphetamine probably triggers cardiomyopathy by causing a chronic excess of catecholamines, similar to what happens in patients with a pheochromocytoma, an adrenal gland tumor, Dr. Robinson told this newspaper. The effects of methamphetamine are exacerbated by its relatively long half-life, 8-12 hours. In contrast, the half-life of cocaine is 30-60 minutes.

NEW ORLEANS — Patients with heart failure who also have hypoalbuminemia have a two- to threefold increased risk of death, compared with patients with normal serum albumin levels, according to results from a study in about 1,000 patients.

It's possible that this elevated mortality risk may be controlled using nutritional supplements or treatments aimed at cutting the inflammation associated with hypoalbuminemia, Tamara Horwich, M.D., said at the annual scientific sessions of the American Heart Association.

It's unclear what links hypoalbuminemia with worse survival during heart failure (HF), but several candidate mechanisms exist. These include hemodilution, cardiac cachexia, biventricular HF, reduced colloid osmotic pressure causing pulmonary edema, and reduced tolerability and use of optimal medical therapy, said Dr. Horwich of the University of California, Los Angeles.

Prior studies had linked hypoalbuminemia with a higher risk of death in a variety of disease states, including cancer, end-stage renal disease, infections, and cardiac surgery. But until now, few studies had examined whether a similar association exists in patients with HF.

To assess this potential link, Dr. Horwich and her associates reviewed case records for 1,162 HF patients who were treated at UCLA Medical Center from December 1983 through June 2004. Some patients were excluded because their left ventricular ejection fraction was greater than 40% or they had inadequate follow-up. The study focused on the 1,039 eligible patients who remained. Their average age was 52 years, and their mean ejection fraction was 23%.

Patients were diagnosed with hypoalbuminemia if their serum albumin was less than 3.4 g/dL. About 25% of the patients in this study had hypoalbuminemia, a prevalence consistent with reports from prior studies of HF patients. Low albumin levels were most prevalent in lean patients, with a prevalence of 29%, but hypoalbuminemia was also common in overweight and obese patients, with prevalences of 15% and 20%, respectively.

The 1-year survival rate in patients who were hypoalbuminemic at baseline was 68%, compared with more than 80% in those with normal baseline levels.

In a multivariate analysis that adjusted for potential confounders, including age, sex, and body mass index, patients who had low serum albumin were 2.8-fold more likely to die, compared with patients with a serum albumin level within the normal range, Dr. Horwich said.

NEW ORLEANS — Patients with heart failure who also have hypoalbuminemia have a two- to threefold increased risk of death, compared with patients with normal serum albumin levels, according to results from a study in about 1,000 patients.

It's possible that this elevated mortality risk may be controlled using nutritional supplements or treatments aimed at cutting the inflammation associated with hypoalbuminemia, Tamara Horwich, M.D., said at the annual scientific sessions of the American Heart Association.

It's unclear what links hypoalbuminemia with worse survival during heart failure (HF), but several candidate mechanisms exist. These include hemodilution, cardiac cachexia, biventricular HF, reduced colloid osmotic pressure causing pulmonary edema, and reduced tolerability and use of optimal medical therapy, said Dr. Horwich of the University of California, Los Angeles.

Prior studies had linked hypoalbuminemia with a higher risk of death in a variety of disease states, including cancer, end-stage renal disease, infections, and cardiac surgery. But until now, few studies had examined whether a similar association exists in patients with HF.

To assess this potential link, Dr. Horwich and her associates reviewed case records for 1,162 HF patients who were treated at UCLA Medical Center from December 1983 through June 2004. Some patients were excluded because their left ventricular ejection fraction was greater than 40% or they had inadequate follow-up. The study focused on the 1,039 eligible patients who remained. Their average age was 52 years, and their mean ejection fraction was 23%.

Patients were diagnosed with hypoalbuminemia if their serum albumin was less than 3.4 g/dL. About 25% of the patients in this study had hypoalbuminemia, a prevalence consistent with reports from prior studies of HF patients. Low albumin levels were most prevalent in lean patients, with a prevalence of 29%, but hypoalbuminemia was also common in overweight and obese patients, with prevalences of 15% and 20%, respectively.

The 1-year survival rate in patients who were hypoalbuminemic at baseline was 68%, compared with more than 80% in those with normal baseline levels.

In a multivariate analysis that adjusted for potential confounders, including age, sex, and body mass index, patients who had low serum albumin were 2.8-fold more likely to die, compared with patients with a serum albumin level within the normal range, Dr. Horwich said.

NEW ORLEANS — Patients with heart failure who also have hypoalbuminemia have a two- to threefold increased risk of death, compared with patients with normal serum albumin levels, according to results from a study in about 1,000 patients.

It's possible that this elevated mortality risk may be controlled using nutritional supplements or treatments aimed at cutting the inflammation associated with hypoalbuminemia, Tamara Horwich, M.D., said at the annual scientific sessions of the American Heart Association.

It's unclear what links hypoalbuminemia with worse survival during heart failure (HF), but several candidate mechanisms exist. These include hemodilution, cardiac cachexia, biventricular HF, reduced colloid osmotic pressure causing pulmonary edema, and reduced tolerability and use of optimal medical therapy, said Dr. Horwich of the University of California, Los Angeles.

Prior studies had linked hypoalbuminemia with a higher risk of death in a variety of disease states, including cancer, end-stage renal disease, infections, and cardiac surgery. But until now, few studies had examined whether a similar association exists in patients with HF.

To assess this potential link, Dr. Horwich and her associates reviewed case records for 1,162 HF patients who were treated at UCLA Medical Center from December 1983 through June 2004. Some patients were excluded because their left ventricular ejection fraction was greater than 40% or they had inadequate follow-up. The study focused on the 1,039 eligible patients who remained. Their average age was 52 years, and their mean ejection fraction was 23%.

Patients were diagnosed with hypoalbuminemia if their serum albumin was less than 3.4 g/dL. About 25% of the patients in this study had hypoalbuminemia, a prevalence consistent with reports from prior studies of HF patients. Low albumin levels were most prevalent in lean patients, with a prevalence of 29%, but hypoalbuminemia was also common in overweight and obese patients, with prevalences of 15% and 20%, respectively.

The 1-year survival rate in patients who were hypoalbuminemic at baseline was 68%, compared with more than 80% in those with normal baseline levels.

In a multivariate analysis that adjusted for potential confounders, including age, sex, and body mass index, patients who had low serum albumin were 2.8-fold more likely to die, compared with patients with a serum albumin level within the normal range, Dr. Horwich said.

A new certification program for the implantation of left ventricular assist devices was released for review by the Joint Commission on Accreditation of Healthcare Organizations.

The certification will be conducted within the Disease‐Specific Care Certification program. Organizations seeking certification will have to meet the standards, practice guidelines, and performance measurements of the specific‐care program, as well as left ventricular assist device (LVAD)‐specific requirements based on those used in the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial, according to the Association for the Advancement of Medical Instrumentation (AAMI). The AAMI expects the requirements to be ready for Centers for Medicare and Medicaid Services review by April.

A new certification program for the implantation of left ventricular assist devices was released for review by the Joint Commission on Accreditation of Healthcare Organizations.

The certification will be conducted within the Disease‐Specific Care Certification program. Organizations seeking certification will have to meet the standards, practice guidelines, and performance measurements of the specific‐care program, as well as left ventricular assist device (LVAD)‐specific requirements based on those used in the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial, according to the Association for the Advancement of Medical Instrumentation (AAMI). The AAMI expects the requirements to be ready for Centers for Medicare and Medicaid Services review by April.

A new certification program for the implantation of left ventricular assist devices was released for review by the Joint Commission on Accreditation of Healthcare Organizations.

The certification will be conducted within the Disease‐Specific Care Certification program. Organizations seeking certification will have to meet the standards, practice guidelines, and performance measurements of the specific‐care program, as well as left ventricular assist device (LVAD)‐specific requirements based on those used in the Randomized Evaluation of Mechanical Assistance for the Treatment of Congestive Heart Failure (REMATCH) trial, according to the Association for the Advancement of Medical Instrumentation (AAMI). The AAMI expects the requirements to be ready for Centers for Medicare and Medicaid Services review by April.

SEATTLE — The long-term use of β‐blockers in heart failure patients with chronic obstructive pulmonary disease and/or asthma did not increase the risk of respiratory complications, results from a large retrospective study have shown.

“Although a history of asthma and/or COPD is still considered a relative contraindication to the use of β‐blockers in the management of [heart failure], our study found that long‐term use did not increase the risk for respiratory complications,” Jay I. Peters, M.D., said at a press briefing during the annual meeting of the American College of Chest Physicians. “We did not see any differences in outcome with the use of cardioselective vs. noncardioselective β‐blockers. The proven mortality benefit of β‐blocking medication in [heart failure] mandates their use whenever possible.”

During the 1960s, physicians viewed β‐blockers as contraindicated in patients with HF. “Subsequent research revealed that the use of cardioselective β‐blockers upregulated the β‐receptor and was useful” in patients with HF, said Dr. Peters of the division of pulmonary diseases and critical care medicine at the University of Texas Health Science Center at San Antonio.

In fact, studies have shown improved survival among HF patients on β‐blockers: For every 20 patients treated with these drugs, one life is saved (Ann. Intern. Med. 2001;134:550‐60; N. Engl. J. Med. 2001;344:1711‐2).

“Unfortunately, many review articles and guidelines often list asthma and COPD as relative contraindications to using β‐blockers. Many physicians in the community are hesitant to use these medications if the patient has any history of obstructive lung disease,” he noted.

A recent metaanalysis of data on 141 patients concluded that cardioselective β‐blockers are not associated with increased respiratory symptoms or inhaler use, and that β‐blockers may enhance the effect of inhaled β‐agonist (Cochrane Database Syst. Rev. 2002;4:CD002992). But “the duration of the studies was only 3 days to 4 weeks, and only 46 patients had pulmonary function tests,” Dr. Peters said.

In a study funded by the U.S. Department of Defense, he and his associates evaluated the prevalence of β‐blocker use and the prevalence of respiratory events in patients with COPD and/or asthma. Their retrospective analysis of prospectively collected data included 1,067 patients with HF who were followed over 18 months. Investigators reviewed every nonroutine office visit, ER visit, and hospitalization over the 18‐month period to evaluate respiratory symptoms and cardiac symptoms.

The prevalence of asthma was 5.9%, and that of COPD was 11.2%; 2.5% of patients had both COPD and asthma. “Overall, 19.6% of patients had obstructive lung disease and could have benefited from β‐blockers,” he said.

Only 39% of patients with asthma and COPD were on β‐blockers. About 45% of asthmatics and 35% of patients with COPD were on β‐blockers. In addition, 49% of the patients were prescribed cardioselective β‐blockers “that are felt to be safer in patients with obstructive lung disease.”

Patients with HF and any respiratory diagnosis had a threefold increase in respiratory encounters, compared with patients who had a diagnosis of HF alone.

Overall, the use of β‐blockers in patients with asthma and/or COPD did not increase the number of respiratory encounters in terms of unscheduled office visits, ER visits, or hospitalizations.

β‐Blocker use in patients with asthma and COPD statistically lowered the rate of respiratory events, he noted, “but the number of patients in this group was small, and larger studies will be needed to confirm this finding.”

SEATTLE — The long-term use of β‐blockers in heart failure patients with chronic obstructive pulmonary disease and/or asthma did not increase the risk of respiratory complications, results from a large retrospective study have shown.

“Although a history of asthma and/or COPD is still considered a relative contraindication to the use of β‐blockers in the management of [heart failure], our study found that long‐term use did not increase the risk for respiratory complications,” Jay I. Peters, M.D., said at a press briefing during the annual meeting of the American College of Chest Physicians. “We did not see any differences in outcome with the use of cardioselective vs. noncardioselective β‐blockers. The proven mortality benefit of β‐blocking medication in [heart failure] mandates their use whenever possible.”

During the 1960s, physicians viewed β‐blockers as contraindicated in patients with HF. “Subsequent research revealed that the use of cardioselective β‐blockers upregulated the β‐receptor and was useful” in patients with HF, said Dr. Peters of the division of pulmonary diseases and critical care medicine at the University of Texas Health Science Center at San Antonio.

In fact, studies have shown improved survival among HF patients on β‐blockers: For every 20 patients treated with these drugs, one life is saved (Ann. Intern. Med. 2001;134:550‐60; N. Engl. J. Med. 2001;344:1711‐2).

“Unfortunately, many review articles and guidelines often list asthma and COPD as relative contraindications to using β‐blockers. Many physicians in the community are hesitant to use these medications if the patient has any history of obstructive lung disease,” he noted.

A recent metaanalysis of data on 141 patients concluded that cardioselective β‐blockers are not associated with increased respiratory symptoms or inhaler use, and that β‐blockers may enhance the effect of inhaled β‐agonist (Cochrane Database Syst. Rev. 2002;4:CD002992). But “the duration of the studies was only 3 days to 4 weeks, and only 46 patients had pulmonary function tests,” Dr. Peters said.

In a study funded by the U.S. Department of Defense, he and his associates evaluated the prevalence of β‐blocker use and the prevalence of respiratory events in patients with COPD and/or asthma. Their retrospective analysis of prospectively collected data included 1,067 patients with HF who were followed over 18 months. Investigators reviewed every nonroutine office visit, ER visit, and hospitalization over the 18‐month period to evaluate respiratory symptoms and cardiac symptoms.

The prevalence of asthma was 5.9%, and that of COPD was 11.2%; 2.5% of patients had both COPD and asthma. “Overall, 19.6% of patients had obstructive lung disease and could have benefited from β‐blockers,” he said.

Only 39% of patients with asthma and COPD were on β‐blockers. About 45% of asthmatics and 35% of patients with COPD were on β‐blockers. In addition, 49% of the patients were prescribed cardioselective β‐blockers “that are felt to be safer in patients with obstructive lung disease.”

Patients with HF and any respiratory diagnosis had a threefold increase in respiratory encounters, compared with patients who had a diagnosis of HF alone.

Overall, the use of β‐blockers in patients with asthma and/or COPD did not increase the number of respiratory encounters in terms of unscheduled office visits, ER visits, or hospitalizations.

β‐Blocker use in patients with asthma and COPD statistically lowered the rate of respiratory events, he noted, “but the number of patients in this group was small, and larger studies will be needed to confirm this finding.”

SEATTLE — The long-term use of β‐blockers in heart failure patients with chronic obstructive pulmonary disease and/or asthma did not increase the risk of respiratory complications, results from a large retrospective study have shown.

“Although a history of asthma and/or COPD is still considered a relative contraindication to the use of β‐blockers in the management of [heart failure], our study found that long‐term use did not increase the risk for respiratory complications,” Jay I. Peters, M.D., said at a press briefing during the annual meeting of the American College of Chest Physicians. “We did not see any differences in outcome with the use of cardioselective vs. noncardioselective β‐blockers. The proven mortality benefit of β‐blocking medication in [heart failure] mandates their use whenever possible.”

During the 1960s, physicians viewed β‐blockers as contraindicated in patients with HF. “Subsequent research revealed that the use of cardioselective β‐blockers upregulated the β‐receptor and was useful” in patients with HF, said Dr. Peters of the division of pulmonary diseases and critical care medicine at the University of Texas Health Science Center at San Antonio.

In fact, studies have shown improved survival among HF patients on β‐blockers: For every 20 patients treated with these drugs, one life is saved (Ann. Intern. Med. 2001;134:550‐60; N. Engl. J. Med. 2001;344:1711‐2).

“Unfortunately, many review articles and guidelines often list asthma and COPD as relative contraindications to using β‐blockers. Many physicians in the community are hesitant to use these medications if the patient has any history of obstructive lung disease,” he noted.

A recent metaanalysis of data on 141 patients concluded that cardioselective β‐blockers are not associated with increased respiratory symptoms or inhaler use, and that β‐blockers may enhance the effect of inhaled β‐agonist (Cochrane Database Syst. Rev. 2002;4:CD002992). But “the duration of the studies was only 3 days to 4 weeks, and only 46 patients had pulmonary function tests,” Dr. Peters said.

In a study funded by the U.S. Department of Defense, he and his associates evaluated the prevalence of β‐blocker use and the prevalence of respiratory events in patients with COPD and/or asthma. Their retrospective analysis of prospectively collected data included 1,067 patients with HF who were followed over 18 months. Investigators reviewed every nonroutine office visit, ER visit, and hospitalization over the 18‐month period to evaluate respiratory symptoms and cardiac symptoms.

The prevalence of asthma was 5.9%, and that of COPD was 11.2%; 2.5% of patients had both COPD and asthma. “Overall, 19.6% of patients had obstructive lung disease and could have benefited from β‐blockers,” he said.

Only 39% of patients with asthma and COPD were on β‐blockers. About 45% of asthmatics and 35% of patients with COPD were on β‐blockers. In addition, 49% of the patients were prescribed cardioselective β‐blockers “that are felt to be safer in patients with obstructive lung disease.”

Patients with HF and any respiratory diagnosis had a threefold increase in respiratory encounters, compared with patients who had a diagnosis of HF alone.

Overall, the use of β‐blockers in patients with asthma and/or COPD did not increase the number of respiratory encounters in terms of unscheduled office visits, ER visits, or hospitalizations.

β‐Blocker use in patients with asthma and COPD statistically lowered the rate of respiratory events, he noted, “but the number of patients in this group was small, and larger studies will be needed to confirm this finding.”