Titrating beta-blockers likely improves outcomes in HF patients with systolic dysfunction
Titrating beta-blocker doses up to a carvedilol equivalent of 50 mg/d appears to have benefit in patients with heart failure (HF) and systolic dysfunction, according to a new study.
Titrating beta-blocker doses up to a carvedilol equivalent of 50 mg/d appears to have benefit in patients with heart failure (HF) and systolic dysfunction, according to a new study.
Researchers analyzed results from HF-ACTION (Heart Failure: A Controlled Trial Investigating Outcomes of Exercise Training) to determine whether beta-blocker dose at baseline was associated with outcomes in patients with ambulatory HF and systolic dysfunction.
The 2,331 patients in HF-ACTION were randomly assigned to exercise training versus usual care and were followed for a median of 2.5 years. The relationship between beta-blocker dose and all-cause mortality, all-cause hospitalization and secondary cardiovascular endpoints was analyzed with and without adjustment for outcome-associated variables. Although different agents were used by the participating centers in the study, beta-blocker dose at baseline was standardized by converting these different treatments into equivalent doses of carvedilol for evaluation; baseline daily dose was then analyzed in dose groups (0 mg/d, 1 to 13 mg/d, 14 to 25 mg/d, 26 to 50 mg/d, and 51 to 100 mg/d) and as a continuous variable.
The study was published online May 2 by the Journal of the American College of Cardiology.
Most of the study patients (approximately 95%) were receiving a beta-blocker. A significant inverse relationship was found between beta-blocker dose and all-cause death or hospitalization, with a linear benefit seen up to 50 mg daily. Other cardiovascular endpoints were not found to be associated with beta-blocker dose in adjusted analyses. At three months, beta-blocker dose was also significantly associated with change in peak VO2. Higher beta-blocker doses did not appear to increase bradycardia.
The authors acknowledged that their study was a post hoc analysis and excluded patients who were not ambulatory and those with preserved systolic function. They also pointed out that dose conversions are not a perfectly accurate method of comparison and that higher doses of beta-blockers may be less tolerable in sicker patients.
However, they concluded that a significant inverse relationship existed between beta-blocker dose and all-cause death or all-cause hospitalization, even after adjustment, and that bradycardia did not increase with higher doses.
“These data support the current clinical guideline recommendations that [beta-blocker] therapy should be titrated to moderate-to-high doses as used in randomized, controlled clinical trials,” they wrote.