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Investigational and emerging therapies for heart failure

Author
Wilson S Colucci, MD
Section Editor
Stephen S Gottlieb, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC

INTRODUCTION

Treatment of heart failure (HF) is aimed at three goals: improvement in symptoms, slowing of disease progression, and prolongation of survival [1]. (See "Overview of the therapy of heart failure due to systolic dysfunction".)

Investigational and emerging therapies for heart failure will be reviewed here. These interventions have been shown to have promise in small studies, as described below, but the risk/benefit ratio and efficacy remain to be proven. Standard therapies for systolic and diastolic HF are discussed elsewhere. (See "Overview of the therapy of heart failure due to systolic dysfunction" and "Treatment and prognosis of diastolic heart failure".)

MODULATION OF HEART RATE OR AUTONOMIC TONE

Sinus node inhibition — The SHIFT trial found that the selective sinus node inhibitor ivabradine improved clinical outcomes in patients with systolic heart failure (HF), but the role of ivabradine in the treatment of systolic HF is uncertain given the stronger evidence for beta blocker therapy in this setting.

In patients with HF, an elevated heart rate is associated with worse cardiovascular outcomes. An elevated heart rate reflects, in part, activation of the sympathetic nervous system and withdrawal of parasympathetic activity, reflecting components of the neurohumoral response to HF. (See "Predictors of survival in heart failure due to systolic dysfunction", section on 'Neurohumoral activation and heart rate'.)

The SHIFT trial investigated the effect of heart rate reduction using the selective sinus node inhibitor ivabradine on outcomes in HF [2]. Six thousand, five hundred and fifty-eight patients with HF, a left ventricular ejection fraction ≤35 percent, and a sinus heart rate of ≥70 beats per minute were randomly assigned to ivabradine or placebo and followed for a median of 23 months. The primary end point was a composite of cardiovascular death or hospital admission for worsening HF. Patients in the ivabradine group experienced the primary end point less frequently than those in the placebo group (24 versus 29 percent) largely due to reduced hospitalizations for HF (hazard ratio [HR] 0.74, 95% confidence interval [CI] 0.66-0.83) and reduced deaths due to HF (HR 0.74, 95% CI, 0.58-0.94). Patients in the ivabradine group with an achieved heart rate less than 60 bpm at 28 days had fewer primary end point events than those with higher heart rates [3].

                          

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Literature review current through: Apr 2015. | This topic last updated: Apr 23, 2015.
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