Abstract
Resting heart rate (HR) is increased in patients with heart failure (HF). Sustained tachycardia can cause HF. The magnitude of HR reduction in treatment trials of patients with HF is associated with a reduction in mortality. Yet, the mechanistic and causal role of HR in HF is unclear, and recent trials with selective HR reduction have not consistently achieved benefit: the BEAUTIFUL trial in patients with coronary artery disease and left ventricular dysfunction did not achieve a significant benefit in the primary endpoint, and only the coronary outcome, not the HF outcome, was improved; in the SHIFT trial, however, patients with symptomatic heart failure had a significant benefit in the primary endpoint of cardiovascular mortality and hospitalization for worsening HF. The present review addresses the pathophysiology of tachycardia-induced HF, the force-frequency relationship, and the clinical potential of HR reduction in HF.
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