title: Update on ivabradine for heart failure.
abstract: Despite dramatic advances in therapy for heart failure (HF) during the past 3 decades, hospitalization and mortality rates remain relatively high. In recent decades, it has become apparent that HF is divisible into two equally lethal but pathophysiologically different sub-classes, the first comprising patients with LV systolic dysfunction [heart failure with reduced ejection fraction (HFrEF)] and the other, approximately equal in size, involving patients with "preserved" systolic function [heart failure with preserved ejection fraction (HFpEF)]. Evidence-based event reducing therapy currently is available only for HFrEF. With the completion of seminal trials of beta blockers, now part of standard therapy for HFrEF, it was apparent that heart rate slowing is an underlying basis of clinical effectiveness of HFrEF therapy. With the discovery of the "f current" that modulates the slope of spontaneous diastolic depolarization of the sino-atrial node, a non-beta blockade approach to heart rate slowing became available. Ivabradine, the first FDA-approved f-current blocker for HFrEF, markedly reduces hospitalizations for worsening heart failure, while also progressively reducing mortality as pre-therapy heart rate increases, and also promotes beneficial left ventricular remodeling, improves health-related quality of life and is effective despite a wide range of comorbidities. The drug is well tolerated and adverse effects are relatively few. Ivabradine represents an important addition to the armamentarium for mitigation of HFrEF.
authors.affiliation: The Howard Gilman Institute for Heart Valve Disease, and the Schiavone Institute for Cardiovascular Translational Research, State University of New York Downstate Medical Center, Brooklyn and New York, NY. Electronic address: jsborer1@gmail.com.
authors.forename: Jeffrey S
authors.initials: JS
authors.lastname: Borer
authors.affiliation: GVM Care&Research, Ettore Sansavini Health Science Foundation, Cotignola, Italy.
authors.forename: Luigi
authors.initials: L
authors.lastname: Tavazzi
mesh_terms: D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000627:therapeutic use*; D001552:Benzazepines / Q000009:adverse effects / Q000627:therapeutic use*; D054815:Cyclic Nucleotide-Gated Cation Channels / Q000037:antagonists & inhibitors / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000401:mortality / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D000077550:Ivabradine; D011788:Quality of Life; D015398:Signal Transduction / Q000187:drug effects; D012849:Sinoatrial Node / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000187:drug effects; D020257:Ventricular Remodeling / Q000187:drug effects
chemical_list: D000889:Anti-Arrhythmia Agents; D001552:Benzazepines; D054815:Cyclic Nucleotide-Gated Cation Channels; D000077550:Ivabradine
keywords: Clinical pharmacology; Heart failure; Heart rate slowing; Systolic heart failure