Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
3019698 | Revista Española de Cardiología Suplementos | 2007 | 14 Pages |
Abstract
The heart rate is the main determinant of both myocardial oxygen demand and coronary blood flow. Heart rate is determined by spontaneous electrical activity in the pacemaker cells of the sinoatrial node. These cells exhibit a diastolic depolarization phase that drives the membrane potential towards the threshold value for initiating a new action potential, which propagates throughout the myocardium and triggers a contractile response. The If current, an inward current of Na+ and K+ ions through hyperpolarization-activated cyclic-nucleotide-gated (HCN) channels, is the main determinant of the slope of the slow diastolic depolarization phase. These channels open in response to membrane hyperpolarization and are modulated by the intracellular cAMP concentration. Ivabradine specifically blocks the If current. To do so, it crosses the membrane and binds to a receptor located on the intracellular side of the channel pore. As a result, ivabradine produces a dose-dependent decrease in heart rate that reduces myocardial oxygen demand and increases coronary blood flow. However, at therapeutic concentrations, it does not affect other cardiac ionic currents, which is why ivabradine does not alter blood pressure, cardiac contractility, or cardiac electrophysiological parameters. This article reviews ivabradine's mechanism of action, pharmacodynamic and pharmacokinetic properties, side effects, and interactions.
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Authors
Miguel Vaquero, Ricardo Gómez, LucÃa Núñez, Ricardo Caballero, Eva Delpón, Adriana Barana, Juan Tamargo,