Article Ivabradine Therapy in Heart Failure Management: Optimizing O...
Ivabradine affects heart rate primarily by selectively inhibiting the If (funny current) channels in the sinoatrial node of the heart. These channels play a crucial role in regulating the heart's pacemaker activity by allowing the influx of sodium and potassium ions during the diastolic phase, which contributes to the spontaneous depolarization of cardiac pacemaker cells.
By blocking the If channels, ivabradine slows down the rate at which these pacemaker cells depolarize, effectively prolonging the duration of the diastolic phase of the cardiac cycle. This action leads to a reduction in heart rate without directly affecting myocardial contractility or the force of cardiac contraction.
In contrast to beta-blockers, which exert their effects on heart rate and contractility by blocking beta-adrenergic receptors, ivabradine specifically targets the If channels in the sinoatrial node, making it a selective and direct modulator of heart rate. This mechanism of action allows ivabradine to lower heart rate without compromising cardiac function, making it particularly useful in conditions such as heart failure and angina where controlling heart rate is beneficial.