Ferrari Roberto, Cargnoni Anna, Ceconi Claudio
University of Ferrara, Italy.
Pharmacol Res. 2006 May;53(5):435-9. doi: 10.1016/j.phrs.2006.03.018. Epub 2006 Mar 28.
Ivabradine, the first representative of a new class of exclusive heart rate-reducing agents, selectively inhibits the I(f) current in the sinoatrial node. The direct electrophysiological consequence of this inhibition is a reduction in the slope of the diastolic depolarisation curve and a decrease in heart rate. Pharmacological inhibition of the I(f) current with ivabradine has been shown to preserve coronary vasodilatation upon exercise, i.e., myocardial perfusion, with no negative inotropic effects and maintenance of cardiac contractility. Ivabradine protects the myocardium during ischaemia, improves left ventricular function in congestive heart failure, and reduces remodelling subsequent to myocardial infarction. Pure heart rate reduction by specific and selective I(f) inhibition decreases oxygen demand, improves myocardial energetics and improves perfusion of the ischaemic myocardium. We can expect distinct clinical benefits from long-term heart rate reduction in patients with chronic ischaemic disease.
伊伐布雷定是新型专一性降低心率药物的首个代表药物,可选择性抑制窦房结的If电流。这种抑制作用直接产生的电生理效应是舒张期去极化曲线斜率降低及心率下降。已证实,使用伊伐布雷定对If电流进行药理抑制可在运动时维持冠状动脉舒张,即维持心肌灌注,且无负性肌力作用,并能保持心脏收缩力。伊伐布雷定在心肌缺血时可保护心肌,改善充血性心力衰竭患者的左心室功能,并减少心肌梗死后的重塑。通过特异性和选择性抑制If电流来单纯降低心率可减少氧需求,改善心肌能量代谢,并改善缺血心肌的灌注。我们可以预期,长期降低慢性缺血性疾病患者的心率会带来明显的临床益处。