Reicher-Reiss H
Heart Institute, Chaim Sheba Medical Center, Tel Hashomer, Israel.
Eur Heart J. 1988 Jun;9 Suppl H:101-4. doi: 10.1093/eurheartj/9.suppl_h.101.
Calcium channel blocking drugs improve systolic function, due to a decrease in left ventricular afterload, and may thus be particularly suitable for therapy of patients with concomitant congestive heart failure and myocardial ischaemia. Since ischaemic heart disease is a major cause of congestive heart failure and further ischaemia may contribute to further left ventricular dysfunction, studies were performed to establish the therapeutic role of calcium channel blockers. Concern has been raised that at high doses, calcium channel blockers have a negative inotropic effect and may lead to deterioration of myocardial systolic function. Clinical studies assessing the role of verapamil and diltiazem in congestive heart failure are scarce, because these drugs may result in a further decrease in cardiac output, especially in the presence of pre-existing left ventricular dysfunction. In vitro observations show that nifedipine is more potent on vascular smooth muscle than on myocardium. It has been suggested that in man, nifedipine does not usually reach concentrations high enough to depress myocardium and the vasodilating left ventricular unloading effect becomes dominant. Analysis of the available clinical data is difficult, but published data concerning the oral or sublingual administration of nifedipine in congestive heart failure suggest that the major haemodynamic effect is a decrease in systemic vascular resistance by 33%, resulting in an increase in cardiac output of 24%. Heart rate was generally unchanged. Right atrial pressures showed minimal change, whereas pulmonary capillary wedge pressure decreased by 16%. The response is more favourable if the congestive heart failure is more severe. A new dihydropyridine, nisoldipine, was evaluated during chronic administration over 8 weeks in patients with severe congestive heart failure.(ABSTRACT TRUNCATED AT 250 WORDS)
钙通道阻滞剂可改善收缩功能,这是由于左心室后负荷降低,因此可能特别适用于伴有充血性心力衰竭和心肌缺血患者的治疗。由于缺血性心脏病是充血性心力衰竭的主要病因,且进一步的缺血可能导致左心室功能进一步恶化,因此开展了多项研究以确定钙通道阻滞剂的治疗作用。有人担心,高剂量的钙通道阻滞剂具有负性肌力作用,可能导致心肌收缩功能恶化。评估维拉帕米和地尔硫䓬在充血性心力衰竭中作用的临床研究较少,因为这些药物可能导致心输出量进一步降低,尤其是在已有左心室功能障碍的情况下。体外观察表明,硝苯地平对血管平滑肌的作用强于对心肌的作用。有人提出,在人体中,硝苯地平通常不会达到足以抑制心肌的浓度,血管舒张的左心室减负作用占主导地位。对现有临床数据进行分析很困难,但已发表的有关硝苯地平口服或舌下给药治疗充血性心力衰竭的数据表明,主要的血流动力学效应是全身血管阻力降低33%,心输出量增加24%。心率通常不变。右心房压力变化极小,而肺毛细血管楔压降低了16%。充血性心力衰竭越严重,反应越有利。一种新的二氢吡啶类药物尼索地平,在重症充血性心力衰竭患者中进行了为期8周的长期给药评估。(摘要截短于250词)