Haemodynamic and clinical effects of an intravenous potassium channel opener--a review

Abstract

Intravenous nicorandil (4-12 mg) produced a significant decrease in mean arterial blood pressure (-5 to -15%), systemic vascular resistance (-8 to -27%), pulmonary capillary wedge pressure (-15 to -41%) and left ventricular end-diastolic pressure (-8 to -18%) in patients with coronary artery disease, myocardial infarction or congestive heart failure. Cardiac output was significantly increased (+3 to +19%) in most studies. These haemodynamic effects of intravenous nicorandil (4-8 mg) were comparable to those of nitroglycerin (0.3 mg), although a greater decrease in preload was produced by nitroglycerin. Moreover, no significant haemodynamic tolerance developed over a 12 to 24 h period during continuous infusion of nicorandil (2.4 micrograms.kg-.min-1) in patients with heart failure, in contrast to nitroglycerin infusion (0.65 microgram.kg-1 x min-1). Intravenous nicorandil (4-12 mg) was also shown to produce a slightly smaller increase (8-27%) in the diameter of the large coronary arteries compared to that of sublingual nitroglycerin (0.3 mg) (16-32%) and to cause a significant decrease in coronary vascular resistance (-9 to -53%) and a significant increase in coronary sinus flow (+6 to +81%) in patients with coronary artery disease. The efficacy of intravenous nicorandil (2-6 mg.h-1) in unstable angina pectoris has been compared with that of isosorbide dinitrate (2-5 mg.h-1) in a double-blind, multicentre trial. Over a 3 to 9 day period, nicorandil therapy tended to be more effective in abolishing anginal attacks and decreasing nitroglycerin consumption.