A Different Mechanism in the Treatment of Ischemic Heart Disease: K+ Channel Activation and Nicorandil

Nicorandil, investigated in many studies in the last 10 years, has a structure and mode of action similar to organic nitrates in addition to its K+ channel opener effect, a different and probably wider therapeutic spectrum can be achieved by this property of the drug. Nicorandil decreases both preload by means of cGMP-induced vasodilatation and afterload by K+ channel activation, but it does not give rise to an increase in heart rate. Tolerance, the greatest problem of nitrates, does not develop during treatment with this drug. Nicorandil decreases both systemic vascular resistance, left ventricular end-diastolic pressure and pulmonary artery wedge pressure and increases both ejection fraction and cardiac index despite having no primary inotropic effect in patients with congestive heart failure. In addition, nicorandil, by its K+ channel activating effect, decreases area of infarction and reperfusion injury independent from its hemodynamic effects. Many further large and long-term studies are needed to confirm these.