Effetti dei calcio antagonisti nella protezione antiaritmica: studi sperimentali.

The calcium overload, secondary to myocardial ischemia and also to post-ischemic reperfusion, produces biochemical changes which in turn affect cardiac electrophysiology creating a substrate favorable for the genesis of ventricular tachycardia and fibrillation. Besides the more obvious effects on normal automaticity and reentry there is growing evidence suggesting a critical link between calcium influx, afterdepoarizations and triggered activity. When life-threatening arrhythmias are induced by the combination of acute myocardial ischemia and of sympathetic hyperactivity, class I antiarrhythmic agents are almost completely unable to produce protection, whereas a significant but incomplete reduction in the incidence of ventricular fibrillation is achieved by adrenergic blocking agents. By contrast, a complete suppression of these malignant arrhythmias follows administration of either verapamil or diltiaziem; nifedipine, partly acting through different mechanisms, provides e significant but incoplete protection. When ventricular tachyarrhythmias are produced by reperfusion, diltiazem is very effective provided that is administered prior to coronary occlusion. Calcium blockers with a favorable ratio between positive cardiac electrophysiologic effects and negative inotropic effects can be expected to significantly contribute to the reduction of ischemia-related sudden cardiac death.