MODEL OF CARDIAC-ARRHYTHMIAS AND SUDDEN-DEATH - CANTHARIDIN-INDUCED TOXIC CARDIOMYOPATHY

Abstract

Toxic cardiomyopathy may result in fatal arrhythmias. To develop a model to study ventricular fibrillation and asystole, the effect of cantharidin in the production of cardiac arrhythmias and myocardial damage was studied. Conscious albino rabbits, weighing between 1.8 to 2.8 kg, received an i.v. bolus injection of cantharidin ranging from 0.6 to 1.9 mg/kg or a control injection of solvent. The ECG was continuously monitored on tape before and after injection for extended periods of time. Dose-related effects were observed with the following: presence, magnitude and duration of ST depression after injection; occurrence of fatal arrhythmias; survival time (high doses were usually fatal within 3 h); and EM evidence of mitochondrial swelling, intramitochondrial granules and myofibrillar degeneration. The most common arrhythmias associated with the high doses of cantharidin were frequent ventricular ectopics, ventricular tachycardia, ventricular fibrillation or asytole. The arrhythmias could not be explained by alterations in blood pressure, electrolytes or blood gases. Cardiotoxic properties of cantharidin and its ability to produce fatal cardiac arrhythmias are shown. It may serve as a model to study sudden death and the efficacy of antiarrhythmic drugs.