In a feline model, delayed myocardial repolarization (QT prolongation) precedes hydrocarbon-catecholamine-induced ventricular fibrillation.
No immediate clinical implications; extends feline evidence linking QT prolongation to catecholamine VF but leaves human translation open.
An increase in the QT interval and the QT/RR ratio was observed prior to the onset of multiple focal ventricular tachycardia and fibrillation induced by petroleum ether and epinephrine or norepinephrine in cats under pentobarbital anesthesia. This prolongation of the QT interval before experimental ventricular tachycardia and fibrillation was significantly greater than that produced by these catecholamines in the absence of arrhythmias. Isoproterenol, which did not lead to ventricular tachycardia after petroleum ether, also failed to increase the duration of the QT interval. The appearance of the electrocardiogram preceding these experimental arrhythmias suggested that a delay in the repolarization of the myocardium was a factor in the precipitation of ventricular fibrillation during hydrocarbon-catecholamine syncope.
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Hutcheon et al. (1963) studied this question.
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