Abstract
The aim was to determine the effect of myocardial hypertrophy on the incidence and severity of arrhythmias following reperfusion after experimental coronary artery occlusion, and to establish if the effect differed between pressure overload hypertrophy and volume overload hypertrophy. The experiments were performed in rats. Pressure overload hypertrophy was induced by aortic banding, and volume overload hypertrophy by perforation of the aortic valve. Four weeks after surgery, coronary artery occlusion and reperfusion experiments were performed. Both pressure and volume overloaded hearts exhibited a similar degree of left ventricular hypertrophy of about 45% weight gain compared to control animals. The total number of ventricular premature beats during reperfusion was not significantly increased in either model of hypertrophy. In contrast to volume overload, the incidence of reperfusion induced ventricular fibrillation was significantly increased in pressure overloaded hearts. Furthermore, there was a significant correlation between number of ventricular premature beats and degree of left ventricular hypertrophy, as well as between duration of ventricular tachycardia and degree of hypertrophy in the pressure overloaded group. Such correlations were not observed in hypertrophy due to volume overload. Neither volume nor pressure overload hypertrophy significantly increased mortality from ventricular fibrillation. An increase in cardiac mass per se does not necessarily aggravate reperfusion arrhythmias. The susceptibility to arrhythmias in this model seems to be critically dependent on the nature of the stimulus triggering left ventricular hypertrophy.
Published Version
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