Abstract

In 30 dogs, acute myocardial infarction was produced by coronary artery ligation, and the dogs were divided into three groups. Group A animals (n = 10) had coronary ligation only. In Group B (n = 12), paired ventricular pacing was initiated 30 minutes following infarction. Group C (n = 8) was identical to Group B except that propranolol, 0.2 mg per kilogram of body weight, was given intravenously 10 minutes before the initiation of paired ventricular pacing. High-fidelity left ventricular pressures, acceleration of aortic flow (max dQ/dt), coronary sinus creatine phosphokinase (CPK), and epicardial mapping were recorded serially before and after coronary artery ligation. The incidence of ventricular fibrillation was not statistically different in Groups A and C (2/10 and 2/8, respectively), but it was higher in Group B (6/12) ( p < 0.05). The maximum first derivative of left ventricular pressure divided by isovolumic-developed pressure [(dP/ dt)/P] and max dQ/dt during the 30 minutes following ligation were similar in all groups; however, in Group B, max (dP/dt)/P and max dQ/dt increased after the initiation of paired ventricular pacing ( p < 0.01) while in Group C the same factors increased insignificantly. Coronary sinus CPK as well as the sum of ST segment elevations and the number of sites showing ST segment elevation increased significantly more in Group B and significantly less in Group C compared with control Group A. This study suggests that in experimental acute myocardial infarction, the combined effects of paired ventricular pacing and propranolol decrease myocardial ischemic injury without altering left ventricular performance or increasing the incidence of ventricular fibrillation.

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