Effect of paired ventricular pacing upon myocardial infarction size

Abstract

Although paired ventricular pacing may improve cardiodynamics following acute myocardial infarction, its effect on myocardial infarct size is not known. In 22 dogs, acute myocardial infarction was produced by selective coronary artery ligation. High fidelity left ventricular pressure, dp dt max , acceleration of aortic flow ( dQ dt ), coronary flow and epicardial mapping were recorded before and at 15-min intervals following acute myocardial infarction for a total of 90 min. Coronary sinus CPK was measured before coronary occlusion and then every 30 min for a period of 150 min. In Group A ( n = 10) animals had an acute myocardial infarction only, while in Group B ( n = 12), paired ventricular pacing was initiated 30 min postinfarction and continued throughout the study. Two dogs from Group A and six from Group B developed ventricular fibrillation and were excluded from the study. In Group A dp dt p , dQ dt and heart rate did not change, while in Group B dp dt p increased from 20.0 ± 1.5 to 30.2 ± 1.5 ( P < 0.05) and dQ dt increased from 19.0 ± 1.7 to 27.1 ± 2.5 ( P < 0.05). Coronary flow, arterial and coronary sinus blood gases were similar in both groups. CPK increased more in Group B than in Group A ( P < 0.05). ΣST was unchanged in Group a between 30 and 90 min post-infarction while in Group B ΣST increased at the same period from 36.0 ± 2.8 to 62.5 ± 8.6 ( P < 0.05). These data indicate that paired ventricular pacing increased ischemic injury in acute myocardial infarction, due to increased oxygen consumption resulting from the positive inotropic effect exceeding the influence of a decreased heart rate.