Arrhythmogenic effects of graded coronary blood flow reductions superimposed on prior myocardial infarction in dogs.

BACKGROUND: We studied arrhythmogenesis and its underlying pathophysiology during graded reductions of coronary blood flow, superimposed on prior myocardial infarction to test the hypothesis that spontaneous ventricular fibrillation and induced ventricular tachycardia are dependent on different patterns of coronary flow reduction in hearts with prior myocardial infarction. METHODS AND RESULTS: In 10 sham-operated dogs (control group) and 24 dogs with 3-week-old experimental apical myocardial infarction, the left circumflex coronary artery was constricted to produce four grades of flow reduction: 25%, 50%, 75%, and 100%. Among the sham-operated control animals, only one of 10 (10%) developed spontaneous ventricular fibrillation and only two of nine (22%) were inducible into sustained ventricular tachycardia during 100% circumflex coronary artery flow reduction. No spontaneous ventricular fibrillation or inducible ventricular tachycardia occurred with lesser grades (25%, 50%, or 75%) of flow reduction among the control animals. In the myocardial infarction group, five of 24 dogs (21%) were inducible before flow reduction. However, 50% flow reduction in the myocardial infarction group resulted in inducibility of ventricular tachycardia in 12 of 24 dogs (50%); nine of 16 (56%) during 75% flow reduction; and six of 11 (55%) with 100% flow reduction. In addition, none of the dogs in the myocardial infarction group developed spontaneous ventricular fibrillation during 25% or 50% flow reduction, whereas six of 22 (27%) developed ventricular fibrillation during 75% flow reduction and 10 of 21 (48%) during 100% flow reduction. In dogs with spontaneous ventricular fibrillation during flow reduction, the total myocardial mass of the ischemic "risk" zone and infarcted zone was significantly greater than in those without spontaneous ventricular fibrillation (68 +/- 5% versus 56 +/- 6% p less than 0.01). There was no difference in the total myocardial mass of the ischemic risk zone and infarcted zone between dogs with and without inducible ventricular tachycardia during flow reduction. CONCLUSIONS: In canine model of subacute myocardial infarction, superimposed ischemia increased the likelihood of inducible sustained ventricular tachycardia with lesser grades of coronary flow reduction compared with that necessary to allow spontaneous ventricular fibrillation. The underlying pathophysiology appears to differ between spontaneous ventricular fibrillation and electrically induced sustained ventricular tachycardia.