Exercise-induced ischemic arrhythmias in patients with previous myocardial infarction: Role of perfusion and tissue viability

Objectives. This study sought to investigate whether residual viability of infarcted myocardium may play role in the pathogenesis of exercise-induced ventricular arrhythmias. Background. We previously showed that transient ischemi within partially infarcted areas often precipitates ventricular arrhythmias during exercise that are consistently obliterated by intravenous nitrates. Methods. We studied 60 patients with chronic stable angin and previous myocardial infarction. All underwent at least two consecutive exercise stress tests, coronary angiography and stress/rest myocardial perfusion tomography by Tc-99m 2-methoxy isobutyl isonitrile (MIBI). In the last 26 consecutive patients, residual viability was assessed by single-photon emission computed tomography (SPECT) using fluorine (F)-18 fluorodeoxyglucose. Perfusion and metabolic dat were evaluated qualitatively by three independent observers in blinded manner. Results. With exercise, 30 patients (group A) consistently developed ventricular arrhythmias (>10 ventricular ectopic beats/min, couplets, nonsustained ventricular tachycardia); the remaining 30 patients (group B) did not. The severity of coronary artery disease (Gensini score) was similar in the two groups. Postexercise SPECT showed partial reperfusion of an infarcted are in 28 of 30 patients of group but in only 9 of 30 of group B (p < 0.0001). Uptake of F-18 fluorodeoxyglucose was observed within the infarcted zone in 10 of 13 and 1 of 13 patients in groups and B, respectively (p = 0.0003). Conclusions. In patients with myocardial infarction, exercise-induced ventricular arrhythmias appear to be triggered by transient ischemi occurring within partially necrotic are containing large amounts of viable myocardium. Therefore, occurrence of arrhythmias during exercise may represent clue to the presence of residual viability within previously infarcted area.