Encircling endocardial ventriculotomy for refractory ischemic ventricular tachycardia. II. Effects on regional myocardial blood flow.

Previous experimental studies of the encircling endocardial ventriculotomy (EEV) have shown a significant alteration of normal local electrical activity within the encompassed region. Although this procedure may result in isolation of ventricular arrhythmias, the data are more suggestive of a less specific effect on regional myocardial blood flow. This study examines the effect of EEV on local myocardial blood flow using the radioactive tracer microsphere technique in 10 dogs. Flows were determined before and after an EEV with the animals on cardiopulmonary bypass at controlled perfusion pressures, temperatures, and heart rates. Blood flow was studied at subepicardial and subendocardial levels inside, outside, and bordering the EEV. Prior to performance of the EEV, subepicardial blood flow in the left ventricular myocardium ranged from 0.81 +/- 0.07 to 0.89 +/- 0.08 ml/gm/min. Subendocardial flows ranged from 0.80 +/- 0.07 to 0.91 +/- 0.09 ml/gm/min. There was no significant difference between any of the flows across each respective layer of myocardium. Following the EEV procedure, blood flow to the subendocardium within the EEV fell to 0.33 +/- 0.07 ml/gm/min, while flow to the subendocardium of the normal regions of the same hearts actually increased to 1.21 +/- 0.23 ml/gm/min. Similar changes occurred at subepicardial levels, with flow at the center of the EEV falling to 0.66 +/- 0.10 ml/gm/min despite a tendency for normal subepicardial flow to increase to 1.78 +/- 0.24 ml/gm/min. Superimposed ischemia to the EEV-encompassed myocardium, created by occlusion of the distal left anterior descending coronary artery (LAD), accentuated this abnormality by demonstrating that the region continues to receive some flow from epicardially based coronary vessels. The data from this study show that the EEV decreased regional blood flow to the encompassed myocardium and suggests that myocardial ischemia may be responsible for ablation of the delicate re-entrant mechanisms that sustain ventricular tachyarrhythmias.