JACC March 6, 2002 1160-109 Mechanisms Underlying the Reentrant Circuit of Ventricular Tachycardia in Isolated Canine Left Ventrlcular Preparation Using Optical Mapping

The cellular mechanisms underlying the reentrant circuit of ventdcular tachycardia (VT) after myocardial infarction (MI) have not yet been clearly understood. Using optical mapping and microelectroda recording in isolated canine left ventdcular preparation, we charactadzed the reentrant circuit of V'I" and its relationship to action potentials recorded in the infarction border zone (BZ). The preparation was isolated from left ventricular free wall and perfused with Tyrode's solution through the left circumflex artery (LCX). MI was created by completely tightening one of the LCX branches. No VT was induced before MI by programmed extrastimuli ($1 to $4). However, 4 hrs after MI, sustained monomorphic VTs at cycle lengths of 375±12 ms were induced in all 6 preparations. Optical mappings during sustained VT showed 2 types of reentrant circuits as functional spiral waves reentry (n=4) using only part of the BZ and anatomic reentry rotating around the obstacle of infarction tissue (n=2). Low amplitude tractionatad electrograms were obtained from site of slow conduction within the BZ. Compared to the non-ischemic normal tissue, action potentials recorded from the BZ (n=6) showed decrease in amplitude (87.5±2.5 vs. 62.2±4.5 mV, p<0.0t), maximal diastolic potential (80.4±2.2 vs. 58.7±5.4 mV, p<0.05), dV/dt (156.6±12.7 vs. 26.4±6.5 V/sec, p<0.05), and ADPg0 (208.3±7.2 vs. 145.2±7.4 ms, p<0.01), consistent with slow conduction and unidirectional block occurred in the BZ. In conclusion, sustained monomorphic VTs developed after MI were due to functional spiral wave reentry or anatomic macroreentry around the infarction area. Both types of reentries involved in the BZ with delayed conduction and unidirectional block.