ANISOTROPIC CONDUCTION CHARACTERISTICS IN ISCHEMIA-REPERFUSION INDUCED CHRONIC MYOCARDIAL-INFARCTION

Objectives: Anisotropic properties of cardiac tissue play an important role in initiation and perpetuation of ventricular tachycardia. Howev er, anisotropic conduction properties in different morphologic types o f chronic myocardial infarctions as well as frequency dependency still need to be elucidated. In the present study, the characteristics of a nisotropic conduction were investigated in situ in the setting of isch emia-reperfusion induced chronic myocardial infarction. Methods: Myoca rdial infarction was induced in 12 dogs by a percutaneous transcathete r left anterior descending coronary artery occlusion-reperfusion techn ique. Four additional dogs served as normal controls. After 14 to 20 d ays, epicardial mapping was performed using simultaneous unipolar reco rdings from 240 electrodes of a plaque electrode array placed on the e picardial border zone overlying the infarctions. Constant rate pacing with five cycle lengths (CL) ranging from 500 to 200 ms as well as pro grammed electrical stimulation (PES) with four basic cycle lengths (BC L) ranging from 430 to 300 ms and single extrastimuli (S2) were perfor med. Results: Two anatomically different patterns of epicardial surfac e morphology were analyzed, designated as type I and type II. In seven animals, there was a continuous thin layer of surviving epicardial mu scle fibers overlying the infarction (type I). During pacing with CL o f 500 vs 200 ms, conduction velocity longitudinal to fiber orientation (theta L) decreased significantly in the infarcted animals compared t o control group (10.9 % vs 5.2 %, p<0.05) whereas conduction Velocity transverse to fiber axis (theta T) decreased to a similar degree in co ntrol and infarcted animals (6.9 vs 7.4 %, n.s.). After premature stim ulation, there was considerably greater reduction in theta L in infarc ted animals than in controls (39.8 % vs 31.5 %, p<0.05) whereas theta T decreased to a similar extend in infarcted and control animals (22.2 % vs 21.4 %, n.s.). During constant rate pacing and premature stimula tion, no functional conduction block was induced in type I infarctions . In five animals, the transmural infarctions clearly extended to the epicardial surface, but continuous strands of surviving epicardial mus cle fibers traversed the area of necrosis (type II). During PES with S 2, functional conduction block and areas of very slow conduction were observed in each case. Conclusions: In ischemia-reperfusion induced ch ronic myocardial infarctions, different epicardial patterns of morphol ogy were observed. Anisotropic conduction was frequency dependent in t he longitudinal but not in the transverse direction. In type I infarct ions, functional conduction block was not inducible during PES whereas in type II infarctions, prerequisites for reentrant arrhythmias like functional conduction block and very slow conduction were induced in e ach case by single extrastimuli.