ANISOTROPIC CONDUCTION CHARACTERISTICS IN CHRONIC MYOCARDIAL-INFARCTION - SIGNIFICANCE FOR INITIATION AND PERPETUATION OF VENTRICULAR-TACHYCARDIA

The underlying mechanism of most ventricular tachycardias in the setti ng of chronic myocardial infarction is reentrant excitation. At that t ime, the active membrane properties like upstroke velocity and amplitu de of action potentials of muscle fibers surviving in the border zone of the infarction have returned nearly completely to normal. Anisotrop ic conduction characteristics, however, importantly contribute to the electrophysiologic properties of the epicardial and/or endocardial bor der zones in chronic myocardial infarction. In normal myocardial tissu e with tight coupling between muscle fibers, conduction velocity is sl ower for impulses propagating transverse to fiber orientation compared to longitudinal to fiber orientation due to a higher effective axial resistivity (''uniform'' anisotropy). With infarct healing, connective tissue invading into the epicardial border zone separates surviving m uscle fiber bundles and thereby decreases cell-to-cell coupling (''non -uniforrn' anisotropy). In this setting, excitation waves propagate tr ansverse to fiber orientation in an irregular sequence and conduction velocity in this direction is significantly reduced without occurrence of acute ischemia. Block of conduction waves propagating longitudinal ly to fiber orientation may lead to activation of the area distal to t he block with long delay by very slow transverse wavefronts. This long delay allows fibers proximal to the line of block to regenerate excit ability, and reentrant excitation may be initiated. The common pathway of figure-eight tachycardias preferentially orientates longitudinally to fiber orientation. Very slow conduction transverse to fiber orient ation at the pivoting points of reentrant circuits may lead to the occ urrence of excitable gaps.