ELECTRICAL ACTIVATION DURING VENTRICULAR-FIBRILLATION IN THE SUBACUTEAND CHRONIC PHASES OF HEALING CANINE MYOCARDIAL-INFARCTION

Background Little information is available regarding the effects of my ocardial infarction on the characteristics of ventricular fibrillation (VF). Epicardial activation during VF can be characterized by the cyc le length and by the characteristics of activation wave fronts. Method s and Results VF was induced by programmed stimulation in 6 dogs with subacute healing (1 week) myocardial infarction (MI), 5 dogs with chro nic (8 week) healing MI, and 6 dogs without MI. Using a plaque electro de array with a 2.5-mm interelectrode distance, 112 electrograms were recorded and 91 Vector loops were created for each cycle of VF from ei ther the anterior (infarcted) or lateral (noninfarcted) wall. Directio n of maximum epicardial activation was determined at each site for the first 10 cycles of VF (early) and for 10 cycles after 5 seconds of VF (late). Wave front size was determined based on a similarity in epica rdial activation directions within a given area and by a statistical a nalysis that determined the degree of spatial linking at varying dista nces over the recording plaque. VF cycle length was defined as the mea n interval of 10 consecutive local activation times. Differences among groups and differences between the anterior and posterolateral walls were determined by ANOVA. The mean wave front area was significantly l arger in the presence of subacute MI (97+/-4 mm(2), early; 78+/-3 mm(2 ), late) or chronic MI (94+/-5 mm(2), early, 78+/-5 mm(2), late) than in noninfarcted animals (73+/-5 mm(2), early; 61+/-3 mm(2), late). The degree of linking of epicardial activation directions was similar in the three groups at distances of 2.5 and 5.0 mm but was lower at a dis tance of 7.5 mm among animals without infarction, confirming a smaller wave front size and suggesting less organization of activation. VF cy cle length was significantly longer in the presence of infarction (98/-5 ms, normal control animals; 121+/-13 ms, subacute MI; 127+/-13 ms, chronic MI). VF cycle length was significantly longer over the anteri or than the lateral wall in the presence of subacute MI (131+/-8 ms, a nterior; 109+/-5 ms, lateral) or chronic MI (136+/-9 ms, anterior; 119 +/-6 ms, lateral) but not in noninfarcted animals (99+/-5 ms, anterior ; 97+/-5 ms, lateral). The prolongation of VF cycle length among anima ls with infarction was associated with slower estimated conduction vel ocities during VF. Conclusions During VF, in animals with subacute or chronic healing MI, (1) the size of activation wave fronts is larger, (2) the cycle length of VF is longer, (3) the conduction velocities ar e slower, and (4) the degree of organization is greater than in contro l animals. Thus, the characteristics of VF throughout the heart are al tered by the presence of regional myocardial infarction. The implicati ons of these findings for the initiation and maintenance of VF in the presence of different underlying myocardial substrates require further study.