DISPERSION OF REFRACTORINESS IN NONINFARCTED MYOCARDIUM OF PATIENTS WITH VENTRICULAR-TACHYCARDIA OR VENTRICULAR-FIBRILLATION AFTER MYOCARDIAL-INFARCTION

Background Postinfarction ventricular tachycardias (VTs) may degenerat e into ventricular fibrillation (VF), but this does not happen in all patients. The underlying mechanism is not exactly known, but dispersio n of refractory periods is considered a major factor in both induction and persistence of reentrant arrhythmias in general. Hypertrophied, n oninfarcted myocardium has altered electrophysiological characteristic s. We hypothesized that noninfarcted ventricular tissue may provide th e heterogeneities that cause the transition from VT into VF. Local fib rillation intervals, ie, the average interval between local activation s during VF, have previously been shown to correlate well with local r efractoriness in human and canine atrium and in porcine and canine ven tricle and may therefore be used as an index of local refractoriness. This technique permits simultaneous assessment of refractoriness at mu ltiple sites. Methods and Results We measured local fibrillation inter vals at 32 to 64 sites in the noninfarcted part of the left ventricle in patients undergoing antiarrhythmic surgery for symptomatic, drug-re fractory, postinfarction ventricular tachyarrhythmias. The grid of ele ctrodes (interelectrode distance, 7 mm) was attached to the epicardium of the left ventricle remote from the infarcted tissue. Group 1 consi sted of 7 patients with hemodynamically tolerable sustained VT (VT gro up). Group 2 consisted of 7 patients with cardiac arrest and documente d VF (VF group). With the patients on cardiopulmonary bypass, VF was i nduced by multiple premature stimulation. The VF interval was not sign ificantly different in the two study groups (VT group, 136+/-5.5 ms; V F group, 129+/-3.4 ms, mean+/-SEM). However, spatial dispersion of the VF intervals (remote from the infarcted area) expressed as the coeffi cient of variation of VF intervals (SDX100/mean VF interval in each he art) was significantly larger in the VF group. It was 3.63+/-0.56 in t he VF group and 1.55+/-0.40 in the VT group (mean+/-SEM; P<.01). Diffe rences between the shortest and longest VF intervals in one and the sa me heart and the largest difference between two adjacent sites were al so larger in the VF group (P<.02 and P<.05, respectively). Conclusions This study shows larger dispersion in VF intervals and therefore sugg ests larger dispersion of refractory periods in parts of the myocardiu m remote from the infarction in patients with postinfarction VF than i n patients with postinfarction VT.