Objectives. The objective of this study was to determine why sustained ventricular tachycardias (VT) sometimes stop without outside intervention. Background. Sustained, monomorphic VT in patients with ischemic heart disease is often caused by reentrant excitation. These tachycardias can degenerate into rapid polylmorphic rhythms or occasionally terminate spontaneously. Methods. Sustained VT was induced by programmed stimulation in dog hearts 4 to 5 days after ligation of the left anterior descending coronary artery. Activation in reentrant circuits in the epicardial border zone of the infarct was mapped using 192 to 312 bipolar electrodes. Results. Spontaneous termination of sustained VT always occurred when the reentrant wave front blocked in the central common pathway in reentrant circuits with a figure- of-eight configuration. Two major patterns of termination were identified from activation maps of the circuits that were not distinguishable from each other on the surface electrocardiogram: 1) Abrupt termination was not preceded by any change in the pattern of activation or cycle length. It could occur at different locations within the central common pathway, was not related to the directions of the muscle fiber orientation and was not ca caused by a short excitable gap. 2) Termination caused by premature activation (after a short cycle) either resulted from shortening of the functional lines of block around which the reentrant impulse circulated or was caused by wave fronts originating outside the reentrant circuit. In only one episode were oscillations of cycle length associated with termination. Conclusions. The mechanisms for termination of reentry in functional circuits causing VT are different from those in anatomic circuits where oscillatory behavior precedes termination.
Schmitt, H., Wit, A. L., Coromilas, J., & Waldecker, B. (1998). Mechanisms for spontaneous termination of monomorphic, sustained ventricular tachycardia: Results of activation mapping of reentrant circuits in the epicardial border zone of subacute canine infarcts. Journal of the American College of Cardiology, 31(2), 460–472. https://doi.org/10.1016/S0735-1097(97)00513-5