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

Citation
H. Schmitt et al., 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), 1998, pp. 460-472
Citations number
40
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
31
Issue
2
Year of publication
1998
Pages
460 - 472
Database
ISI
SICI code
0735-1097(1998)31:2<460:MFSTOM>2.0.ZU;2-T
Abstract
Objectives. The objective of this study was to determine why sustained ventricular tachycardias (VT) sometimes stop without outside interven tion. Background. Sustained, monomorphic VT in patients with ischemic heart disease is often caused by reentrant excitation, These tachycard ias can degenerate into rapid polymorphic rhythms or occasionally term inate spontaneously. Methods. Sustained VT was induced by programmed s timulation in dog hearts 4 to 5 days after ligation of the left anteri or descending coronary artery, Activation in reentrant circuits in the epicardial border zone of the infarct was mapped using 192 to 312 bip olar electrodes. Results. Spontaneous termination of sustained VT alwa ys occurred when the reentrant wave front blocked in the central commo n 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 a ny change in the pattern of activation or cycle length, It could occur at different locations within the central common pathway, was not rel ated to the directions of the muscle fiber orientation and was not cau sed by a short excitable gap, 2) Termination caused by premature activ ation (after a short cycle) either resulted from shortening of the fun ctional lines of block around which the reentrant impulse circulated o r 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 i n functional circuits causing VT are different from those in anatomic circuits where oscillatory behavior precedes termination. (C) 1998 by the American College of Cardiology.