Mechanisms for absence of inverse relationship between coupling intervals of premature impulses initiating reentrant ventricular tachycardia and intervals between premature and first tachycardia impulses.
BACKGROUND
During initiation of tachycardias by programmed stimulation (PES), an inverse relationship between the coupling interval of the premature impulse (V1V2) and the interval between the premature impulse and the first impulse of tachycardia (V2T1) has been proposed to be a specific indicator of reentry. However, an inverse relationship has not always been observed during initiation of clinical reentrant ventricular tachycardias (VTs).


RESULTS
Reentrant VT was initiated by PES in twelve 4-day-old infarcted dog hearts. The relationship between V1V2 and V2T1 was always direct. Mapping of the epicardial border zone (EBZ) indicated that initiation of VT was secondary to functional orthodromic block of V2, propagation of V2 around the line of block, and antidromic propagation through the original location of the block. In 7 dogs, the line of orthodromic block and the pathway of orthodromic propagation were similar for different V1V2 coupling intervals. Orthodromic conduction time around the line to its distal side was longer at shorter V1V2 intervals, but a shorter antidromic delay in the area of unidirectional block for shorter V1V2 intervals, possibly reflecting small changes in the conduction pathway involving deeper layers of the EBZ, resulted in shorter V2T1 intervals. In the other 5 dogs, the orthodromic conduction pathway of V2 around the line of block changed markedly, with a shorter pathway for shorter V1V2 intervals resulting in shorter V2T1 intervals.


CONCLUSIONS
An inverse relationship between V1V2 and V2T1 is not a specific indicator of functional reentry.
Cabo
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Department of Pharmacology, College of Physicians and Surgeons of Columbia University, New York, NY 10032, USA.
Deruyter
B
B
Coromilas
J
J
Wit
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AL
D000818:Animals; D004285:Dogs; D004562:Electrocardiography; D006329:Heart Conduction System / Q000502:physiology; D017180:Tachycardia, Ventricular / Q000209:etiology*