Spectrum of electrophysiologic and electropharmacologic characteristics of verapamil-sensitive ventricular tachycardia in patients without structural heart disease.
Verapamil-sensitive ventricular tachycardia (VT) is a well-recognized clinical entity that some authorities believe may result from triggered activity. Despite its uniform response to verapamil, however, there is evidence that this uncommon form of VT may not be as homogeneous as first believed. Standard intracardiac electrophysiologic techniques were used to study verapamil-sensitive VT in 32 patients (aged 38 years +/- 20 years) without evidence of structural heart disease. More than half of these patients (69%) exhibited VT with a right bundle branch block-type QRS pattern, with the remainder (31%) displaying VT with a left bundle branch block pattern. In 31% of the patients the VT could be induced by fixed-cycle length atrial pacing, whereas in 59% of patients fixed-cycle length ventricular pacing was necessary. A critical range of cycle lengths for VT induction was required in 66% of the patients. Ventricular tachycardia was initiated with single atrial premature extrastimuli in 16% of patients, single ventricular extrastimuli in 50% of patients, and double ventricular premature extrastimuli in 9% of patients. Ventricular tachycardia displaying cycle-length alternans was observed in 28% of patients. In only 19% of patients was it possible to entrain VT during pacing from the right ventricular apex. Isoproterenol infusion was required for tachycardia induction in 50% of patients, 44% of whom had VT with a left bundle branch block QRS pattern, with the remaining 56% exhibiting VT with a right bundle branch block pattern. Beta-adrenergic blockers suppressed 53% of verapamil-sensitive VT in patients tested, whereas adenosine terminated VT in 50% of patients, with 81% of these patients exhibiting either a left bundle branch block QRS pattern or isoproterenol dependence. Ventricular tachycardia exhibiting a left bundle branch block pattern was more likely to be isoproterenol dependent (p <0.05) and adenosine sensitive (p <0.001). However, verapamil-sensitive, catecholamine-dependent VT was no more likely to be adenosine sensitive than the catecholamine-independent form of the arrhythmia (p >0.5). Verapamil-sensitive VT exhibits properties expected of both a reentrant and triggered arrhythmia, and it is inconsistently dependent on both exogenous catecholamines for induction and intravenous adenosine for termination. Verapamil-sensitive VT encompasses a heterogeneous group of tachycardias that may result from multiple cellular electrophysiologic mechanisms.
Lee
K L
KL
Cardiac Electrophysiology Service, Stanford University School of Medicine, California 94305, USA.
Lauer
M R
MR
Young
C
C
Lai
W T
WT
Tai
Y T
YT
Chun
H
H
Liem
L B
LB
Sung
R J
RJ
D000241:Adenosine / Q000494:pharmacology; D000328:Adult; D002037:Bundle-Branch Block / Q000503:physiopathology; D002395:Catecholamines / Q000494:pharmacology; D004562:Electrocardiography / Q000187:drug effects; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D008875:Middle Aged; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000503:physiopathology*; D014700:Verapamil / Q000494:pharmacology / Q000627:therapeutic use
D002395:Catecholamines; D014700:Verapamil; D000241:Adenosine; D007545:Isoproterenol