CHARACTERISTICS OF SLOW CONDUCTION ZONE DEMONSTRATED DURING ENTRAINMENT OF IDIOPATHIC VENTRICULAR-TACHYCARDIA OF LEFT-VENTRICULAR ORIGIN
Citation
K. Okumura et al., CHARACTERISTICS OF SLOW CONDUCTION ZONE DEMONSTRATED DURING ENTRAINMENT OF IDIOPATHIC VENTRICULAR-TACHYCARDIA OF LEFT-VENTRICULAR ORIGIN, The American journal of cardiology, 77(5), 1996, pp. 379-383
Categorie Soggetti
Cardiac & Cardiovascular System
SICI code
0002-9149(1996)77:5<379:COSCZD>2.0.ZU;2-0
Abstract
Idiopathic ventricular tachycardia (VT) with the right bundle branch b
lock pattern and left-axis deviation has been shown to be due to reent
ry, but the property of the slow conduction zone within the reentry ci
rcuit is little understood. In 7 patients (mean VT cycle length [CL]:
361 +/- 49 ms), rapid pacing from the right ventricular outflow tract
was performed during VT while recording electrograms at the early acti
vation site in the left ventricle and at the right ventricular apex; a
lso, conduction times from the pacing site to these recording sits (St
-A and St-B intervals, respectively) were measured. Both constant fusi
on (except for the last paced beat) and progressive fusion were seen i
n all patients, indicating VT entrainment, The left ventricular site w
as captured orthodromically with an St-A interval of 394 +/- 57 ms at
the pacing CL of 351 +/- 47 ms during entrainment, while the right ven
tricular apex was captured directly with an St-B interval of 63 +/- 19
ms. The St-A interval was gradually prolonged with the shortening of
the pacing CL, whereas the St-B interval remained unchanged. VT was in
terrupted in all patients at the pacing CL of 279 +/- 39 ms. The effec
ts of intravenous lidocaine (1 mg/kg) and verapamil (1 mg) were examin
ed in 5 and 7 patients, respectively. Neither drug terminated VT but t
he VT-CL was increased to 369 +/- 57 ms after lidocaine (p < 0.05) and
to 413 +/- 69 ms after verapamil (p < 0.05) (p < 0.05 vs after lidoca
ine). The St-A interval was significantly increased after lidocaine (p
< 0.05) and after verapamil (p < 0.05), while the St-B interval remai
ned unchanged. A significant correlation between changes in St-A inter
val and VT-CL after verapamil was noted (p < 0.001). In conclusion, th
e slow conduction zone of this VT shows tachycardia-dependent conducti
on delay, and the mechanism of this slow conduction involves mainly ca
lcium channel-dependent conduction and partly depressed sodium channel
-dependent conduction.