MECHANISM OF PREVENTION OF SUDDEN-DEATH BY NADOLOL - DIFFERENTIAL ACTIONS ON ARRHYTHMIA TRIGGERS AND SUBSTRATE AFTER MYOCARDIAL-INFARCTION IN THE DOG

[摘要] Electrocardiographic monitoring and provocative ventricular pacing were used to evaluate control and nadolol treatment groups 6 to 24 hours after left anterior descending coronary artery ligation in the dog. During the 6 to 24 hour period, the control group (n=20) developed ventricular triplets at rates exceeding 270/min. Seven dogs spontaneously developed sustained monomorphic ventricular tachycardia (421 .+-. 12 beats/min) at 13 .+-. 2 hours. Sustained monomorphic ventricular tachycardia was present for 38 .+-. 8 seconds before ventricular fibrillation developed. One dog developed recurrent monomorphic ventricular tachycardia, with six episodes lasting from 8 to 72 seconds (375 to 425 beats/min). At 24 hours, ventricular pacing producing sustained monomorphic ventricular tachycardia (378 .+-. 12 beats/min) in 9 of 13 surviving animals. Nadolol administration 6 hours after coronary artery ligation (n=19) lowered both the rate (241 .+-. 8 versus 328 .+-. 8 beats/min; p=0.001) and the incidence (8 .+-. 6 versus 198 .+-. 61 per hour; p=0.004) of rapid ventricular triplets and prevented sudden arrhythmic death (0%; p = 0.005). Nadolol failed to prevent sustained monomorphic ventricular tachycardia (88%; 365 .+-. 12 beats/min) produced by ventricular pacing. The data suggest that nadolol prevents spontaneous sustained monomorphic ventricular tachycardia by selectively suppressing the arrhythmia trigger (rapid ventricular triplets) without altering the underlying arrhythmia substrate.

[发布日期] 1986-12-01