Respective role of sympathetic tone and of cardiac pauses in the genesis of 62 cases of ventricular fibrillation recorded during Holter monitoring

Sixty-two Holter recordings of sudden death due to ventricularfibrillation (VF) were analysed by full disclosure and computerizedprocessing. Thirteen sudden deaths were due to torsades de pointesin non coronary subjects (11/13), related to quinidine-likedrugs and/or hypokalaemia: they were always initiated by a longRR cycle due to a post-extrasystolic pause, and announced bya progressive decrease of mean heart rate (from 77.5 ±2.5 to 60.6 ± 2.7 beats min^–1, P<0.001), inthe three preceding hours. The other cases occurred in coronarypatients (45/49), with acceleration of ventricular tachycardia( VT), monomorphic in 24 cases, polymorphic in 13, the ventricularrate increasing from 220.6 ±55 to 241.5 ±69 beatsmin^–1, rather than with primary VF (12 cases). A cardiacpause (RR cycle exceeding 125% of the mean five preceding cycles)was present in 22/49 cases immediately before the onset of VT/VF.The coupling interval of the extrasystole initiating VT/ VFwas shorter than the shortest value encountered before: 377.6±± 94.5 ms vs 421.4 ± 92.3. The prematurityindex (coupling interval/preceding RR cycle ratio) was lowerin primary VF than in VT leading to VF. In the last hour precedingVF, ST changes were unusual (five cases), whereas heart rateincreased from82.8±20 to 92.0 ± 26.7 beats min^–1,(P<0001).This acceleration was in fact present only in caseswithout pauses before the onset of VT/VF: from 85.0±22.8to 99.1 + 31.1 (n = 27, P<0.001) whereas no changeoccurredin cases with preceding pause: from 79.8 ±15.5 to 80.8±16.3 (n = 22, P = NS). As a result, VT/VF without apreceding pause occurs in the setting of a higher heart rate,most probably reflecting a higher sympathetic drive. Preventionof these two main determinants by pacing and beta-blocking therapyshould bemore efficient than the use of antianginal or antiarrhythmicdrugs.