Primary ventricular fibrillation is associated with increased paced right ventricular electrogram fractionation

The mechanisms of spontaneous ventricular fibrillation (primary VF) in patients without structural heart disease are obscure. A new technique has shown that in patients with hypertrophic cardiomyopathy conduction of fractionated ventricular paced beats, recorded at several right ventricular sites, is prolonged in individuals who have suffered a VF arrest, and this may reveal one component of a reentrant substrate. Patients with primary VF were studied with the same methods to determine whether similar abnormalities are present in this group.

Nine patients with primary VF were studied by pacing one right ventricular (RV) site by use of a constant drive train with an extrastimulus inserted every third beat and reducing the extrastimulus coupling interval (S1S2 interval) by 1 ms on each occasion while recording at three other sites. The delay of each fractionated potential in the high-pass-filtered electrograms in response to the extrastimulus was determined and used to form conduction curves of delay versus the S1S2 interval. These curves were repeated by pacing each RV site in turn and recording from the other three sites. The curves were characterized by determining the S1S2 interval at which electrogram components increased in delay by 0.75 ms/20 ms reduction in S1S2 interval and the increase in electrogram duration between a coupling interval of 350 ms and 1 ms above refractoriness. Seven control patients were studied using the same method. The mean increase in electrogram duration in VF patients was 13 ms (range, 3 to 23 ms) compared with 4 ms (range, -2 to 14 ms) in unaffected control patients. The extrastimulus coupling interval at which delay increased was 318 ms (range, 293 to 334 ms) in VF patients and 274 ms (range, 265 to 284 ms) in control patients (P < .01). There was no difference between the number of fractionated potentials in VF patients and control patients.

In primary VF patients, the individual potentials within fractionated electrograms have increased delays when compared with control patients. This may identify one component of a reentrant arrhythmic substrate.