Sudden Death in Noncoronary Heart Disease Is Associated With Delayed Paced Ventricular Activation

Abstract

Background— Slowed or delayed myocardial activation and dispersed refractoriness predispose to reentrant excitation that may lead to ventricular fibrillation (VF). Increased ventricular electrogram duration (ΔED) in response to extrastimuli and increased S1S2 coupling intervals at which electrogram duration starts to increase (S1S2 delay ) are seen both in hypertrophic cardiomyopathy (HCM) in those at risk of VF and in patients with idiopathic VF (IVF). Methods and Results— ΔED and S1S2 delay have been measured using paced electrogram fractionation analysis in 266 patients with noncoronary heart disease. Of these, one group of 61 patients had a history of VF and included 21 HCM, 17 IVF, 13 long-QT syndrome (LQTS), 5 dilated cardiomyopathy (DCM), and 5 others. These were compared with 205 patients with similar diseases with no VF history (non-VF group) and a control group (n=12) without heart disease. Results from HCM VF patients (ΔED, 19±3.3 ms; S1S2 delay , 350±9.7 ms) differed sharply from observations in HCM non-VF patients (ΔED, 7.3±1.35 ms; S1S2 delay , 312±6.7 ms; P <0.001). DCM VF patients had longer delays (ΔED, 14.3±5.9; S1S2 delay , 344±11.2) than DCM non-VF patients (ΔED, 5.8±1.87 ms; S1S2 delay , 311±5.7 ms; P <0.001), with major differences also seen comparing LQTS VF (ΔED, 12.4±5.3 ms; S1S2 delay , 343±13.8 ms) and LQTS non-VF patients (ΔED, 11.0±2.7 ms; S1S2 delay , 320±5.4 ms; P <0.001). IVF patients had both severely abnormal and normal areas of myocardium. Conclusions— Slowed or delayed myocardial activation is a common feature in patients with noncoronary heart disease with a history of VF, and its assessment may allow the prospective prediction of VF risk in these patients.