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(Circulation. 2003;107:2595.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

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

Richard C. Saumarez, PhD, MRCP; Lidia Chojnowska, MD, PhD; Richard Derksen, MD; Mariusz Pytkowski, MD; Maciej Sterlinski, MD; Christopher L.-H. Huang, MD, PhD; Nicolas Sadoul, MD; Richard N.W. Hauer, MD; Witold Ruzyo, MD; Andrew A. Grace, PhD, FRCP

From the Department of Cardiology, Papworth Hospital (R.C.S., A.A.G.) and Departments of Biochemistry and Medicine (R.C.S., A.A.G.), Engineering (R.C.S.), and Physiology (C.L.-H.H.), University of Cambridge, UK; Institute of Cardiology (L.C., M.P., M.S., W.R.), Warsaw, Poland; Heart Lung Centre Utrecht (R.D., R.N.W.H.), University Medical Centre, Utrecht, the Netherlands; and University Hospital (N.S.), Nancy, France.

Correspondence to Dr Richard C. Saumarez, Department of Cardiology, Papworth Hospital, University of Cambridge, Cambridge CB3 8RE, UK. E-mail rcs23{at}eng.cam.ac.uk

Background— Slowed or delayed myocardial activation and dispersed refractoriness predispose to reentrant excitation that may lead to ventricular fibrillation (VF). Increased ventricular electrogram duration (ED) 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— ED 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 (ED, 19±3.3 ms; S1S2_delay, 350±9.7 ms) differed sharply from observations in HCM non-VF patients (ED, 7.3±1.35 ms; S1S2_delay, 312±6.7 ms; P<0.001). DCM VF patients had longer delays (ED, 14.3±5.9; S1S2_delay, 344±11.2) than DCM non-VF patients (ED, 5.8±1.87 ms; S1S2_delay, 311±5.7 ms; P<0.001), with major differences also seen comparing LQTS VF (ED, 12.4±5.3 ms; S1S2_delay, 343±13.8 ms) and LQTS non-VF patients (ED, 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.

Key Words: death, sudden • electrophysiology • cardiomyopathy • long-QT syndrome

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