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43(15) ms in the patients (P < 0 01). Q to the onset of mitral regurgitation was also short (50(15)) ms, and correlated inversely with PR interval (r. = -0-67, n = 73, P < 0*01). Early potentials (< 40 uV) were recorded on the signal averaged electrocardiogram in 33 representative patients and in all controls. Their overall duration was 30(12) ms in the patients, much longer than normal (12(7), P < 0.01)). Early potential time correlated positively with PR interval (r = 0'75, P < 0.01) and QRS duration (r = 0-60, P < 0.01) on a 12 lead electrocardiogram, and negatively with apparent electromechanical delay (r = -071, P < 0.01, n = 33), but not with true electromechanical delay (73 (15) (Br HeartJ7 1994;72:167-174) Prolonged ventricular activation, as shown by a broad QRS complex, is common in patients with dilated cardiomyopathy' 2 and may independently impair systolic and diastolic ventricular function.2' Such patients are often said to have "left bundle branch block", but the body of direct information from humans underlying this diagnosis is surprisingly scanty. The electrocardiographic pattern in these patients is very variable, particularly as to the presence or absence of a septal q wave. Also, the QRS duration is unimodally distributed in a large population of such patients,2 which would be surprising if the long QRS complex were indeed due to the presence or absence of a localised block of a single anatomical structure. In our study, therefore, we have attempted to clarify some of these questions by combining detailed findings of regional ventricular wall motion with information from standard 12 lead and signal averaged electrocardiograms in a group of patients with dilated cardiomyopathy. Patients and methods PATIENTSWe studied 77 patients aged 59(SD13). All the patients had dilated cardiomyopathy, defined as left ventricular end diastolic dimension 6-0 cm or more and shortening fraction < 15% on an M mode echocardiogram. Four

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