Nature of ventricular activation in patients with dilated cardiomyopathy: evidence for bilateral bundle branch block.

Abstract

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

Effect of Pacing Chamber and Atrioventricular Delay on Acute Systolic Function of Paced Patients With Congestive Heart Failure

“…19 This relationship may explain why a sufficiently wide QRS and left bundle-branch block tend to predict short-term pacing benefit. Patients may not benefit from pacing unless the conduction disorder and underlying ventricular incoordination are suitably abnormal.…”

Conditional expression of a G i -coupled receptor causes ventricular conduction delay and a lethal cardiomyopathy

“…In the United States, about half of the cases of dilated cardiomyopathy are associated with myocarditis or coronary artery disease, and half are considered idiopathic (1)(2)(3)(4). Ventricular conduction delay, as shown by a prolonged depolarization in the electrocardiogram (wide QRS complex), is associated with up to 70% of IDC cases (5) and is an independent risk factor for death among IDC patients (6,7). Several lines of evidence implicate altered G i signaling in the development of cardiomyopathies such as IDC, but a direct relationship between G i signaling and cardiomyopathy has not been demonstrated in vivo.…”

Differentiation of Ischemic From Nonischemic Cardiomyopathy During Dobutamine Stress by Left Ventricular Long-Axis Function

“…10 Furthermore, stress-induced changes in long-axis function can be measured objectively. 11,12 Our study thus aimed to compare long-axis behavior at rest and during stress in ischemic and nonischemic cardiomyopathy, with and without LBBB, and thus define criteria for differentiating between them.…”