Resting and ambulatory ECG predictors of mode of death in dilated cardiomyopathy

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

“…In contrast to previous data suggesting that up-regulation of the G i pathway in cardiomyopathy is a compensatory response to hyperactive G s signaling, our findings suggest a causal role for the G i pathway. Second, our PTX experiments prove that G i signaling causes ventricular conduction delay, a cardinal feature of dilated cardiomyopathy associated with a poor prognosis (6,7). The cause of ventricular conduction delay in human cardiomyopathy is unknown.…”

“…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.…”

Bundle branch block patterns and long-term outcomes in heart failure

“…However, these studies did not find a consistent mortality effect after multiple covariate adjustment. Although two small studies concluded that left bundle branch block was not independently associated with higher risk of death [21,22], others have suggested that its presence is a predictor of mortality in chronic HF [23,24]. In the setting of acute HF, the impact of left bundle branch block is unclear, with studies reporting contrasting effects [15,17,20].…”

Detection of Abnormal High-Frequency Components in the QRS Complex by the Wavelet Transform in Patients With Idiopathic Dilated Cardiomyopathy

“…[1][2][3][4] From the histological viewpoint, it is likely that myocardial fiber degeneration and fibrotic replacement, resulting in the disruption of cell-to-cell connections, 5,6 would not only reduce left ventricular mechanical performance but would also produce electrophysiological abnormalities, such as disruptions of the depolarization wavefront and regional conduction delays, that would provide an appropriate substrate for arrhythmogenicity. The incidence of sudden cardiac death presumably due to fatal ventricular tachyarrhythmia increases with the progression of heart failure and the reduction of the left ventricular EF, 7,8 which suggests that the potential for fatal ventricular arrhythmia due to electrophysiological derangement may progress insidiously with left ventricular mechanical dysfunction, whether or not there is a history of symptomatic malignant ventricular tachycardia.…”