Hemodynamic implications of left bundle branch block

Left bundle branch block (LBBB), traditionally viewed as an electrophysiolo gic abnormality, is increasingly recognized for its profound hemodynamic ef fects. LBBB causes asynchronous myocardial activation, which, in turn, may trigger ventricular remodeling. Exercise nuclear studies frequently show re versible perfusion defects in the absence of obstructive coronary artery di sease and some patients with intermittent LBBB develop angina coincident wi th the onset of LBBB. It is uncertain, however, if these phenomena are beca use of myocardial ischemia or ventricular asynergy. LBBB is associated with impaired systolic and diastolic function. In patients with dilated cardiom yopathy (DCM), LBBB is accompanied by progressive left ventricular (LV) dil atation and mitral regurgitation. It is not known whether LBBB is the cause or the consequence of LV dilatation. DCM patients with LBBB, as compared t o those with normal intraventricular conduction, are more likely to have a nonischemic etiology, profound LV dilatation, lower ejection fraction, incr eased symptomatology, and shorter survival. Patients with DCM and accelerat ion-dependent LBBB may benefit from restoration of a narrow QRS complex by suppressing the heart rate with beta -blocker. There is extensive research underway in patients with DCM and LBBB to evaluate the short and long-term effects of normalization of ventricular activation sequence with high septa l, LV, or biventricular pacing.