Ventricular dyssynchrony is defined as uncoordinated regional myocardial contraction and relaxation and may be either interventricular or intraventricular. Most of the clinical focus has been on left ventricular (LV) intraventricular dyssynchrony, which in principle may have 3 different origins. First, dyssynchrony may have an electric origin as in left bundle-branch block, which causes nonuniform timing of electric activation. Second, there may be disturbances in excitation-contraction coupling, and this would be apparent as delay in electromechanical activation time. Presently, there are limited data on the clinical relevance of such disturbances. Third, dyssynchrony may have a primary mechanical origin and may occur in ventricles with regional impairment of function, as in myocardial ischemia when systolic shortening in different segments is out of phase. Furthermore, a primary mechanical origin may be found in ventricles with nonuniform distribution of load, and this may occur when there are regional differences in LV wall thickness or differences in local radius of curvature, including septal curvature. In these cases, segmental differences in systolic wall stress may lead to differences in timing of peak contraction. Article see p 1687 Cardiac resynchronization therapy (CRT) is established as an effective treatment option in patients with severe heart failure (HF) and LV electric dyssynchrony as indicated by a wide QRS complex.1 Because CRT corrects electric dyssynchrony, it would a priori seem less likely that patients with narrow QRS should be responders because they presumably have relatively normal electric conduction. Consistent with this notion, Beshai et al2 found no benefit of CRT in patients with severe HF with QRS <130 ms and echocardiographic evidence of mechanical dyssynchrony. In apparent contradiction to this, Williams et al,3 in this issue of Circulation , demonstrate that CRT causes marked immediate improvement in LV function in HF patients with narrow QRS and no …