Chronic secondary mitral regurgitation (SMR) is a complex entity that is often clinically underappreciated.1 It complicates either ischemic heart disease or dilated cardiomyopathy; its prevalence varies among series but may reach ≤50% in patients with heart failure.2 When present, SMR may exhibit a broad range of severity and confers an adverse prognosis, which is worse with increasing severity of mitral regurgitation (MR).3,4 The management of SMR poses a unique set of challenges, based partly on the complexity of the valve disorder and the still-evolving adoption of the optimal therapeutic approach.5 Noninvasive imaging and, in particular, echocardiography, plays a critical role for the initial and longitudinal assessment, for individual risk stratification and outcome prediction, and for guiding intervention in patients with chronic SMR.6 SMR develops because of a combination of mitral leaflet tethering secondary to left ventricular (LV) dilatation/deformation with papillary displacement/discoordination, annular dilatation/dysfunction, insufficient LV-generated closing forces attributable to reduction of LV contractility, and global LV/papillary muscle dyssynchrony.1,5 Tethering of the mitral leaflets is the principal lesion of SMR and results in restriction of systolic leaflet motion, namely type IIIb of Carpentier’s classification. SMR does not typically occur in global LV dysfunction without tethering. However, once tethering occurs, leaflet closure is further impaired by LV dysfunction because there is decreased force opposing tethering.6–9 The key event in the pathogenesis of SMR is the distortion of normal LV geometry—regional and global LV remodeling—with subsequent apical and lateral displacement of papillary muscles, which, in turn, draws the chordae tendineae away from the line of coaptation.7,8 The extent of LV systolic dysfunction and dilatation is weakly correlated to the degree of SMR unless accompanied by geometric distortion in the region of the papillary muscles.1,9 …