Papillary muscle relocation

Ischemic mitral regurgitation results from the progressive interactions of left ventricular remodeling and dilatation following transmural infarction and mitral annular dilatation, primarily along the posterior annulus. As the left ventricle dilates and the sphericity index increases, the papillary muscles are displaced laterally toward the apex and the interpapillary distance increases, resulting in distortion of the subvalvular apparatus and leafl et tethering (Carpentier type IIIb mitral regurgitation). As this occurs, the mitral annulus becomes dilated (Carpentier type I mitral regurgitation). Repair of ischemic mitral regurgitation with reduction annuloplasty has become the standard approach to restoring the normal anteroposterior dimension of the dilated mitral annulus, yet recurrence of mitral regurgitation following this procedure occurs in a signifi- cant number of patients. In one study comparing preoperative and postoperative echocardiograms of 585 patients undergoing isolated annuloplasty for ischemic mitral regurgitation, moderate to severe mitral regurgitation was present in 85 % of patients preoperatively. This was reduced to >10 % of patients in the immediate postoperative period but increased to affect 28 % of patients within 6 months of repair, after which time rates of recurrence stabilized. Use of an undersized ring did not correlate with postoperative regurgitation grade, suggesting other mechanisms of disease for surgical intervention (McGee et al., J Thorac Cardiovasc Surg 128:916–924, 2004). To further characterize these observations, a recent series compared mitral leafl et configurations before and after annuloplasty for ischemic mitral regurgitation. While tethering of both anterior and posterior leafl ets contributes to preoperative disease, it is progressive tethering of the posterior leafl et following annuloplasty that results in early and late persistent/recurrent mitral regurgitation (Zhu et al., Circulation 112:I396–I401, 2005; Kuwahara et al., Circulation 114:I529–I534, 2006). This augmented tethering is likely due to an imbalance between a mobile posterior annulus, shifted anteriorly during repair, and a relatively fixed papillary muscle. Therefore, the emphasis has shifted to incorporating the subvalvular apparatus into the repair of ischemic mitral regurgitation.