Suture Relocation of the Posterior Papillary Muscle in Ischemic Mitral Regurgitation

Despite advances in our understanding of the pathophysiology of ischemic mitral regurgitation as well as advances in surgical technique and perioperative care, surgical treatment of ischemic mitral regurgitation is associated with mortality rates as high as 20% in some series. It is generally agreed that in the majority of cases, mitral valve repair results in superior short- and mid-term outcomes when compared with mitral valve replacement. In our own series of patients with ischemic mitral regurgitation, the hospital mortality rate for patients undergoing concomitant coronary artery bypass grafting and mitral valve repair was significantly less (1.9%) than patients undergoing coronary artery bypass grafting/mitral valve replacement (10.7%). There is some debate remaining as to whether repair or replacement is best suited for the sickest patients. Given the fact that ischemic mitral regurgitation occurs in the substrate of an often poorly functioning ventricle, it is not surprising that surgical mortality rates are higher for this lesion than for other causes of mitral regurgitation. However, in many cases, failure of the mitral valve repair technique to adequately treat the mechanism of the individual patient’s ischemic mitral regurgitation may significantly impact the clinical outcome.

Observational studies in both experimental animals and clinical patients reveal that the mechanisms of ischemic mitral regurgitation are varied. Carpentier’s classification of leaflet motion reveals 2 plausible mechanisms. In patients with Carpentier’s type I dysfunction (Fig. 1), leaflet motion is unrestricted and ischemic mitral regurgitation occurs on the basis of annular dilation, with resultant failure of leaflet coaptation. This is ordinarily treated adequately by ring annuloplasty. In the case of Carpentier’s type IIIb dysfunction (Fig. 2), there is tethering of A3 and P3 segments to the anterior and posterior leaflets, respectively. This results from posterior displacement of the posterior papillary muscle and subjacent left ventricle as a product of myocardial infarction. This mechanism is poorly treated by simple mitral annuloplasty as abundant clinical experience has shown. Ring annuloplasty fails to restore adequate leaflet coaptation as the leaflet edges remain tethered below the annular level. Adequate treatment will only result if the leaflet edges can be allowed to return to the annular level. In addition, the combination of annular dilation as well as leaflet tethering may be at play with individual patients. These patients are also inadequately treated by ring annuloplasty alone. These latter 2 mechanisms are likely the mechanisms responsible for reports of up to 20% residual and/or progressive mitral regurgitation after annuloplasty alone.

A number of procedures have been developed to try to improve results of mitral repair in these cases. Asymmetric mitral rings have been developed which attempt to deal with the more eccentric mitral leak. The Alfieri repair, in which the anterior and posterior leaflets are sewn together, has been used by us and others with mixed results. In our hands, long-term improvement in mitral regurgitation has been poor. Kon’s method of patch anterior leaflet augmentation attempts to let the level of leaflet coaptation fall more posteriorly toward the level of the displaced papillary muscles.

Various types of ventricular modeling procedures also have been tried to restore papillary muscle geometry. We developed a method of suture relocation of the posterior papillary muscle that relieves A3 and P3 leaflet restriction. The procedure is simple and quick, which is of benefit in these generally unhealthy patients. In cases where the left ventricle is markedly enlarged, a Dor procedure is added to both stabilize the position of the papillary muscles and prevent late apical migration of the subvavular apparatus.