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Ann Thorac Surg 2007;83:1919-1920
© 2007 The Society of Thoracic Surgeons

Correspondence

The Mechanisms of Chronic Ischemic Mitral Regurgitation

Marc A. Radermecker, MD, PhDa, Patrizzio Lancellotti, MD, PhDb

a Department of Cardiothoracic and Vascular Surgery, CHU Sart-Tilman, University of Liège, Liège, 4000 Belgium
b Department of Cardiology, CHU Sart-Tilman, University of Liège, Liège, 4000 Belgium

(Email: mradermecker{at}chu.ulg.ac.be).

To the Editor:

In their practical review of ischemic mitral regurgitation (IMR), Borger and colleagues [1] have rightly emphasized the heterogeneity of clinical conditions confounding the study of "true chronic IMR." They appropriately suggest restricting the use of the terms "chronic IMR" to a condition in which mitral regurgitation occurs more than 1 week after myocardial infarction and is associated to one or more segmental wall motion abnormalities with significant coronary disease in the corresponding territory and, most importantly, structurally normal mitral valve (MV) leaflets and chordae tendineae.

Post-ischemic fibrotic elongation of papillary muscles (PM) after myocardial infarction is an unusual, although well-recognized, ischemic lesion that we have encountered in 4% of our surgical experience with chronic IMR. The macroscopic pathologic aspect of this lesion is a whitish, usually thin, elongated papillary muscle. Although the whole PM is often involved, the PM heads may be more affected than other regions. In this situation the MV dysfunction is caused either by some degree of leaflet tethering (type IIIb) possibly associated with focal leaflet prolapse (type II) or mainly leaflet prolapse with varying amount of annular dilatation (type I). In many instances, especially when evaluated by inexperienced teams, the mechanism of MV dysfunction is not readily apparent.

It is our contention that this type of IMR, which fully complies with the previously described definition, should be kept in mind when dealing with chronic IMR. Because this type differs significantly from the mechanism of leaflet tethering due to outward and apical PM displacement with restriction of leaflet motion and reduction of their surface of coaptation (type IIIb) [2], none of the current techniques used to manage the usual form of chronic IMR will be satisfactory.

In this subgroup of chronic IMR, PM plication and shortening associated with annuloplasty has been reported to be effective [3]. In our experience we have observed recurrent prolapse after repair of fibrotic PM. In cases of complex ischemic remodelling of the PM and underlying left ventricular wall, MV replacement with conservation of the subvalvular apparatus may be a wise option.


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  1. Borger MA, Alam A, Murphy PM, Doenst T, David TE. Chronic ischemic mitral regurgitation: repair, replace or rethink Ann Thorac Surg 2006;81:1153-1161.[Abstract/Free Full Text]
  2. Lancellotti P, Lebrun F, Piérard LA. Determinants of exercise-induced changes in mitral regurgitation in patients with coronary artery disease and left ventricular dysfunction J Am Coll Cardiol 2003;42:1921-1928.[Abstract/Free Full Text]
  3. Fasol R, Lakew F, Pfannmuller B, Slepian MJ, Joubert-Hubner E. Papillary muscle repair surgery in ischemic mitral valve patients Ann Thorac Surg 2000;70:771-776.[Abstract/Free Full Text]

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Michael A. Borger and Tirone E. David
Ann. Thorac. Surg. 2007 83: 1920-1921. [Extract] [Full Text] [PDF]



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Ann. Thorac. Surg., May 1, 2007; 83(5): 1920 - 1921.
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