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Ann Thorac Surg 2007;83:1920-1921
© 2007 The Society of Thoracic Surgeons


Correspondence

Reply

Michael A. Borger, MD, PhDa, Tirone E. David, MDb

a Division of Cardiovascular Surgery, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, M5G 2C4 Canada
b Division of Cardiovascular Surgery, Toronto General Hospital, 200 Elizabeth St, Toronto, Ontario, M5G 2C4 Canada

(Email: michael.borger{at}utoronto.ca; tirone.david{at}uhn.on.ca).

To the Editor:

We appreciate the comments of Radermecker and Lancellotti [1] regarding our recent review article on ischemic mitral regurgitation (IMR) [2]. The important work performed by Pierard and Lancellotti [3] has markedly improved our understanding of the pathophysiology of IMR.

We agree with the authors that segmental mitral valve (MV) leaflet prolapse may occasionally occur in patients with chronic IMR secondary to papillary muscle (PM) fibrosis and elongation, or even rupture of a head of the PM [4]. The prolapse may be difficult to visualize on echocardiography, particularly if it involves a small portion of the leaflets or is confined to the posteromedial commissure. Further complicating the issue is the fact that such PM elongation may paradoxically decrease the amount of mitral regurgitation in patients with apical displacement and tethering of the PM [5]. We have also observed a combined prolapse of a MV segment and tethering of other segments in some IMR patients.

Ischemia-induced PM elongation may only be recognized during direct intraoperative inspection of the subvalvular apparatus. The PM elongation results in prolapse of the corresponding segment of the MV, which should be carefully compared with the remainder of the MV leaflets. It is important to note that the leaflets themselves will be normal, which distinguishes this entity from other forms of MV prolapse. If MV repair is to be attempted in patients with ischemic PM elongation, the subvalvular length must be corrected to result in normal leaflet motion. Surgical options for MV repair include chordal or PM shortening, chordal transposition, or neo-chordae construction with Gore-Tex sutures (Gore Medical, Flagstaff, AZ) [4, 6].

The exact prevalence of PM elongation-induced IMR is unknown, because relatively little has been written about this entity. The authors of the previously mentioned letter [4] estimate that PM elongation is present in 4% of their patients with IMR, although others have noted a higher prevalence [4].

It is important to distinguish chronic ischemic PM elongation or rupture from acute ischemic PM rupture. Patients with acute PM rupture are clinically unstable and echocardiography reveals marked MV leaflet prolapse and mitral regurgitation. Direct surgical inspection reveals a large amount of acutely necrotic muscle and a ruptured PM head, and MV replacement is the preferred surgical option for these patients. In contrast, chronic IMR may result from a small subendocardial infarct that eventually leads to localized rupture of the PM head. Such patients are clinically stable and their ejection fraction may be near normal.

Although we wholeheartedly agree with the authors that PM elongation is important to describe when discussing IMR, we disagree that our definition of IMR would result in the exclusion of such patients. Our definition (ie, mitral regurgitation greater than 1 week post-infarct with one or more segmental wall motion abnormalities, corresponding coronary disease, and structurally normal leaflets and chordae tendinea) does not specifically exclude patients with mitral leaflet prolapse due to an ischemic, elongated PM. Such patients will still exhibit the three criteria included in our definition, although the segmental wall motion abnormality may be mild. However, it is critically important to stress that the MV leaflets and chordae are otherwise structurally normal in such patients. This will distinguish ischemic, elongated PM-induced prolapse from the much more common myxomatous degeneration-induced prolapse, which is associated with a much better natural history and prognosis.

We suggest that future studies of IMR use our definition to obtain a homogeneous patient population that can be compared across studies.


    References
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 References
 

  1. Radermecker MA, Lancellotti P. The mechanisms of chronic ischemic mitral regurgitation(letter) Ann Thorac Surg 2007;83:1919-1920.[Free Full Text]
  2. 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]
  3. Pierard LA, Lancellotti P. The role of ischemic mitral regurgitation in the pathogenesis of acute pulmonary edema N Engl J Med 2004;351:1627-1634.[Abstract/Free Full Text]
  4. Jouan J, Tapia M, Cook R, Lansac E, Acar C. Ischemic mitral valve prolapse: mechanisms and implications for valve repair Eur J Cardiothorac Surg 2004;26:1112-1117.[Abstract/Free Full Text]
  5. Uemura T, Otsuji Y, Nakashiki K, et al. Papillary muscle dysfunction attenuates ischemic mitral regurgitation in patients with localized basal inferior left ventricular remodeling: insights from tissue Doppler strain imaging J Am Coll Cardiol 2005;46:113-119.[Abstract/Free Full Text]
  6. 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]

Related Article

The Mechanisms of Chronic Ischemic Mitral Regurgitation
Marc A. Radermecker and Patrizzio Lancellotti
Ann. Thorac. Surg. 2007 83: 1919-1920. [Extract] [Full Text] [PDF]




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