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Eur J Cardiothorac Surg 2005;28:361-362
© 2005 Elsevier Science NL
Letter to the Editor |
Department of Cardiovascular Surgery, Heart Center, Ankara University School of Medicine, Dikimevi, 06340 Ankara, Turkey
Received 17 February 2005; accepted 26 April 2005.
* Corresponding author. Tel.: +90 5055279680; fax: +90 3123625639. (Email: rakar{at}medicine.ankara.edu.tr).
Key Words: Ischemic mitral regurgitation • Mitral valve repair
We read the original article by Jouan and colleagues [1] with great interest, highlighting the mechanisms of ischemic mitral valve prolapse and implications for mitral valve repair, which appeared in the December 2004 issue of EJCTS. The results of this retrospective observational study suggest that ischemic mitral valve prolapse (Carpentier type-II) represents one-third of the cases in their series. We wish to congratulate the authors on a very interesting paper; however, we feel that certain issues must be addressed.
Ischaemic mitral regurgitation (IMR) is a common complication of coronary artery disease caused by partial or complete obstruction of one or more coronary arteries [2]. By definition, patients with IMR have structurally normal valve leaflets and chordae but valvular incompetence usually occurs as a complication of regional or global LV dysfunction [3]. As described by Steven Bolling, ‘IMR is a ventricular disease, not a valvular disease’. Exception to this might be the patients with chronic mitral valve prolapse without mitral regurgitation (a subgroup of patients with Barlow's disease), the most common valve abnormality involving approximately 3–5% of the adult population [3]. If the patients in this subgroup develop mitral regurgitation only after a myocardial infarction, they can be included in IMR series. Patients exhibit different pathological features, clinical presentation and outcome than those having MR of other aetiology. Taking this into account, it is essential that the authors demonstrate previous ischemic myocardial injury for all patients in their series. However, the authors reported no wall motion abnormality in 22.7% of their patients [1]. Furthermore, the mean ejection fraction in this patient population was 54.9±13.8% and end diastolic left ventricular diameter was 60.9±8.9mm [1]. The authors also failed to mention the duration between the myocardial infarction and surgery for their series, although 34.1% were operated upon within 60 days following acute myocardial infarction. They did not investigate histological or ultrastructural analysis of mitral valve specimens in patients undergoing quadrangular resection, either. However, they overcame this limitation by discussing mechanisms of papillary muscle dysfunction after ischemic injury and detailed description of papillary muscle anatomy, which deserves attention.
Thus, some of Carpentier's geneous mitral valve repair techniques, including quadrangular resection and chordal transposition are questionable when applied to IMR. Better understanding of the complex inter-relationship of the obstructed coronary artery, left ventricular muscle and competency of the mitral valve would certainly help to develop new management strategies for IMR, which is a subject of intense debate. Certain mitral valve pathologies and concomitant coronary artery disease continue to create a dilemma for diagnosis of IMR and reporting outcome in this patient population.
References
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