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Research Article | Volume 15 Issue 1 (, 2009) | Pages 1 - 10
Characterization of mitral valve anterior leaflet perfusion patterns
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1
Department of Cardiothoracic Surgery, Stanford University School of Medicine, Stanford, CA 94305-5247, USA
Under a Creative Commons license
Open Access
DOI : 10.61336
Published
Sept. 19, 2009
Abstract

Background and aim of the study: Although previous histologic studies have demonstrated the presence of blood vessels in the anterior mitral leaflet (AML) and second-order chordae (SC), little is known of the pattern of leaflet perfusion. Hence, the pattern and source of AML perfusion was investigated in an ovine model.

Methods: Fluorescein angiograms were obtained in 17 ovine hearts immediately after heparinization and cardioplegic arrest, using non-selective left coronary artery (LCA) and selective left anterior descending (LAD), proximal, mid- and distal left circumflex (LCx) perfusion. Serial photographs using a flash/filter system to optimize fluorescence were obtained through a left atriotomy.

Results: The proximal half of the AML was seen to be richly vascularized. A loop of vessels was consistently observed in the mitral annulus and AML; these vessels ran along the annulus, extended to the sites of SC insertion, and created anastomoses between these insertions. The SC contributed to the AML perfusion and the anastomotic loop. Selective perfusion of the LAD or proximal LCx artery (ligated before the first obtuse marginal artery) did not perfuse the AML (n = 6). Perfusion of the mid- and distal LCx (n = 7) consistently supplied the AML via SC insertion sites and annular branches.

Conclusion: The ovine AML is perfused by vessels that run through the SC and annulus simultaneously, and then create a communicating arcade in the leaflet. These vessels originate from the mid- and distal portions of the LCx. A loss of perfusion as a result of microvascular disease could have adverse implications. Derangements in the extensive vascular component of the mitral valve could be an important contributing factor to valve disease.

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