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J Thorac Cardiovasc Surg 2005;129:525-531
© 2005 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Imbalanced chordal force distribution causes acute ischemic mitral regurgitation: Mechanistic insights from chordae tendineae force measurements in pigs

Department of Cardiothoracic and Vascular Surgery and Institute of Clinical Medicine, Skejby Sygehus, Aarhus University Hospital, Aarhus, Denmark

Received for publication April 15, 2004; revisions received July 21, 2004; accepted for publication July 26, 2004.

^* Address for reprints: Sten Lyager Nielsen, MD, Department of Cardiothoracic and Vascular Surgery, Skejby Sygehus, Aarhus University Hospital, 8200 Aarhus N, Denmark (E-mail: lyager{at}ki.au.dk).

BACKGROUND: Ischemic mitral regurgitation is caused by an imbalance of the entire mitral-ventricular complex. This interaction is mediated through the chordae tendineae force distribution, which may perturb several elements of the mitral valve apparatus. Our objective was to investigate the association between the mitral valvular 3-dimensional geometric perturbations and chordae tendineae force redistribution in a porcine model of acute ischemic mitral regurgitation.

METHODS: In 9 pigs, acute ischemic mitral regurgitation was induced by repeated microembolization of the left circumflex coronary artery. Mitral leaflet coaptation geometry was determined by 2-dimensional echocardiography and reconstructed 3-dimensionally. Leading edge chordal forces were measured by dedicated miniature force transducers at control and during ischemic mitral regurgitation.

RESULTS: During acute ischemic mitral regurgitation, there was a decreased tension of the primary chorda from the ischemic posterior left ventricular wall to the anterior leaflet (0.295 ± 0.063 N vs 0.336 ± 0.071 N [control]; P < .05). The tension of the chorda from the nonischemic anterior left ventricular wall to the anterior leaflet increased (0.375 ± 0.066 N vs 0.333 ± 0.071 N [control]; P < .05). In accordance, relative leaflet prolapse was observed at the ischemic commissural side, whereas there was an increase in the leaflet surface area at the nonischemic commissural side, indicating localized leaflet tethering.

CONCLUSIONS: Acute ischemic mitral regurgitation due to posterior left ventricular wall ischemia was associated with focal chordal and leaflet tethering at the nonischemic commissural portion of the mitral valve and a paradoxical decrease of the chordal forces and relative prolapse at the ischemic site of the anterior mitral valve leaflet.

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