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J Thorac Cardiovasc Surg 2005;130:783-790
© 2005 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

Mitral valve stiffening in end-stage heart failure: Evidence of an organic contribution to functional mitral regurgitation

^a Department of Bioengineering, Rice University, Houston, Tex
^b Department of Biomedical Engineering, Cleveland Clinic Foundation, Cleveland, Ohio
^c Department of Biostatistics, Cleveland Clinic Foundation, Cleveland, Ohio
^d Department of Cardiovascular Medicine, Cleveland Clinic Foundation, Cleveland, Ohio
^e Department of Thoracic and Cardiothoracic Surgery, Cleveland Clinic Foundation, Cleveland, Ohio
^f Kaufman Center for Heart Failure, Cleveland Clinic Foundation, Cleveland, Ohio
^g Northwestern Cardiovascular Institute, Chicago, Ill

Received for publication August 23, 2004; revisions received April 7, 2005; accepted for publication April 25, 2005.

^_* Address for reprints: K. Jane Grande-Allen, PhD, Department of Bioengineering MS 142, Rice University, PO Box 1892, Houston, TX 77251-1892 (Email: grande{at}rice.edu).

OBJECTIVE: Mitral regurgitation is a complication for many patients with congestive heart failure. Although this regurgitation is considered purely functional, we hypothesize that the alterations in cardiac geometry and function induce dysfunctional remodeling of the mitral valve, which can be demonstrated by alterations in the material behavior of the leaflets and chordae.

METHODS: Mitral leaflets and chordae from 23 valves from transplant recipient hearts (11 with dilated and 12 with ischemic cardiomyopathy) and from 21 normal valves (from autopsy) were mechanically tested.

RESULTS: Radially oriented anterior mitral leaflet strips from failing hearts were 61% stiffer and 23% less viscous on average than those from autopsy control hearts. The mean stiffness of circumferentially oriented anterior leaflet strips was 50% higher than that of control hearts. Leaflet extensibility was reduced 35% overall. Likewise, the failing heart chordae were an average of 16% stiffer (all P .05).

CONCLUSIONS: Mitral valves in congestive heart failure have significantly altered mechanics that suggest that the tissue is permanently distended and fibrotic and might be unable to stretch sufficiently to cover the valve orifice. These material changes in the valve tissues accompany the biochemical alterations in extracellular matrix composition that we have previously reported. Our finding of leaflet and chordal remodeling suggests that mitral regurgitation in patients experiencing heart failure might not be purely functional and that these mitral valves should not be considered normal. Moreover, there are implications for strategies of mitral valve surgery or percutaneous approaches in this patient population.

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