Chapter 45

There has been intense interest over the past decade in developing percutaneous catheter-based techniques to manage valvular heart disease.1–4 Although the success has been rapid to the point of being disruptive in catheter treatment of aortic stenosis, progress has been much more modest in correcting mitral regurgitation (MR) percutaneously.5 The success of catheter-based treatment of aortic stenosis can be attributed to a singular pathophysiology of the disease and the successful development of delivery systems and techniques to treat this disorder using conventional imaging techniques. The field of percutaneous mitral valve repair, however, has not progressed nearly as rapidly for a host of reasons. These include the complex pathophysiology of MR with diverse causes as well as challenging imaging and complex delivery issues. These obstacles have led to slower than anticipated clinical adoption of catheter-based approaches for the treatment of MR. To understand the potential for successful therapy, it is first instructive to examine the pathophysiology of the various mechanisms of the disease.

### Pathophysiology of Mitral Regurgitation

The mitral valve is a complex structure composed of two leaflets, a fibrous annulus with varying degrees of continuity and integrity, and a subvalvular apparatus consisting of chordae tendinea and papillary muscles attached to the wall of the left ventricle (LV). The causes of mitral regurgitation range from intrinsic disease of the leaflets mainly owing to degenerative disease or fibroelastic deficiency in patients with mitral valve prolapse, although connective tissue diseases, including Barlow's syndrome, also occur, to functional mitral regurgitation (FMR) in which the valve is anatomically normal but stretched because of tethering and annular dilatation.6 Although the mitral regurgitation in intrinsic disease occurs initially as leaflet disease, secondary annular dilatation occurs in the large majority of patients by the time they present for treatment. The larger proportion of patients with mitral regurgitation, however, are those without intrinsic disease of the leaflets, or FMR. FMR is not a primary valvular pathology but a secondary one caused by ventricular dilation, which leads to apical and lateral distraction of the papillary muscles tethering the mitral leaflets causing central regurgitation owing to failure of coaptation during systole of the anatomically normal leaflets7 (Fig. 45-1). The causes and prognosis are inherently different from intrinsic disease. Although annular dilatation also occurs in this disease, it also is a secondary phenomenon. Surgical correction of FMR is based upon overcorrection of the annular dilatation component by performing an undersized annuloplasty to restore leaflet coaptation.

###### Figure 45-1

Pathophysiology of functional mitral regurgitation with concept of correction of leaflet malcoaptation by a complete and undersized ring annuloplasty.

### Transcatheter Approaches to the Treatment of Mitral Regurgitation

There is a wide spectrum of ingenious devices and creative approaches to manage MR from ...

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