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INTRODUCTION

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Mitral valve repair (MVR) remains the standard of care for patients with severe valve incompetence. MVR is usually accomplished by either an open surgical (sternotomy) approach or by minimally invasive (right lateral minithoracotomy) access techniques. Recently there has been an intense interest in developing percutaneous catheter-based techniques, especially for high-risk patients.1-4

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Although the success of transcatheter aortic valve replacement (TAVR) has been rapid, progress toward percutaneous correction of mitral regurgitation (MR) has been much more modest.5 The success of catheter-based treatment of aortic stenosis can be attributed to a number of factors: the singular pathophysiology of the diseased valve, the aortic valve’s anatomical location that allows for precise valve stent implantations at the annular level, and the successful development of delivery systems using conventional imaging techniques. The field of percutaneous MVR, however, has not progressed so rapidly for a host of reasons including the complex pathophysiology of MR with a diversity of etiologies, as well as challenges in imaging and delivery and secure anchoring of the valve without impingement on surrounding cardiac structures. 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.

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PATHOPHYSIOLOGY OF MITRAL REGURGITATION

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The mitral valve (MV) 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 tendineae and papillary muscles attached to the wall of the left ventricle (LV). The etiology of MR can be categorized into two ways: primary also called degenerative or organic, and secondary or functional MR.

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In primary MR (Carpentier Type II), the intrinsic disease is a result of leaflet degeneration, ranging from fibroelastic deficiency to an excess of connective tissue called Barlow’s disease, in patients with MV prolapse. Although MR of intrinsic disease occurs initially as isolated leaflet disease, secondary annular dilatation occurs in the majority of patients by the time that they present for treatment.

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The largest proportion of patients who present with MR, however, are those with secondary MR (Carpentier Type IIIB), in which the valve is anatomically normal but has been stretched by tethering and ventricular dilatation.6 Secondary MR is not a primary valvular pathology but is a result of a cascade of events initiated by this ventricular dilation. Ventricular dilation leads to apical and lateral distraction of the papillary muscles, which results in tethering of the mitral leaflets. This tethering causes central regurgitation secondary to failure of coaptation of the anatomically normal leaflets during systole.7 The causes and prognosis of secondary MR are inherently different from intrinsic disease. Although annular dilatation also occurs in this disease, it is a secondary phenomenon. The principle utilized during surgical repair of secondary MR is based upon ...

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