Timing of surgery in mitral regurgitation.

The mitral valve apparatus is a complex anatomic and functional unit composed of the mitral annulus, valve leaflets, chordae, papillary muscles, and the underlying left ventricular wall. Normal function depends on both normal anatomy of each of these components and on the overall three dimensional relationships of these structures to each other, including the effects of overall left ventricular size, shape, and systolic function. Diverse mechanisms of mitral regurgitation are associated with different clinical outcomes. In addition, medical or surgical treatment is directed at the specific mechanism of regurgitation in each individual patient. Mitral regurgitation caused by an anatomic abnormality of the leaflets and chordae is termed primary regurgitation, while mitral regurgitation caused by a process primarily affecting the left ventricle is termed secondary mitral regurgitation. Examples of primary mitral regurgitation include myxomatous mitral valve disease which results in mitral regurgitation caused by leaflet prolapse and/or chordal rupture, rheumatic disease which typically causes increased leaflet stiffness with chordal shortening and fusion, and endocarditis with leaflet deformation and destruction. Examples of secondary mitral regurgitation include ischaemic disease that affects the function of the papillary muscles and underlying left ventricular wall, and dilated cardiomyopathy that alters the normal angle between the papillary muscles and mitral annulus (table 1). Echocardiography allows reliable identification of the presence, severity and mechanism of mitral regurgitation. When transthoracic imaging is suboptimal, transoesophageal images provide excellent visualisation of mitral valve anatomy, and allow an accurate assessment of the aetiology of valve disease and the likelihood of surgical repair (fig 1). The severity of mitral regurgitation can be quantitated by several approaches, including calculation of regurgitant volumes and fraction from calculation of volume flow rate at two intracardiac sites, from the proximal isovelocity surface area, or by measurement of the vena contracta on colour flow imaging. However, in practical terms, many clinicians rely on the simpler, albeit less quantitative, evaluation of regurgitation severity by colour flow imaging in multiple views (figs 2 and 3). Assessment of the haemodynamic consequences of regurgitation is even more important than quantitation of regurgitant severity. Specific parameters that are important for clinical decision making are the degree of left ventricular dilation, left ventricular systolic function, left atrial enlargement, and pulmonary hypertension.