Patients with left ventricular (LV) dysfunction often have varying degrees of mitral regurgitation at echocardiography. This is usually termed functional mitral regurgitation (FMR) to emphasize that it is related, not to an anatomic defect of the mitral valve, as in the organic valvular incompetence of mitral prolapse, but to LV dysfunction itself. However, the mechanism of this relationship is unclear. The main cause of FMR is thought to be mitral valve tenting, defined as insufficient systolic leaflet body displacement towards the annulus, with coaptation limited to the leaflet tips, resulting in regurgitation (Figure).
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Annular changes have a contributory role: insufficient coaptation due to tenting is increased by the loss of systolic annular function, separating the leaflets further. Severe FMR in LV dysfunction has major hemodynamic impact, causing pulmonary hypertension and LV overload, which in turn accelerates LV remodeling. FMR predicts a poor prognosis in LV dysfunction due either to cardiomyopathy or ischemia.
The possibility that surgical correction of FMR could improve prognosis in LV dysfunction with a low ejection fraction (EF) was discounted until recendy on the grounds that EF is a significant predictor of outcome after mitral valve surgery, and that surgical correction of low-EF mitral regurgitation has a poor prognosis compared with an equivalent degree of mitral regurgitation with normal EF.
However, these data were mainly derived from patients with structural mitral valve disease undergoing valve replacement. The reduction in EF after correction was due to in part to the elimination of LV decompression due to a low-pressure left atrium and, even more importantly, to the elimination of the volume overload due to organic regurgitation. Thus, the postoperative survival curves produced in these patients probably do not apply to FMR. There is also increasing evidence that the integrity of annular-chordal-papillary muscle continuity, which is usually disrupted during valve replacement, is also an important determinant of postoperative LV function.
Figure. Parasternal long axis view of aorta (Ao), left ventricle (LV) and left atrium (LA) showing systolic apical displacement of the mitral valve leaflets into the left ventricle with a large tenting area (T).
Note how these deformities result in a lack of central coaptation between the anterior and posterior leaflets.
After. Yiu SF, Enrichez-Sarano M, Tribouilloy C, Seward JB, Tajik AJ. Determinants of the degree of functional mitral regurgitation in patients with systolic left ventricular dysfunction. A quantitative clinical study. Circulation. 2000;102: 1400-1406. Copyright ‚© 2000, American Heart Association.
No relationship has been found between mitral valve repair and the low output state often reported after mitral valve replacement. Intraoperative echocardiography has shown that the regional myocardial contractile abnormalities in the anterior and posterior septum resolve immediately after valve repair, but not after replacement. The intraoperative EF also declines significantly during valve replacement, but remains unchanged during repair. It thus appears reasonable to assume that surgical valve repair is associated with improved symptoms and prognosis in LV dysfunction with severe FMR. Unfortunately, conclusive published evidence to this effect is still pending. Only small unrandomized studies are available reporting benefit from surgical intervention.
Severe mitral regurgitation in heart failure warrants surgical correction, whether or not coronary artery bypass grafting is planned. Randomized controlled trials are required to determine whether surgical valve correction alone is indicated in these patients, even in the absence of other planned surgical procedures.
Management; mitral regurgitation; surgical correction; trial.