Functional Mitral Regurgitation скачать в хорошем качестве

Functional Mitral Regurgitation

Description: https://johnsonfrancis.org/profession... https://johnsonfrancis.org/profession... Discussion on functional mitral regurgitation including atrial functional MR, proportionate and disproportionate functional MR. Functional mitral regurgitation occurs due to non-coaptation of mitral leaflets in the setting of left ventricular/mitral annular dilatation. Initial part of the discussion will be on FMR due to LV dilatation and latter part on atrial functional MR. FMR can occur in cardiomyopathies of both ischemic and idiopathic varieties as well as in left ventricular dilatation due to aortic regurgitation. The distorted shape of the left ventricles restricts the mitral valve closure. But the incidence of functional mitral regurgitation is less than what is expected from left ventricular remodeling. This is thought to be due to the enlargement of mitral leaflets in response to left ventricular enlargement and change in morphology. Enlargement of mitral leaflets may not be due to stretch alone, but also due to active growth of cells and matrix. The enlargement of mitral leaflets causing a less than expected rate of functional mitral regurgitation is more likely to occur in slowly progressive left ventricular dilatation as in chronic aortic regurgitation. For this reason, the chance of functional mitral regurgitation is less in chronic aortic regurgitation than in other cases with corresponding severity of left ventricular dilatation. Atrial functional MR occurs typically in atrial fibrillation and heart failure with preserved ejection fraction. It is different from MR secondary to left ventricular dysfunction. In left ventricular dysfunction, tethering of mitral leaflets is an important cause for mitral regurgitation while it is not so in atrial functional MR. There is insufficient leaflet lengthening or remodeling to produce coaptation in the setting of annular dilatation. Hence MR secondary to left ventricular dysfunction is usually an eccentric jet, whereas atrial functional MR produces a central jet as the leaflets fail to co apt in the centre. Atrial functional MR can occur in 6-7% cases of lone atrial fibrillation. The prevalence is much higher in HFpEF. The severity of left atrial dilatation is much more in atrial functional MR when compared to MR secondary to left ventricular failure. Guideline directed medical therapy is the cornerstone in the management of secondary mitral regurgitation. Targeting atrial fibrillation by catheter ablation might prevent progression of HFpEF and potentially atrial functional MR. Surgical restrictive mitral annuloplasty improves leaflet coaptation by reducing annular dimensions. But recurrence rate up to 32.6% has been reported 12 months after an initially successful mitral annuloplasty. At the same time, a chordal sparing mitral valve replacement in the same study had only 2.3% recurrence rate. That study of 251 patients with severe ischemic mitral regurgitation showed that mitral valve replacement provided a more durable correction of mitral regurgitation. There was no significant difference in clinical outcome between repair and replacement in that study. 616 patients with secondary mitral regurgitation underwent the MitraClip procedure in EVEREST II Study. Acceptable safety, reduction of severity of MR, symptomatic improvement and positive ventricular remodeling were documented in the study. Going by the Gorlin hydraulic orifice equation, patients with left ventricular ejection fraction of 30% and a left ventricular end diastolic volume of 220-250 ml and regurgitant fraction of 50% is expected to have an effective regurgitant orifice area of 0.3 cm2. MR in these patients is proportionate to the degree of left ventricular dilatation, independent of specific tethering abnormalities of mitral valve leaflets, and can respond to drugs and devices that reduce LVEDV. Patients with EROA of 0.3 – 0.4 cm2, but with LVEDV of only 160-200 ml have MR disproportionately higher than predicted by the LVEDV. These patients may be preferentially benefitted from interventions directed at the mitral valve. COAPT trial had chronic heart failure patients with reduced left ventricular ejection fraction and severe secondary MR Trans catheter mitral valve repair resulted in lower rate of hospitalization for heart failure and lower all-cause mortality at 2 years than medical therapy alone. Freedom from device related complications was 96.6% at 12 months. There was a significant reduction of left ventricular volumes at 1 year. Mean LVEDV was 192 ml and mean EROA was 41 mm2 indicating disproportionate MR. It has been suggested that the difference in outcome between MITRA-FR and COAPT trials could have been due to the difference in proportionate vs disproportionate functional MR.