Pathophysiology, Echocardiographic Diagnosis, and Treatment of Atrial Functional Mitral Regurgitation: JACC State-of-the-Art Review.

The conventional view holds that functional mitral regurgitation (MR) is caused by restriction of leaflet motion resulting from displacement of the papillary muscle-bearing segments of the left ventricle. In the past decade, evidence has accrued suggesting functional MR can also be caused by left atrial enlargement. This underrecognized cause of secondary MR-atrial functional MR (AF-MR)-is mechanistically linked to annular enlargement, perturbations of annular contraction, and atriogenic leaflet tethering. AF-MR has been described in patients with atrial fibrillation and heart failure with preserved ejection fraction. Preliminary data suggest rhythm control may decrease MR severity in patients with atrial fibrillation. Additionally, several studies have reported reductions in MR and symptomatic improvement with restrictive annuloplasty and transcatheter edge-to-edge repair. This review discusses the pathophysiology, echocardiographic diagnosis, and treatment of AF-MR. AF-tricuspid regurgitation is also discussed.

Efficacy of left atrial plication for atrial functional mitral regurgitation.

OBJECTIVE: Atrial functional mitral regurgitation (AFMR) is caused by atrial fibrillation and left atrial enlargement. Our study aimed to evaluate the efficacy of left atrial plication (LAP) for AFMR. METHODS: Of 1164 mitral valve surgery patients at our hospital from January 2000 to May 2019, 22 patients underwent surgery for AFMR. Our retrospective analysis divided the patients with AFMR into two groups according to whether LAP was performed (LAP + group, n = 9; LAP - group, n = 13). Mitral valve angle (MV angle) (horizontal inclination of mitral valve) was measured by pre- and post-operative computed tomography scan. Individuals with type II mitral regurgitation, left ventricular ejection fraction of < 55%, males with left ventricular endo-diastolic dimension of > 60 mm and females with > 55 mm, aortic valve disease, mitral valve calcification, hypertrophic obstructive cardiomyopathy, and both "redo" and emergency cases were excluded. RESULT: Mitral valve replacement was performed in 6 patients and mitral ring annuloplasty in 16 cases. No recurrence of mitral regurgitation or structural valve deterioration occurred during the follow-up period. There were no hospital deaths; 3 deaths occurred during the follow-up period. Compared to the LAP - group, the LAP + group demonstrated a significantly greater decrease of MV angle (16.6 ± 8.1° vs. 1.2 ± 6.9°, p < 0.01) and left atrial dimension (18.4 ± 7.0 mm vs. 6.9 ± 14.6 mm, p = 0.02). CONCLUSIONS: Surgical results of AFMR were satisfactory. LAP may be appropriate for correcting the angle of a mitral valve tilted horizontally. More cases need to be considered in the future.

Mechanistic insights into atrial functional mitral regurgitation: Far more complicated than just left atrial remodeling.

Recent studies lend credibility to the notion that lone atrial fibrillation (AF) can cause functional mitral regurgitation (MR), commonly referred to as atrial functional MR (AF-MR). The conventional view holds that left atrial enlargement associated with AF causes annular dilatation which gradually moves the mitral valve leaflets apart resulting in inadequate coaptation and regurgitation. Recent findings, however, suggest that AF-MR is not solely related to left atrial remodeling, but that important structural and functional abnormalities of the left ventricle also play a role in its pathogenesis.

Novel pathogenetic mechanisms and structural adaptations in ischemic mitral regurgitation.

Ischemic mitral regurgitation (MR) is a common complication of myocardial infarction thought to result from leaflet tethering caused by displacement of the papillary muscles that occurs as the left ventricle remodels. The author explores the possibility that left atrial remodeling may also play a role in the pathogenesis of ischemic MR, through a novel mechanism: atriogenic leaflet tethering. When ischemic MR is hemodynamically significant, the left ventricle compensates by dilating to preserve forward output using the Starling mechanism. Left ventricular dilatation, however, worsens MR by increasing the mitral valve regurgitant orifice, leading to a vicious cycle in which MR begets more MR. The author proposes that several structural adaptations play a role in reducing ischemic MR. In contrast to the compensatory effects of left ventricular enlargement, these may reduce, rather than increase, its severity. The suggested adaptations involve the mitral valve leaflets, the papillary muscles, the mitral annulus, and the left ventricular false tendons. This review describes the potential role each may play in reducing ischemic MR. Therapies that exploit these adaptations are also discussed.