Updated pathophysiological overview of functional MR (ventricular and atrial).

Basic mechanism of ventricular functional mitral regurgitation (FMR) is subvalvular tethering. Left ventricular (LV) dilatation, in association with mitral valve (MV) annular dilatation, causes outward displacement of papillary muscles (PMs), which abnormally pulls or tethers MV leaflets, resulting in MV tenting, reduction in leaflets coaptation and MR. Because surgical annuloplasty does shorten distance between anterior and posterior MV annuli to improve coaptation but does not address this subvalvular tethering, ventricular FMR frequently persists or recurs in the chronic stage after surgical annuloplasty. This high incidence of persistent/recurrent MR requires additional procedures to reduce subvalvular tethering. Although patients occasionally show marked improvements after annuloplasty with surgical tethering reduction procedures such as PM approximation, evidence to support benefits of such surgery is limited, requiring further trials. Recently, MV adaptation or MV leaflets tissue growth associated with LV dilatation attracts attention. Patients with larger MV leaflets with significant LV dilatation/dysfunction show less MV tethering and MR compared to those with smaller MV leaflets but with similar LV remodeling, suggesting the protective or beneficial role of MV leaflets tissue growth against LV remodeling. The MV leaflets tissue growth has the potential to lead to novel strategies of treatment for ventricular FMR. It is well known that atrial FMR is frequent in patients with left atrial dilatation, typically in those with isolated atrial fibrillation. The degree of atrial FMR is usually mild, even when it is present, and occasionally moderate, and severe atrial FMR is really rare. It is known that only severe regurgitation causes heart failure in primary MR, resulting in description on indications of surgery or intervention for only severe MR in current guidelines. Therefore, this atrial FMR up to moderate degree did not attract attention for a long time. However, recent studies have shown that patients with only moderate atrial FMR develop severe heart failure, suggesting more aggressive indication of MV surgery or intervention for "moderate" regurgitation in patients with atrial FMR. Therefore, atrial FMR is now recognized highly important. The unveiled malignant nature of atrial FMR arises many questions, including (1) why patients with only moderate atrial FMR develop heart failure? (2) do patients with mild atrial FMR develop heart failure or not?, and many others. Atrial FMR seems even more mysterious after the unveiling of its significance.

Description and prevalence of ventricular mitral annular disjunction: variation of normality or pathological variant?

INTRODUCTION AND OBJECTIVES: The aim of this study was to investigate a new variation of the atrial wall-mitral annulus-ventricular wall junction along the mural mitral leaflet and commissures: the ventricular mitral annular disjunction (v-MAD). This new variant is characterized by spatial displacement of the mitral leaflet hinge line by more than 2mm toward the left ventricle. METHODS: We examined a cohort of autopsied human hearts (n=224, 21.9% females, 47.9±17.6 years) from patients without known cardiovascular disease to identify the presence of v-MAD. RESULTS: More than half (57.1%) of the hearts showed no signs of MAD in the mural mitral leaflet or mitral commissures. However, v-MAD was found in 23.6% of cases, located within 20.1% of mural leaflets, 2.2% in superolateral commissures, and 1.3% in inferoseptal commissures. V-MAD was not uniformly distributed along the mitral annulus circumference, with the most frequent site being the P2 scallop (19.6% of hearts). The v-MAD height was significantly greater in mural leaflets than in commissures (4.4 mm±1.2 mm vs 2.1 mm±0.1 mm; P<.001). No specific variations in mitral valve morphology or anthropometrical features of donors were associated with the presence or distribution of v-MADs. Microscopic examinations revealed the overlap of the thin layer of atrial myocardium over ventricular myocardium in areas of v-MAD. CONCLUSIONS: Our study is the first to present a detailed definition and morphometric description of v-MAD. Further studies should focus on the clinical significance of v-MAD to elucidate whether it represents a benign anatomical variant or a significant clinical anomaly.

Mitral Annular Calcification-Related Valvular Disease: A Challenging Entity.

Mitral valve annular calcification-related valvular disease is increasingly common due to the rising prevalence of age-related mitral annular calcifications. Mitral annular calcification alters the structure and function of the mitral valve annulus, which in turn causes mitral valve regurgitation, stenosis, or both. As it frequently coexists with comorbid conditions and overlapping symptoms, mitral annular calcification-related valvular disease poses significant diagnostic and therapeutic challenges. For instance, left ventricular diastolic dysfunction hinders the assessment of mitral valvular disease. Detection of mitral annular calcifications and assessment of related mitral valve disease hinge on two-dimensional echocardiography. Comprehensive assessment of mitral annular calcifications and related mitral valve disease may require multidetector computed tomography and three-dimensional echocardiography. Invasive hemodynamic testing with exercise helps identify the cause of symptoms in patients with comorbid conditions, and transcatheter interventions have emerged as a viable therapeutic option for older patients. After an outline of the normal mitral annulus, we examine how mitral annular calcifications lead to mitral valve disease and how to accurately assess mitral regurgitation and stenosis. Lastly, we review surgical and transcatheter approaches to the management of mitral annular calcification-related mitral valve regurgitation, stenosis, or both.

Mitral regurgitation outcomes after transcatheter atrial septal defect closure.

BACKGROUND: Worsening mitral regurgitation (MR) is a complication of intervention for atrial septal defect (ASD). Little is known about mitral valve (MV) characteristics associated with worsening MR. We aimed to elucidate MR outcomes and predictors of worsening MR after transcatheter ASD closure. METHODS: We analyzed changes in MR from prior to transcatheter ASD closure to 6 months after the procedure and predictors of worsening MR via baseline transthoracic echocardiography in 238 patients (64.7% females; mean age, 53 ± 22 years). RESULTS: Worsening MR was defined as worsening to moderate in patients with less than or equal to mild MR at baseline or vena contracta width increasing of ≥2 mm by 6-month follow-up in patients with moderate MR. Worsening MR was observed in 29 patients (12.2%). The associated echocardiographic findings were pseudoprolapse, hamstringing, stiffness, and anteroposterior and intercommissural mitral annulus diameter in the univariable logistic regression analysis (all P < 0.05). Multivariable analysis after adjusting for age; long-standing persistent atrial fibrillation; and ASD size showed that models combining MV leaflet findings such as pseudoprolapse or hamstringing, or anterior leaflet stiffness with the ratio of the sum of anterior and posterior leaflet lengths to intercommissural mitral annulus diameter were statistically significant for predicting worsening MR (R2 = 0.393, P < 0.001 and R2 = 0.385, P < 0.001, respectively). CONCLUSIONS: Worsening MR after transcatheter ASD closure might depend on MV leaflet findings and annulus size in patients with long-standing persistent atrial fibrillation.