Forms Of Mitral Regurgitation Research Articles

A Case of Transient Mitral Regurgitation: Not Everything Is Always What It Seems

Mitral regurgitation (MR) is a common form of valvular heart disease that is associated with significant morbidity and mortality. MR can be broadly classified into 2 different categories: primary and secondary MR. Primary MR usually is caused by leaflet abnormalities, whereas secondary MR is a chronic disease secondary to geometric distortion of both the annulus and subvalvular apparatus because of left ventricular remodeling. Without acute changes in loading conditions, myocardial blood flow, or rhythm disturbances, functional MR typically is not transient. In this E-Challenge, the authors show a transient and completely reversible acute and severe form of functional MR with the use of multimodal echocardiography.

From secondary to tertiary mitral regurgitation: the paradigm shifts, but uncertainties remain

Secondary mitral regurgitation (MR) is the most common and undertreated form of MR, whose contribution to poor prognosis and indications to correction remains under discussion. MR has been characterized into 'proportionate' or 'disproportionate', based on left ventricle (LV) and regurgitant volumes, whereas 'tertiary' MR identifies conditions, in which regurgitation is pathologic per se and actively contributes to LV dysfunction. Echocardiographic and anatomo-pathological studies revealed that secondary MR prompts subtle leaflet maladaptive changes, actively contributing to the dynamic progression of secondary MR. We critically discuss the paradigm shift from secondary to tertiary MR and question the notion that MV leaflets play a passive role in secondary MR. We also review the role of standard transthoracic echocardiography for appraising and quantifying maladaptive MV leaflet changes and LV volumes and call for a more sophisticated and comprehensive imaging framework for classifying MR in future interventional studies.

Early and late mortality after repair or replacement in mitral valve prolapse and functional ischemic mitral regurgitation: A systematic review and meta-analysis of observational studies

Mitral regurgitation (MR) is the most prevalent valvular pathology in the USA affecting 1.7% of the population [1]. The two predominant forms of MR in the Western World are mitral valve prolapse (MVP) and ischemic mitral regurgitation (IMR) [2]. The optimal surgical strategy is still debated in both entities. Previous data comparing mitral valve repair (MVr) and replacement (MVR) approaches are based on a heterogeneous population in terms of LV function and baseline characteristics. The purpose of this study was to perform a systematic review and meta-analysis of all the relevant studies and to compare the mortality between the 2 surgical treatment strategies in patients with MVP and IMR. Using PubMed database, EMBASE, and the Cochrane Library we performed literature searches and thereafter individually reviewed relevant articles, extracted relevant data and entered in Review Manager software ([RevMan] version 5.1.20 (Nordic Cochrane Centre, Copenhagen, Denmark)).

Direct Visualization of Regurgitant Orifice by CMR Reveals Differential Asymmetry According to Etiology of Mitral Regurgitation

This study sought to characterize the shape of regurgitant orifice area (ROA) and mitral apparatus in various forms of mitral regurgitation (MR) by cardiac magnetic resonance (CMR). ROA is an accepted parameter of MR severity. However, there are little data on the shape of the ROA in various forms of MR. Direct assessment of ROA was performed with a 1.5-T CMR scanner using a breath-hold fast imaging with steady-state free precession. The regurgitant orifice shape and the anatomy of the mitral valve apparatus including mitral annulus, mitral leaflet angles, and mitral valve tenting area were assessed. We studied 74 patients. MR severity was mild in 39%, moderate in 27%, and moderate-to-severe or severe in 34%. Mitral valve pathology was degenerative in 26%, prolapse in 22%, flail in 33%, and functional in 19%. For all patients, ROA correlated significantly with regurgitant fraction (r = 0.80, p < 0.001). The ROA shape index as expressed by the ratio of the larger length to the smaller length was a median of 2.04 (interquartile range [IQR]: 1.49 to 3.08) over all patients. CMR revealed significant asymmetry of the ROA geometry in functional MR 3.91 (IQR: 2.79 to 4.84) compared with prolapse 2.14 (IQR: 1.80 to 3.04), flail 2.20 (IQR: 1.69 to 2.91), and degenerative MR 1.24 (IQR: 1.09 to 1.57), all p < 0.01. The assessment of mitral valve geometry demonstrated that patients with functional MR had significantly increased leaflet angles, mitral valve tenting area, and mitral annulus area (all p < 0.05). Of note, the orifice shape index correlated with increasing leaflet angles in patients with functional MR (r = 0.68, p = 0.005). Direct assessment of ROA by CMR revealed significant asymmetry of ROA in various forms of MR, particularly in patients with functional MR. The slitlike appearance in functional MR correlates with a distended mitral apparatus.

Different mechanisms of mitral regurgitation in acute and chronic forms of coronary heart disease.

Contradictory two-dimensional echocardiographic findings have been reported in relation to the role of prolapse of the mitral valve and lack of systolic leaflet coaptation in mitral regurgitation secondary to coronary heart disease. A prospective study of 22 patients with chronic coronary heart disease and mitral regurgitation showed the following: Inferior akinesia was detected in 14 (64%), fibrosis of the postero-medial papillary muscle in 10 (45%), and prolapse of the mitral valve in nine (41%). A combination of the three signs was seen in six patients (27%). Lack of systolic leaflet coaptation was seen in only two patients, both with anterior myocardial infarction. When these results are compared with those reported in the literature, it is apparent that in acute coronary heart disease, lack of leaflet coaptation is frequently visualized (P less than 0.01) and fibrosis of the postero-medial papillary muscle and prolapse of the mitral valve are lacking (P less than 0.01). A unitary explanation of all forms of mitral regurgitation in coronary heart disease is misleading; mechanisms of mitral regurgitation in coronary heart disease depend on the clinical presentation--acute or chronic, the site of infarction, and the presence of cardiac dilatation.

Systolic mitral flutter, an echocardiographic clue to the diagnosis of ruptured chordae tendineae

A new finding of fine systolic fluttering of the mitral leaflet is described in two patients with ruptured chordae tendinease and severe mitral regurgitation. The flutter is caused by the action of high-velocity blood flow upon the leaflet margin that has lost its support. The jet stream of blood evokes a high-frequency vibratory motion of the tensed leaflet as opposed to the previously described, lower frequency, less specific, diastolic flutter. This finding was not seen in the echocardiograms of 75 patients with other forms of mitral regurgitation. Systolic flutter appears to be specific for ruptured chordae tendineae.

The natural history and surgical management of the redundant cusp syndrome (floppy mitral valve)

The incidence of the redundant cusp syndrome (“floppy valve”) was 5 per cent in 294 routine autopsies carried out at St. George’s Hospital. The incidence increased linearly with age. The characteristic pathological features are expansion and thickening of the valve cusps with lengthening and weakening of the chordae tendineae. Fibrous disintegration begins at the tip of the fibrous core of the valve and spreads toward the annulus and into the chordae tendineae. The natural history of the redundant cusp syndrome is usually benign; however, in approximately 8 per cent of the patients, the valve deteriorates and rapidly progressive mitral regurgitation develops. We reviewed the presenting features and surgical management of 16 patients with this syndrome treated at St. Thomas’ Hospital between 1965 and 1972. The reasons for early deterioration in this series were ruptured chordae, subacute bacterial endocarditis, and associated connective tissue disease. The characteristic clinical features are a mid-systolic click and a late systolic murmur. However, when valve function deteriorates, the patient usually is in atrial fibrillation and has a pansystolic murmur, which makes the syndrome difficult to distinguish from other forms of mitral regurgitation. Fourteen patients in this series had mitral valve replacement with no operative mortality but one late death. None had paravalvular leaks and all are virtually asymptomatic. Two patients were treated by valvoplasty. Both have pansystolic murmurs and dyspnea.