Mitral Valve Prolapse Discussion

The abnormality depicted on the transesophageal echocardiogram represents marked myxomatous deformity with prolapse of the posterior mitral valve leaflet. Mitral valve prolapse ( MVP ) is a common clinical entity with a wide spectrum of clinical presentations. The vast majority of patients have modest derangement of mitral valve architecture which is responsible for the characteristic mid-systolic click(s), often accompanied by a mid- to late-systolic mitral regurgitant murmur.

Rarely, MVP can be complicated by severe mitral regurgitation, infective endocarditis , and congestive heart failure . Present in up to 5% of the adult US population, the diagnosis of MVP is generally made on clinical grounds, often augmented by characteristic echocardiographic findings. The prototypical patient is a slender female, often with pectus excavatum and joint hypermobility.

Multiple examining positions may be required to bring about the physical findings that are characteristic of MVP. Sometimes an MVP click that is heard on one exam is not audible on another. Maneuvers which decrease preload such as standing produce an earlier click and a longer murmur (ie, the click moves closer to the first heart sound), while those that increase afterload such as squatting delay the click and shorten the murmur. Some patients can have a systolic click on auscultation with a normal echocardiogram. Others may exhibit characteristic derangements on echo, including marked superior systolic displacement of the one or both mitral leaflets (often in conjunction with myxomatous thickening of the leaflets and chordae tendinaeae) but a murmur may be inaudible. Rarely, chordal rupture resulting in a flail leaflet can be seen. Varying degrees of mitral regurgitation are consequently encountered, which can be underestimated due to the tendency for eccentric jets to hug the left atrial wall.

The underlying structural abnormality often relates to abnormal connective tissue metabolism, so that MVP is associated with conditions such as MarfanÕs syndrome and Ehlers-Danlos syndrome, as well as a variety of congenital cardiac disorders. Redundant myxomatous tissue builds up within the mitral valve leaflets and can extend to the chordae tendineae and mitral annulus. These factors reinforce impairment in valve function and contribute to mitral regurgitation by erosion of chordae and premature calcification and dilatation of the mitral annulus.

The vast majority of patients with MVP are asymptomatic (have no symptoms) and have a benign course. A variety of symptoms have been linked to MVP including anxiety, fatigue, palpitations, and chest pain. Although many theories have been proposed, the exact pathophysiologic relationship with MVP remains unknown. Reassurance, avoidance of stimulants (such as alcohol and caffeine), and low dose beta blockade (eg, lopressor, tenormin, inderal) have been advocated in the management of these symptoms. Progression to severe mitral regurgitation is uncommon, with males and patients over age 50 being at highest risk. Symptomatic severe mitral regurgitation is an indication for surgery; mitral valve repair with or without ring annuloplasty can now be performed at low operative risk and with encouraging long-term results. Endocarditis is also rare and follows a similar demographic profile. It is generally agreed that patients with abnormal valve thickening or significant mitral regurgitation on echocardiography as well as those with an audible murmur should receive antibiotic prophylaxis for infective endocarditis . Stroke (CVA), perhaps related to platelet deposition on the surface of the myxomatous valve leaflet, can occur. Both supraventricular and ventricular arrhythmias may be seen, although it is not clear whether the presence of arrhythmia in patients with MVP represent the chance concurrence of two common cardiac entities or whether a causal relationship exists.