Mitral Valve Prolapse Syndrome: A Patients Perspective

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Even for those who are not experiencing symptoms, if a murmur is detected suggesting mitral valve prolapse, an echocardiogram, or echo, is usually recommended. The echo uses ultrasound to evaluate the characteristics of the valve cusps and how much blood may be leaking regurgitation from the valve when the heart contracts. Other tests may include magnetic resonance imaging MRI , or angiogram. The test results and extent of your symptoms will guide your healthcare provider in determining if further testing is indicated.

In many instances, having MVP will not impact your health and requires no treatment. Talk with your healthcare provider about how best to prevent complications from MVP based on your level of risk. If you are prescribed medication, take it as directed.

What happens during MVP?

MVP very rarely becomes a highly serious condition. However, in the most serious cases, mitral valve prolapse can cause abnormal heartbeats arrhythmias that may eventually become life-threatening. When valve prolapse is severe enough to cause significant valve leakage , it can lead to serious complications like stroke. This happens because a mitral valve leaking regurgitating a significant amount of blood can cause blood clots to form.

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When clots travel from the heart to the arteries or the brain, it can lead to a stroke or heart attack. Know the signs and symptoms of heart attack and stroke. The routine use of antibiotics before having a dental procedure is no longer recommended by the American Heart Association for patients with mitral valve prolapse regardless of whether or not they have any associated symptoms.

Walk through a step-by-step interactive guide explaining your valve issue and treatment options with helpful videos, text summaries and links along the way. The link provided below is for convenience only, and is not an endorsement of either the linked-to entity or any product or service. What is mitral valve prolapse MVP? What happens during MVP? Is mitral valve prolapse dangerous? How is mitral valve prolapse detected?

However, despite the availability of literally millions of patients for study, no convincing association has been found to date. Occasional families with MVP have been identified and an underlying gene defect reported.

In patients with X-linked myxomatous valvular dystrophy, a rare disorder associated with severe MVP, the defect has been linked to chromosome Xq28 The first locus for nonsyndromic MVP has been mapped to chromosome 16p A second locus for autosomal dominant MVP has been mapped to chromosome 11p Thus, even within families with an autosomal dominant mode of inheritance, there appears to be significant genetic heterogeneity.

The role of mechanical stress in the evolution of MVP is also important. The mitral valve opens and closes more than 3 billion times during the course of the normal human lifespan. During each closure period, it must withstand the full force of ventricular contraction. Because of the normal orientation of the leaflets, this force is unevenly applied, affecting the posterior leaflet more than the anterior leaflet, and prolapse of the posterior leaflet is more common observed in two-thirds of cases, with prolapse of both leaflets occurring in the remaining third.

This pattern of involvement and the fact that the valve disruption occurs late in life are consistent with the important role of physiologic stress in the development of MVP. The TGFs are multipotent cytokines that are important modulators of cell growth, proliferation and differentiation, inflammation, extracellular matrix deposition, and apoptosis Their biologic effects are context dependant and vary with tissue type and the activity of other signaling pathways In a study reported in this issue of the JCI , Ng et al.

They compared the morphometry of mitral valves in fibrilin-1—deficient mice to those of wild-type mice and report a progressive increase in leaflet length and thickness in heterozygous versus homozygous mice.

The leaflets exhibited both increased cell proliferation and decreased apoptosis. Similar to human MVP, the murine model pioneered by Ng et al. There are differences, however, among what has been noted in human acquired myxomatous mitral valve disease. Clinically, the MVP that often accompanies Marfan syndrome is not generally considered to be a model of the isolated MVP in the adult for a number of reasons.

Second, severe mitral valve disorders in Marfan syndrome are generally manifest in infants, while in adults, the majority of complications are due to aortic aneurysm formation and dissection. This is in contrast to the clinical paradigm of MVP, where complications are typically not seen before the fifth decade of life. Third, the valvular involvement in Marfan syndrome and in these mice affects the whole valve in a relatively homogeneous way.

In idiopathic MVP, necropsy studies show that the morphologic abnormalities can involve 1 or both leaflets, and the morphological changes may be heterogeneous within the leaflet itself Fourth, in one recent study 29 , prolapse was shown to occur in roughly half of the patients with Marfan syndrome, and in our experience it occurs even less frequently. The mouse model described by Ng et al. The most significant morphologic changes were noted in the homozygous mice.

While homozygous and dual heterozygous forms of FBN1 mutations in children have been reported, they appear to be lethal at an early age 30 , as was the case in the homozygous mice in the Ng et al. Second, although the histology of the valves in this study is not described in detail, the hypercellularity of the leaflets is striking. An increase in interstitial cells has been noted in surgical specimens and valves from MVP patients; however, hypercellularity is not generally a feature of MVP The difference may lie in the fact that the valves available for study in MVP patients generally come from autopsy or have been surgically removed and thus represent advanced disease, while in the Ng et al.

It would be interesting to study the histologic features of the valves in older heterozygous mice to see whether they are similar to those found in clinical MVP. The morphological changes of the mitral valve in this murine model were evident shortly after birth, while idiopathic MVP is uncommon in children and generally becomes manifest after the adolescent growth spurt.

It may be that clinically undetectable changes are present at birth in MVP and only become apparent later in life, but this remains to be shown. Future studies using this model would ideally include a more detailed description of the anatomic features of the murine model. Since in humans there is considerable phenotypic variability among individual genotypes, it would also be interesting to see how consistent the phenotypic expression is in the murine model.

In summary, it appears that MVP is a final common pathway for a variety of genetic and acquired disorders, which presumably weaken connective tissue of the valve and lead to leaflet elongation, thickening, and often degeneration.

However, a great deal of study remains necessary before the pathogenic mechanisms underlying idiopathic MVP and its relationship to more generalized forms of connective tissue disease are clarified. Go to JCI Insight. Top Abstract Mitral valve prolapse: