MVP exhibits a strong hereditary component and in some patients is transmitted as an autosomal dominant trait.
Second common cause is rheumatic fever mostly seen in developing countries.
It is twice as frequent in women as in men.
MVP may occasionally result from Marfan syndrome, Ehler danlos syndrome and osteogenesis imperfecta.
It develops due to myxomatous degeneration of mitral valve in which middle layer of valve leaflet composed of loose, myxomatous material is unusually prominent.
- Most patients with mitral valve prolapse are asymptomatic.
- In symptomatic patients it may present as chest pain, dyspnea, fatigue, palpitation, syncopeand even sudden death.
- Spontaneous rupture of chordea tendinae may cause a sudden worsening of MR that is hemodynamically severe.
- On auscultation there is a mid systolic click in mild cases and pansystolic murmur if there is a significant mitral regurgitation. The click is believed to be produced by sudden tensing of the elongated chordae tendineae of prolapsing leaflets.
- Thoracic deformities are more prevalent in MVP
- BP may be normal or low.
- Infective endocarditis
- Rupture of chordae tendineae causing sudden severe MR.
- Progressive MR
- Arrhythmias and sudden death.
ECG: may be normal or may show arrhthymias such as SVT or atrial or ventricular premature contractions.
Echocardiography: is diagnostic of MVP. It shows one or both mitral leaflets bulging by atleast 2 mm into the left atrium during systole.
- Reassurance: Patients who are asymptomatic and without any arrhythmia on ECG should be reassured without any specific treatment and followed every 3 to 5 years.
- Beta-blockers: are affective for chest pain, SVT or frequent premature beats.
- Aspirin : is given to patients with MVP who have documented focal neurological deficits.
- Infective endocarditis prophylaxsis
- Surgical Treatment: with valve repair or replacement is done if there is hemodynamically significant mitral regurgitation.