Refers to the displacement of some part of one or both leaflets of the mitral valve into the left atrium during systole.
Most common cause of chronic mitral regurgitation in develop countries.
Prevalence in Framingham Offspring Study 2.5%.
Occurs in 3% to 6% of Americans.
Prevalence 6-9% in patients older than 65 years.
Worldwide approximately 150,000,000 people are affected.
The primary cause of chronic organic/degenerative mitral regurgitation in developed countries.
Both acquired and genetic forms exist.
Most cases have mild disease and never need surgery.
While it is largely regarded as a benign condition, the annual rate of sudden cardiac death in individuals with MVP is 0.2-0.4% per year, and is roughly twice that observed in the general population which is 0.1-0.2% per year.
Related to the floppy mitral valve.
May be inherited as part of a recognized heritable disorder.
Several chromosomal loci for autosomal dominant mitral valve prolapse have been identified.
More common in women.
Natural history is variable, and mainly determined by the severity of the mitral regurgitation.
Characterized by billowing of one or both mitral leaflets at least 2 mm beyond the echocardiographic parasternal long axis annular plane.
Approximately 5 to 10% of patients have progression to severe mitral regurgitation, while the majority remain asymptomatic.
Severe regurgitation causes left ventricular dysfunction, heart failure, pulmonary hypertension, and atrial fibrillation.
Much of the increased cardiac death risk is related to left ventricular dysfunction in the setting of severe mitral regurgitation.
Severe mitral regurgitation may lead to rupture of mitral chordae and complications of endocarditis and stroke.
Mortality rate with mitral valve prolapse and severe mitral regurgitation is approximately 67% per year (Ling LH).
Characterized by myxomatous degeneration.
Excess leaflet tissue in young patients with severe myomatous degeneration is known as Barlow’s syndrome.
In older patients mitral valve prolapse is not associated with excess leaflet tissue and is known as fibroelastic deficiency.
Excess leaflet tissue and fibroelastic deficiency can lead to leaflet prolapse, and chordal elongation or rupture, indicating the wide spectrum of degenerative mitral valve disease that exists.
The above anatomic abnormalities prevent the mitral orifice from closing completely during systole resulting in regurgitation.
Over time, annular dilatation may occur resulting in further progression of mitral regurgitation.
Cerebral ischemic events reported in patients with no other source of emboli found to be present.
Common lesion in Marfan syndrome.
Clinical manifestations do not become evident before childhood.
In patients with mitral valve prolapse there is an estimated 4-5 times greater risk of developing Infective endocarditis than does the general population, an estimated incidence of 14 cases per hundred thousand MVP person years
Infective endocarditis is a serious condition associated with severe complications, including CHF, stroke, systemic emboli, abscess formation and death in up to 25% of patients.
Associated with an increased risk of infective endocarditis, particularly in men, and in patients with thickened leaflets, and patients with a systolic murmur.
Symptoms appear to be less common in childhood than in adulthood.
Evaluation includes: postural auscultation, EKG, echocardiogram, assessment of orthostatic, exercise testing, dynamic imaging or hemodynamic studies.