Mitral Valve Prolapse

Believed to be most common form of valvular heart disease, with an incidence of 2–3% in the general population. MVP is a progressive disease that begins in middle age and affects both men and women.

Most common cause of chronic primary MR.

Disease severity varies widely. Complications related to the disease are a consequence of arrhythmias, infective endocarditis, and progressive severity of MR with associated LV dysfunction.

Acute HF or exacerbation of chronic HF as a consequence of MR

Embolic stroke

Arrhythmias

Sudden cardiac death

Severity of MR

Severity of associated LV dysfunction and HF

AFIB, embolic stroke, sudden cardiac death

Associated conditions: Marfan syndrome; Ehlers-Danlos syndrome, osteogenesis imperfecta, pseudoxanthoma elasticum, aneurysms-osteoarthritis syndrome, or hypertrophic cardiomyopathy

Severity of disease varies widely based on the clinical and diagnostic criteria used to establish the diagnosis.

MVP is defined by echocardiography as isolated prolapse of the mitral valve leaflets ≥2 mm beyond the mitral valve annular plane into the LA during systole. The myxomatous degeneration causing MVP is characterized by leaflet thickening, leaflet redundancy, chordal elongation, or chordal rupture. MRI may demonstrate scarring or fibrosis of the papillary muscle or inferobasal segments of the LV

Structural changes lead to weakness and deformity of the valve apparatus. Annular dilation, stretching of leaflets and chordal elongation impair leaflet coaptation causing progression of MR.

Fibrosis or scarring of the valve apparatus may increase the risk of ventricular arrhythmias or sudden cardiac death.

Rupture of weakened chordae results in a flail leaflet and produces acute severe MR.

Chronic MR causes progressive atrial dilation, eccentric LV hypertrophy, HF, and AF.

MVP syndrome is MVP associated with a spectrum of nonspecific symptoms, including atypical chest pain, palpitations, exertional dyspnea, exercise intolerance, syncope, anxiety, lean body habitus, electrocardiographic repolarization abnormalities, and sudden cardiac death. A pathophysiologic link between genetics and the molecular biology of disease expression for MVP and its syndromes has yet to be fully defined.

Onset of HF symptoms, LV dysfunction (ejection fraction <50% or end-systolic diameter >40 mm) and pulm Htn worsen pt prognosis. AF, left atrial enlargement, leaflet thickening (>5 mm), flail segments, and age >50 y is associated with worsening disease.