Mitral Valve Prolapse
A condition where the mitral valve leaflets bulge back into the left atrium during the heart's contraction, sometimes causing a leak (regurgitation).
Emergency Management: Flail leaflet secondary to ruptured chordae tendineae causing acute severe mitral regurgitation and cardiogenic shock. Requires emergent surgical intervention.
Mitral valve prolapse (MVP) is a structural abnormality of the mitral valve where one or both leaflets billow (prolapse) by at least 2 mm into the left atrium during ventricular systole. It is typically caused by myxomatous degeneration of the valve tissue, leading to redundant, thickened leaflets and elongated chordae tendineae.
Detailed Overview
MVP is the most common cause of primary mitral regurgitation in developed countries. While the vast majority of individuals with MVP are asymptomatic and have a benign course, a subset may develop severe mitral regurgitation, infective endocarditis, or sudden cardiac death (malignant MVP syndrome). The condition is frequently identified incidentally during physical examination by the characteristic mid-systolic click and late systolic murmur. Diagnosis and risk stratification heavily rely on echocardiography.
Epidemiology & Demographics
MVP affects approximately 2% to 3% of the general population. It is slightly more prevalent in females, especially in younger age groups, but severe MVP requiring surgery is more common in males > 50 years of age.
Etiological Mechanism
The majority of cases are primary (idiopathic) with familial clustering (autosomal dominant inheritance with variable penetrance, linked to loci on chromosomes 11, 15, and 16). Secondary MVP is associated with connective tissue disorders such as Marfan syndrome (FBN1 mutation) and Ehlers-Danlos syndrome, as well as polycystic kidney disease.
Primary Causes
Idiopathic myxomatous degeneration
Marfan syndrome
Ehlers-Danlos syndrome
Osteogenesis imperfecta
Histologically, MVP is characterized by the proliferation of the spongiosa layer of the valve with accumulation of proteoglycans (myxomatous degeneration), displacing the fibrosa layer. This leads to weakened, redundant valve leaflets and chordae tendineae. During systole, the increased left ventricular pressure forces the weakened leaflets to balloon backwards (prolapse) past the mitral annulus into the left atrium. This abnormal motion can put stress on the papillary muscles and left ventricular myocardium, contributing to arrhythmogenesis.
Diagnostic Criteria & Guidelines
Echocardiographic demonstration of systolic displacement (prolapse) of one or both mitral valve leaflets by ≥ 2 mm into the left atrium beyond the plane of the mitral annulus in the parasternal long-axis view.
For asymptomatic patients without MR or with mild MR, no medical therapy is needed. Reassurance is key. For symptomatic patients with palpitations, chest pain, or anxiety, low-dose beta-blockers (e.g., Metoprolol tartrate 25-50 mg PO BID or Propranolol 10-20 mg PO TID) are first-line. Manage any associated hypertension or arrhythmias according to standard guidelines.
Second-Line & Adjunctive Therapy
If beta-blockers are not tolerated or ineffective, non-dihydropyridine calcium channel blockers (e.g., Diltiazem) can be used. For high PVC burden or malignant arrhythmias, antiarrhythmics or ablation may be considered.
Surgical & Procedural Management
Surgical Mitral Valve Repair is the definitive treatment if the patient develops severe symptomatic mitral regurgitation, or asymptomatic severe MR with LVEF ≤ 60% or LVESD ≥ 40 mm. Repair is preferred over replacement.
Patient Counseling & Advice
Reassure the patient that MVP is usually a benign condition that does not affect life expectancy. Explain the symptoms of progression (shortness of breath, extreme fatigue) and the importance of regular follow-up. Endocarditis prophylaxis is NO LONGER recommended for MVP alone.
Follow-Up & Monitoring Schedule
Asymptomatic patients with MVP and no/mild MR: clinical exam every 3-5 years. If moderate to severe MR: echocardiogram every 6-12 months.
Preventive Strategies
MVP cannot be prevented as it is primarily genetic. Complications can be minimized by avoiding severe hypertension and treating infections promptly.
Generally excellent. The mortality rate is similar to the general population. Less than 10% of patients require surgical intervention over their lifetime.