Mitral Regurgitation

Detailed Overview

MR can be classified as primary (organic), involving intrinsic abnormalities of the mitral valve apparatus (leaflets, chordae tendineae, papillary muscles, or annulus), or secondary (functional), where the valve is structurally normal but fails to close properly due to left ventricular dilation or dysfunction. Chronic MR allows the heart to compensate over time, while acute MR presents with sudden, life-threatening cardiogenic shock and pulmonary edema. The regurgitant volume depends on the size of the regurgitant orifice and the pressure gradient between the LV and LA. Progression of the disease can lead to atrial fibrillation, pulmonary hypertension, and right-sided heart failure.

Epidemiology & Demographics

MR is the most common valvular abnormality, with a prevalence of nearly 10% in the general population. It affects males and females equally. The prevalence increases significantly with age, affecting over 10% of individuals above 75 years of age. Rheumatic heart disease remains a leading cause in developing nations.

Etiological Mechanism

Primary causes include myxomatous degeneration (mitral valve prolapse), infective endocarditis (Staphylococcus aureus, viridans streptococci), rheumatic heart disease (Group A Streptococcus), and chordal rupture. Secondary causes include ischemic heart disease (papillary muscle displacement or rupture post-MI) and dilated cardiomyopathy.

Primary Causes

Myxomatous degeneration of the mitral valve

Infective endocarditis

Rheumatic fever

Ischemic heart disease

Dilated cardiomyopathy

• Prior Myocardial Infarction: Can cause papillary muscle dysfunction or rupture, particularly involving the posteromedial papillary muscle supplied by the right coronary artery.
• Mitral Valve Prolapse: Structural abnormality of the leaflets leading to incomplete closure; present in 2-3% of the population.
• Advanced Age: Associated with degenerative calcification of the mitral annulus (MAC).

During systole, high pressure in the left ventricle forces blood backward through the incompetent mitral valve into the left atrium. This increases LA volume and pressure. In chronic MR, the LA dilates to accommodate the extra volume, maintaining normal pressure, but the LV undergoes eccentric hypertrophy due to volume overload. Eventually, LV contractility declines, leading to reduced forward cardiac output and increased end-systolic volume. In acute MR, the non-compliant LA cannot dilate, resulting in a sudden rise in LA and pulmonary venous pressure, leading to acute pulmonary edema.

Characteristic Clinical Presentation

• Dyspnea on exertion: Shortness of breath during physical activity due to elevated pulmonary venous pressure.
• Orthopnea: Difficulty breathing when lying flat, caused by redistribution of fluid to the lungs.
• Fatigue: Reduced exercise tolerance resulting from decreased forward cardiac output.
• Palpitations: Awareness of heartbeats, often due to the development of atrial fibrillation from LA dilation.

Physical Examination Signs

• Holosystolic murmur best heard at the apex, radiating to the axilla.
• Displaced, hyperdynamic apical impulse.
• S3 gallop (in severe MR with volume overload).
• Soft S1 sound.

• Left-sided heart failure: Resulting from chronic volume overload leading to LV dysfunction.
• Atrial fibrillation: Due to left atrial enlargement; increases the risk of systemic thromboembolism.
• Pulmonary hypertension: Caused by chronic backup of pressure into the pulmonary vasculature.

Diagnostic Criteria & Guidelines

Diagnosis is primarily echocardiographic, requiring visualization of the regurgitant jet. Severe primary MR is defined by: Effective Regurgitant Orifice Area (EROA) ≥ 0.40 cm², Regurgitant Volume ≥ 60 mL/beat, and Regurgitant Fraction ≥ 50%. Severe secondary MR is sometimes defined with lower thresholds (EROA ≥ 0.20 cm²).

Differential Diagnosis

• Aortic Stenosis
• Tricuspid Regurgitation
• Ventricular Septal Defect
• Hypertrophic Cardiomyopathy

Laboratory Tests & Biomarkers

• NT-proBNP: Often elevated (e.g., > 400 pg/mL) indicating ventricular wall stress and heart failure.
• ECG: May show left atrial enlargement (P mitrale), LV hypertrophy, or atrial fibrillation.

Imaging Modalities & Findings

• Transthoracic Echocardiogram (TTE):
• Chest X-ray:

• Stage A
  Patients with MVP, mild valve thickening, or MAC, with no MR jet or trace MR.
• Stage B
  Mild to moderate MR. Regurgitant volume < 60 mL, regurgitant fraction < 50%, EROA < 0.40 cm2.
• Stage C
  Severe MR (Regurgitant volume >= 60 mL, EROA >= 0.40 cm2) but no symptoms. C1: LVEF > 60% and LVESD < 40mm. C2: LVEF <= 60% or LVESD >= 40mm.
• Stage D
  Severe MR with symptoms of heart failure (exertional dyspnea, heart failure).

Second-Line & Adjunctive Therapy

Transcatheter Edge-to-Edge Repair (TEER, e.g., MitraClip) is indicated for patients with symptomatic severe primary MR at high or prohibitive surgical risk, or highly selected patients with chronic severe secondary MR with persistent symptoms despite optimal GDMT (e.g., LVEF 20-50%, LVESD ≤ 70 mm, COAPT criteria).

Surgical & Procedural Management

Mitral Valve Repair is strongly preferred over replacement if technically feasible, especially for degenerative disease. Mitral Valve Replacement (mechanical or bioprosthetic) is performed if repair is not possible. Mechanical valves require lifelong anticoagulation (Warfarin, target INR 2.5-3.5).

Recommended Lifestyle Changes

• Sodium restriction to < 2,000 mg/day to reduce volume retention.
• Aerobic exercise program for asymptomatic patients; avoidance of competitive sports in severe MR.
• Smoking cessation.

Patient Counseling & Advice

Educate the patient on the importance of reporting new symptoms like shortness of breath or palpitations immediately. Explain the need for endocarditis prophylaxis ONLY if a prosthetic valve was implanted or prior endocarditis history exists (Amoxicillin 2g PO 1 hour before dental procedures). Discuss the trajectory of the disease and the timing for surgical intervention.

Follow-Up & Monitoring Schedule

Asymptomatic severe MR requires clinical evaluation and echocardiography every 6-12 months. Mild to moderate MR requires evaluation every 1-2 years.

Preventive Strategies

Prompt treatment of streptococcal pharyngitis (Penicillin V 500 mg PO BID for 10 days) to prevent rheumatic fever. Optimal management of hypertension and coronary artery disease.

Patients with asymptomatic severe MR and normal LV function have a 10-year survival rate of > 80%. Once symptoms or LV dysfunction (LVEF < 60%) develop, mortality increases significantly without surgical intervention.