Mitral Regurgitation

Mitral Regurgitation (MR) is a common valvular lesion that can be acute or chronic. Chronic MR is further divided into Primary (Organic) MR, where the pathology affects the valve apparatus itself (e.g., mitral valve prolapse, endocarditis, or rheumatic fever), and Secondary (Functional) MR, where the valve is structurally normal but fails due to Left Ventricular (LV) dilatation or remodelling (e.g., after MI). In MR, the LV must pump blood both into the aorta and back into the Left Atrium (LA). This leads to volume overload of the LA and LV. Initially, the LV compensates through eccentric hypertrophy to maintain stroke volume. However, chronic volume overload eventually leads to LV dysfunction, heart failure, and pulmonary hypertension. Atrial fibrillation is a frequent complication due to LA stretch. Management depends on the severity of MR, the presence of symptoms, and LV function. Surgical repair is generally preferred over replacement for primary MR.

The mitral valve apparatus consists of the valve leaflets, chordae tendineae, papillary muscles, and the mitral annulus. In Mitral Valve Prolapse (MVP)/Barlow's disease, myxomatous degeneration leads to lengthening of the chordae and redundant leaflets. Acute MR often results from rupture of the chordae tendineae or papillary muscle (classically 2-7 days post-inferior MI). Pathophysiologically, the regurgitant volume depends on the orifice size, the pressure gradient between LV and LA, and the duration of systole. LA compliance also plays a role: in acute MR, the LA is non-compliant, leading to a rapid rise in LA pressure and catastrophic pulmonary oedema. In chronic MR, the LA dilates and becomes more compliant, allowing it to accommodate large volumes at lower pressures for years before heart failure develops.

Chronic MR presents with gradual onset dyspnoea, orthopnoea, and fatigue. Some patients may also complain of palpitations (AF). Acute MR presents with sudden, severe respiratory distress ('flash' pulmonary oedema) and cardiogenic shock. Physical signs include: 1. Pulse: Usually normal volume (unless low CO/Shock); may be irregular (AF). 2. Apex: Displaced (down and out) and hyperdynamic (volume overload). 3. Auscultation: A pansystolic murmur at the apex radiating to the axilla (best heard with the diaphragm in the left lateral position). A third heart sound (S3) is common in severe MR due to rapid ventricular filling. Complications include atrial fibrillation, pulmonary hypertension, and right-sided heart failure.

1. Bedside: 12-lead ECG (LA enlargement - P mitrale; LVH; AF).
2. Imaging: Chest X-ray (Cardiomegaly, LA enlargement seen as a 'double shadow' on the right heart border, pulmonary venous congestion). Echocardiogram (TTE is diagnostic; TOE provides better detail for surgical planning).
3. Specialized: Cardiac MRI (quantify regurgitant volume); Exercise testing (to unmask symptoms in 'asymptomatic' patients).

1. Medical: Not curative. Diuretics (Furosemide) for fluid overload. Standard heart failure therapy (ACEi, Beta-blockers) if LV dysfunction present. Anticoagulation if AF occurs.
2. Acute MR: Urgent stabilization with IV nitrates/diuretics; intra-aortic balloon pump (IABP) to reduce afterload; urgent surgery.
3. Surgical (Primary MR): Mitral valve repair is preferred over replacement as it preserves the subvalvular apparatus and LV function. Indicated for symptomatic patients or asymptomatic patients with LV dysfunction (EF <60% or LVESD >40mm).
4. Surgical/Percutaneous (Secondary MR): Management focused on underlying HF; 'MitraClip' (edge-to-edge repair) for high-risk patients.