Mitral Regurgitation (MR)

Definition & Overview

Classification

Primary (Organic/Degenerative) MR

Secondary (Functional) MR

• Dilated cardiomyopathy → papillary muscle displacement, apical tethering of leaflets
• Ischemic LV dysfunction → papillary muscle ischemia/infarction
• Atrial fibrillation → annular dilation causing malcoaptation
• ~75% of patients with heart failure with reduced ejection fraction have some degree of secondary MR; severe in ~20%

Pathophysiology — Three Phases

Phase A: Acute MR

Acute MR: EDV 170 mL, ESV 30 mL — forward SV only 70 mL; LA pressure elevated to 25 mmHg. Result: pulmonary congestion + low cardiac output.

Phase B: Chronic Compensated MR

Chronic compensated MR: EDV increases to 240 mL; eccentric hypertrophy restores forward SV to 95 mL; LA pressure normalizes to 15 mmHg.

Phase C: Chronic Decompensated MR

Chronic decompensated MR: Contractile dysfunction causes ESV to rise to 110 mL; forward SV falls to 65 mL despite massive LV dilation (EDV 260 mL).

Key point: Reduced afterload occurs only in acute severe primary MR. In chronic MR, the increased LV radius returns wall stress to normal.

Clinical Features

Symptoms

• Often asymptomatic for years during compensation
• Exertional dyspnea and fatigue (earliest symptoms as LV function begins to decline)
• Orthopnea, PND, and pulmonary edema (advanced disease)
• Right-sided heart failure symptoms if pulmonary hypertension develops
• Acute severe MR: cardiogenic shock, flash pulmonary edema

Physical Examination

In acute MR: the large LA v-wave rapidly equilibrates LA and LV pressure, shortening/softening the murmur — the murmur can be deceptively soft despite severe regurgitation.

In secondary (functional) MR: the murmur may be unimpressive or even inaudible due to reduced LV contractile force.

Diagnosis

ECG

• Left atrial enlargement (notched P wave in II, biphasic P in V1)
• LV hypertrophy (voltage criteria)
• Atrial fibrillation (common complication)

Chest X-Ray

• Cardiomegaly (LV + LA enlargement)
• Pulmonary vascular congestion in decompensated states
• Absence of cardiomegaly suggests mild MR or acute onset

Echocardiography (Primary Investigation)

• TTE: LV and LA size/function, valve morphology, Doppler quantification of MR severity
• Color-flow Doppler: Identifies and semi-quantifies the regurgitant jet — but can over/underestimate severity, especially with eccentric jets
• Quantitative methods (preferred for clinical decisions):
  • Vena contracta width
  • PISA (Proximal Isovelocity Surface Area) — regurgitant volume and effective regurgitant orifice area (EROA)
  • Pulmonary vein flow reversal (systolic flow reversal = severe MR)
• TEE: Superior valve anatomy, leaflet pathology, surgical planning; also used intraprocedurally
• 3D echocardiography: Pathoanatomic detail for surgical repair planning

Cardiac MRI

• Precise quantification of regurgitant fraction when echo is inconclusive
• Phase-contrast imaging: directly measures regurgitant volume

Cardiac Catheterization

• Reserved for cases where non-invasive assessment is inconclusive
• Coronary angiography if >40 years or ischemic symptoms suspected

Severity Grading (Echocardiographic)

Management

Medical Therapy

• Goal: ↑ forward cardiac output, ↓ regurgitant volume
• Arterial vasodilators (nitroprusside): reduce SVR, preferentially increase forward flow
• Intra-aortic balloon counterpulsation: if hypotension precludes vasodilators (increases diastolic pressure, reduces afterload)
• Emergent surgical repair/replacement is often required

• ACE inhibitors/ARBs (e.g., lisinopril 20 mg/day): reduce LV volume, improve symptoms
• Beta-blockers: observational benefit
• Diuretics: relieve congestion
• Rate/rhythm control if AF present; anticoagulation mandatory with AF

• Vasodilators have not been shown to benefit patients with normal afterload
• Treat hypertension aggressively per guidelines

Surgical Therapy

• Symptomatic severe primary MR with any LVEF
• Asymptomatic severe primary MR with:
  • LVEF ≤60%, or
  • LV end-systolic diameter (LVESD) ≥40 mm
• New-onset AF attributable to MR
• Pulmonary hypertension (PASP >50 mmHg at rest)

• Repair is strongly preferred when technically feasible:
  • Preserves LV geometry and function
  • Lower operative mortality (~1%), better long-term survival
  • No need for long-term anticoagulation (unlike mechanical valve)
  • Annuloplasty ring ± leaflet/chordal procedures
• Replacement (MVR) indicated when leaflets are fused, calcified, have shortened/fused chordae, or when durable repair is not achievable

Transcatheter Edge-to-Edge Repair (TEER) — MitraClip

• Primary MR: prohibitive surgical risk (FDA approved)
• Secondary MR: symptomatic severe MR despite GDMT in HFrEF patients (LVEF 20–50%, LVESD <70 mm, PASP <70 mmHg) — shown to reduce HF hospitalizations and all-cause mortality vs. medical therapy alone (COAPT trial)

• Reduction of MR to grade <2 in 84–93% of patients
• 30-day mortality: ~5–6% in high-risk elderly cohorts
• Significant improvement in NYHA class and QoL at 12 months

Complications

Prognosis

• Severe asymptomatic MR with preserved LV function: ~10% per year risk of developing symptoms, LV dysfunction, or AF
• Surgery before LVEF declines below 60% or LVESD exceeds 40 mm is associated with better postoperative outcomes and potentially reversible LV dysfunction
• Once LV contractile dysfunction develops, it may not be fully reversible even after surgery