Educational

Mitral Regurgitation

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by

Saim Khalid
in

1. Introduction

Mitral regurgitation (MR) is the backward flow of blood from the left ventricle (LV) into the left atrium (LA) during systole, caused by incompetence of the mitral valve. It is the second most common valvular heart disease worldwide, after aortic stenosis, and has a wide range of etiologies, mechanisms, and clinical implications.

The mitral valve is a complex apparatus consisting of leaflets, chordae tendineae, papillary muscles, and the annulus. Any disruption in these structures can lead to MR. Importantly, MR is broadly classified into:

  • Primary (organic) MR: due to structural abnormalities of the mitral valve apparatus itself.
  • Secondary (functional) MR: due to left ventricular or left atrial remodeling, with structurally normal valve leaflets.

Understanding these distinctions is crucial, as management strategies differ significantly between primary and secondary MR.

2. Structural vs Functional MR

2.1 Primary (Organic) Mitral Regurgitation

  • Definition: MR resulting from intrinsic structural abnormalities of the mitral valve components.
  • Causes:
    • Degenerative (myxomatous) disease: Mitral valve prolapse (Barlow’s disease, fibroelastic deficiency).
    • Rheumatic heart disease: Leaflet thickening, chordal fusion, restricted motion.
    • Infective endocarditis: Leaflet perforation or chordal rupture.
    • Congenital malformations: Cleft mitral valve.
    • Radiation-induced valvulopathy.

Key feature: Valve leaflets and/or subvalvular apparatus are diseased or damaged.

2.2 Secondary (Functional) Mitral Regurgitation

  • Definition: MR caused by distortion of left ventricular or atrial geometry, with structurally normal valve leaflets.
  • Causes:
    • Ischemic MR: Following myocardial infarction with papillary muscle displacement.
    • Dilated cardiomyopathy: Annular dilation and papillary muscle tethering.
    • Left atrial enlargement: Atrial fibrillation leading to atrial functional MR.

Key feature: Valve leaflets are normal, but the valve fails to coapt due to ventricular or atrial remodeling.

2.3 Clinical Distinction

  • Primary MR: Valve pathology evident on echocardiography (e.g., prolapse, flail leaflet).
  • Secondary MR: Normal valve morphology but poor leaflet coaptation due to altered ventricular mechanics.

3. Pathophysiology of Volume Overload

MR creates a volume overload state, leading to adaptive and eventually maladaptive changes.

3.1 Hemodynamic Consequences

  • During systole, part of LV stroke volume is ejected back into the LA.
  • The LV must accommodate both:
    • Forward stroke volume into the aorta.
    • Regurgitant volume into the LA.
  • This causes:
    • LV volume overload.
    • LA volume and pressure overload.

3.2 Acute vs Chronic MR

Acute MR

  • Causes: Papillary muscle rupture, chordal rupture, endocarditis.
  • Pathophysiology:
    • LA is non-compliant → rapid rise in LA pressure.
    • Severe pulmonary congestion and edema.
    • No time for LV or LA adaptation.
  • Clinical picture: Severe dyspnea, pulmonary edema, cardiogenic shock.

Chronic MR

  • LV and LA gradually adapt to regurgitant volume.
  • Adaptations:
    • LA dilation → accommodates regurgitant flow with lower pressure rise.
    • LV eccentric hypertrophy → increases chamber size to maintain forward output.
  • Eventually, decompensation occurs: LV systolic dysfunction, pulmonary hypertension, right-sided failure.

3.3 Determinants of Severity

  • Regurgitant orifice size.
  • Pressure gradient between LV and LA.
  • Systolic duration.
  • LV and LA compliance.

4. Clinical Signs and Auscultatory Findings

Clinical evaluation is critical in MR, though diagnosis must be confirmed with imaging.

4.1 Symptoms

  • Acute MR: Severe dyspnea, orthopnea, pulmonary edema, hypotension, cardiogenic shock.
  • Chronic MR (early): Often asymptomatic.
  • Chronic MR (progressive): Fatigue, exertional dyspnea, orthopnea, palpitations (AF).
  • End-stage MR: Right heart failure (edema, ascites, hepatomegaly).

4.2 Physical Examination

Pulse and Blood Pressure

  • Often normal in compensated chronic MR.
  • In advanced disease: atrial fibrillation with irregular pulse.

Cardiac Auscultation

  1. Classic Murmur:
    • High-pitched, blowing holosystolic murmur.
    • Best heard at apex.
    • Radiates to axilla (sometimes to base or back).
  2. First Heart Sound (S1):
    • Soft or absent in severe MR (valve does not close effectively).
  3. Third Heart Sound (S3):
    • Often present due to rapid filling of LV.
    • Indicates severe volume overload and possible LV dysfunction.
  4. Fourth Heart Sound (S4):
    • May be heard in early MR with stiff LV.
  5. Other findings:
    • Mid-systolic click in mitral valve prolapse.
    • Loud P2 if pulmonary hypertension develops.

Apical Impulse

  • Displaced and hyperdynamic in chronic MR due to LV enlargement.

Jugular Venous Pulse

  • Elevated in advanced disease with right-sided involvement.

4.3 Clinical Clues to Etiology

  • Mitral valve prolapse: Late systolic murmur with midsystolic click.
  • Ischemic MR: History of MI, new holosystolic murmur.
  • Rheumatic MR: Associated with mitral stenosis, opening snap.

5. Diagnostic Approach

While physical exam provides strong suspicion, imaging—especially echocardiography—confirms diagnosis and guides management.

5.1 Echocardiography (Gold Standard)

  • Transthoracic echocardiography (TTE):
    • Defines leaflet morphology and motion.
    • Measures regurgitant volume, effective regurgitant orifice area (EROA).
    • Assesses LV size, function, and LA enlargement.
  • Transesophageal echocardiography (TEE):
    • Superior resolution; essential for surgical planning.
    • Useful in endocarditis, prosthetic valves, intraoperative evaluation.

Quantitative criteria for severe MR:

  • Regurgitant volume ≥60 mL.
  • EROA ≥0.40 cm².
  • Regurgitant fraction ≥50%.
  • Vena contracta ≥0.7 cm.

5.2 Doppler and Color Flow Mapping

  • Detects MR jet size, direction, and eccentricity.
  • Helps differentiate central vs eccentric jets.

5.3 Stress Echocardiography

  • Assesses exercise-induced changes in MR severity and pulmonary pressures.
  • Useful in borderline cases.

5.4 Cardiac Catheterization

  • Historically gold standard; now reserved for:
    • Inconclusive echo.
    • Assessment of coronary artery disease prior to surgery.

5.5 Cardiac MRI

  • Accurate quantification of regurgitant volume and fraction.
  • Excellent for serial follow-up.

5.6 Other Investigations

  • ECG: May show LA enlargement, AF, LVH.
  • Chest X-ray: Cardiomegaly, pulmonary venous congestion.
  • BNP levels: Elevated with symptomatic MR, correlate with prognosis.

6. Distinguishing Primary vs Secondary MR in Diagnosis

  • Primary MR:
    • Abnormal valve morphology (flail, prolapse, thickening).
    • Surgery often required, especially with symptoms or LV dysfunction.
  • Secondary MR:
    • Normal leaflets with annular dilation or tethering.
    • Management focuses on treating underlying LV disease (HF therapy, CRT, revascularization).
    • Surgical repair/replacement considered in selected cases.

7. Prognosis

  • Asymptomatic MR: May remain stable for years.
  • Symptomatic MR: Poor prognosis without intervention.
  • Primary MR: Valve repair offers excellent outcomes if performed early.
  • Secondary MR: Prognosis tied to underlying cardiomyopathy; treatment more complex.

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