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Clinical Subject Page

Mitral Regurgitation

Also called

Leaky Mitral Valve

ICD-10

I34.0

Specialty

Cardiology

Onset

Acute & Chronic

Reviewed

June 2026
On This Page

Overview

Mitral regurgitation (MR) is a leakage of blood from the left ventricle back into the left atrium because the mitral valve does not close completely during systole. This reduces the amount of blood pumped forward and can eventually lead to left-sided heart failure.

Etiology & Risk Factors

Primary (Organic) MR

Caused by disease of the mitral valve itself.

  • Mitral valve prolapse (most common degenerative cause)

  • Mitral annular calcification

  • Ruptured chordae tendineae

  • Rheumatic fever

  • Infective endocarditis

  • Ischemic MR (e.g., papillary muscle rupture after acute myocardial infarction)

Secondary (Functional) MR

Caused by left ventricular disease leading to valve incompetence.

  • Coronary artery disease (CAD)

  • Previous myocardial infarction (MI)

  • Dilated cardiomyopathy

  • Left-sided heart failure

Risk Factors

  • Mitral valve prolapse

  • Coronary artery disease

  • Previous myocardial infarction

  • Dilated cardiomyopathy

  • Heart failure

  • Rheumatic fever

  • Infective endocarditis

  • Mitral annular calcification

Pathophysiology

Acute MR

  • The mitral valve fails to close, causing blood to flow back from the left ventricle (LV) into the left atrium (LA) during systole.

  • This causes:

    • Rapid increase in LA pressure

    • Pulmonary venous congestion

    • Pulmonary edema

    • Increased LV volume overload to maintain cardiac output

 

Chronic MR

  • Long-term volume overload causes:

    • Left atrial enlargement

    • Left ventricular dilation (eccentric hypertrophy)

  • Initially, the heart compensates and maintains cardiac output.

  • Over time, LV dysfunction develops, leading to:

    • Reduced stroke volume

    • Increased LA and LV pressures

    • Pulmonary congestion

    • Pulmonary hypertension

    • Right heart strain

 

Simple Flow

Mitral valve doesn’t close properly → Blood leaks back into LA during systole → LA & LV volume overload → LV dilation → Heart failure → Pulmonary hypertension (late)

Clinical Presentation

Acute MR

Symptoms

  • Sudden dyspnea

  • Pulmonary edema

  • Palpitations

  • Symptoms of left-sided heart failure

  • Cardiogenic shock (severe cases)

Examination

  • Soft decrescendo murmur (may be absent in severe MR)

  • S3 heart sound may be present

Chronic MR

Symptoms

  • Exertional dyspnea

  • Fatigue

  • Palpitations (often due to atrial fibrillation)

  • Dry cough

  • Symptoms of left-sided heart failure

  • Later, symptoms of right-sided heart failure

Examination

    • Holosystolic (pansystolic), high-pitched blowing murmur

      • Best heard at the apex

      • Radiates to the left axilla

    • Quiet S1

    • S3 heart sound (advanced disease)

    • Displaced apical impulse

Mitral Regurgitation Case Overview
Mitral Regurgitation Overview

History Taking

  • “Do you get short of breath when walking or climbing stairs?”
  • “Do you become short of breath when lying flat?”
  • “Do you wake up at night feeling short of breath?”
  • “Do you feel your heart racing or skipping beats?”
  • “Do you feel tired more easily than before?”
  • “Do you have a dry cough?”
  • “Have you had chest pain or a recent heart attack?”
  • “Have you ever had rheumatic fever or infective endocarditis?”
  • “Do you have swelling in your legs or ankles?”

Mitral Stenosis Vs Mitral Regurgitation

Cardiology · Valvular Heart Disease — Mitral Stenosis vs Mitral Regurgitation

🚧 Mitral Stenosis
Narrowed mitral valve orifice → obstructed LA→LV flow
Normal area: 4–6 cm²  |  Severe: <1 cm²
Most common cause: Rheumatic fever
↺ Mitral Regurgitation
Incompetent mitral valve → systolic backflow LV→LA
Volume overload of both LA and LV
Most common cause: MVP / rheumatic / ischaemic
Pathophysiology
Mitral Stenosis
Valve orifice narrows → pressure gradient across MV during diastole
LA pressure rises → LA enlargement + pulmonary venous HTN
Pulmonary HTN → RV pressure overload → cor pulmonale
LV is underfilled (preload ↓) — LV function usually preserved
AF common due to LA dilation → risk of LA thrombus → stroke
Mitral Regurgitation
Systolic backflow LV→LA → LA volume overload
LA enlarges → increased pulmonary venous return → LV volume overload
Compensated phase: LV dilates (eccentric hypertrophy), EF appears normal
Decompensated: LV contractility fails → EF falls → HF
Acute MR (papillary rupture/chordae): no time to compensate → flash pulmonary oedema
Auscultation & Heart Sounds
Mitral Stenosis
Murmur Mid-diastolic rumble at apex
Timing Diastolic — after S2, continues toward S1
Radiation Does not radiate
Character Low-pitched, rumbling
Special Loud S1  |  Opening snap after S2
Positional Louder in left lateral decubitus

S1┈┈┈S2┈OS┈╾╾╾rumble╿╿╿┈S1
└ Shorter S2–OS interval = more severe stenosis (higher LA pressure)
Presystolic accentuation (if sinus rhythm) — murmur increases just before S1
S1 loudness ↓ as stenosis worsens (valve less mobile)
Mitral Regurgitation
Murmur Pansystolic (holosystolic) murmur at apex
Timing Throughout systole — S1 to S2
Radiation Axilla / left infrascapular
Character Blowing, high-pitched
Special Soft/absent S1  |  S3 gallop (volume overload)
Positional Louder with squatting & expiration

S1┈╾╾╾╾╾╾╾╾╾S2┈┈┈┈┈┈S1
└ Uniform throughout systole — does not change with S1 or S2
MVP exception: late systolic murmur preceded by mid-systolic click
Acute MR may have a soft or early systolic murmur (LA pressure equalises rapidly)
ECG Findings
Mitral Stenosis
P wave Broad, notched P in II — “P mitrale” (>120 ms)
P in V1 Biphasic — prominent negative terminal deflection
QRS Usually normal (LV not overloaded)
Late finding RVH pattern (RAD, dominant R in V1) if pulmonary HTN
Rhythm Atrial fibrillation common (LA dilation)

┈/╾╿┈P-mitrale┈┈┈┈narrow QRS┈┈┈┈
└ P mitrale = LA enlargement signature — notched P >2.5 mm wide in II
Mitral Regurgitation
P wave Broad, notched P — “P mitrale” (LA enlargement)
QRS LVH pattern — tall R in V5/V6, deep S in V1/V2
Axis LAD (LV volume overload)
Rhythm AF common (LA dilation, same as MS)
Key diff LVH present in MR — absent in MS

┈/╾╿┈P-mitrale┈┈tall QRS (LVH)┈┈
└ LVH on ECG = volume overload — key distinguisher from pure MS
CXR Findings
Mitral Stenosis
LA enlargement: double shadow right heart border, splaying of carina (>70°), posterior displacement of oesophagus on lateral
Pulmonary venous HTN: upper lobe diversion → Kerley B lines → pulmonary oedema
Mitral valve calcification visible on lateral CXR
LV size normal (underfilled)
Late: RV enlargement, prominent pulmonary arteries
Mitral Regurgitation
LA enlargement (same signs as MS but often more prominent in chronic MR)
LV enlargement — cardiomegaly with leftward and downward cardiac apex displacement
Pulmonary oedema in acute MR or decompensated chronic MR
Key difference: LV enlargement present in MR — absent (or even small LV) in MS
Echocardiography
Mitral Stenosis
Hockey stick deformity of anterior mitral leaflet (doming in diastole)
Reduced E-F slope on M-mode (slow valve opening)
Planimetry of MVA <1 cm² = severe; PHT method for area
Mean gradient >10 mmHg = severe (Doppler)
LA enlarged, LV normal or small; leaflet calcification/fusion assessed for PTMC suitability (Wilkins score)
Mitral Regurgitation
Colour Doppler: systolic jet from LV into LA (direction indicates mechanism)
EROA ≥0.4 cm² or RVol ≥60 ml = severe (PISA method)
LV dilated (EDV ↑) with preserved or reduced EF
LA enlarged; pulmonary vein systolic flow reversal in severe MR
Surgery indicated when EF ≤60% or ESD ≥40 mm (LV decompensation threshold)
Symptoms & Clinical Features
Mitral Stenosis
Exertional dyspnoea → orthopnoea → PND (pulmonary venous HTN)
Haemoptysis (pulmonary venous rupture or Eisenmenger)
Palpitations (AF) → systemic embolism / stroke
Malar flush (mitral facies) — peripheral vasoconstriction + facial telangiectasia
Hoarseness — Ortner syndrome (enlarged LA compressing recurrent laryngeal nerve)
Symptoms precipitated by: pregnancy, tachycardia, AF (loss of atrial kick)
Mitral Regurgitation
Chronic: long asymptomatic phase — compensated for years
Exertional dyspnoea, fatigue (reduced forward CO)
Palpitations (AF), orthopnoea, PND
Acute MR: sudden flash pulmonary oedema, cardiogenic shock (ruptured papillary muscle post-MI)
Hyperdynamic apex, laterally displaced (LV volume overload)
Feature Mitral Stenosis Mitral Regurgitation
Murmur timingMid-diastolic rumblePansystolic blowing
Best heardApex, left lateral decubitusApex, radiates to axilla
S1Loud (early) → soft (late/calcified)Soft / obscured
Extra soundsOpening snap (OS) after S2S3 gallop (volume overload)
ECG P waveP mitrale (broad, notched)P mitrale (broad, notched)
ECG QRSNormal (RVH if pulm HTN)LVH pattern
CXR heart sizeLA enlarged, LV normalLA + LV both enlarged
Pulmonary oedemaChronic (gradual venous HTN)Acute (sudden decompensation)
LV functionPreserved (underfilled)Dilated → EF may fall
AF riskVery high (thrombus → stroke)High (LA dilation)
Main causeRheumatic feverMVP, rheumatic, ischaemic, IE
InterventionPTMC (balloon) or MVRRepair preferred over replacement
Surgery triggerMVA <1.5 cm² + symptomsEF ≤60% or ESD ≥40 mm

Investigations

1. Transthoracic Echocardiography (TTE) – Gold Standard

  • First-line and diagnostic test of choice

  • Assesses:

    • Severity of mitral regurgitation

    • Mitral valve anatomy

    • Left atrial and left ventricular size and function

2. Transesophageal Echocardiography (TEE)

  • If TTE is inadequate

  • Performed before surgery to better evaluate the valve

3. ECG

  • May show:

    • Atrial fibrillation

    • Left ventricular hypertrophy (LVH)

    • Left atrial enlargement (P mitrale)

    • Right heart strain in advanced disease

4. Chest X-ray

  • Assesses for:

    • Pulmonary edema

    • Pulmonary congestion

    • Left atrial enlargement

    • Left ventricular enlargement (chronic MR)

5. Laboratory Tests

  • Troponin (to rule out myocardial infarction)

  • BNP

  • Blood cultures if infective endocarditis is suspected

6. Additional Tests (when indicated)

    • Cardiac MRI

    • Stress echocardiography

    • Coronary angiography (especially if ischemic MR is suspected or before surgery)

Diagnosis

Mitral Regurgitation · Diagnostic Criteria

DIAGNOSIS IS PRIMARILY ECHOCARDIOGRAPHIC (TTE ± TEE) Severity is graded using a multiparametric, integrative approach per ASE/ESC guidelines — no single measurement is diagnostic in isolation. Combine qualitative, semi-quantitative and quantitative parameters with clinical context.
Diagnostic Approach
1
Qualitative
Valve morphology — flail leaflet, prolapse, vegetation, calcification. Color Doppler jet size (subjective, least reliable alone).
Screening
2
Semi-Quantitative
Vena contracta width, jet area/LA area ratio, pulmonary vein flow pattern, CW Doppler density/contour.
Supporting
3
Quantitative
Regurgitant volume, regurgitant fraction, EROA via PISA or volumetric method. Most robust for severity grading.
Most reliable
4
Clinical Correlation
Symptoms, exam findings, ECG/CXR, LA/LV remodeling and pulmonary pressures to confirm chronicity and impact.
Integration
Parameter Mild Moderate Severe
Regurgitant Volume (RVol) <30 mL 30–59 mL ≥60 mL
Regurgitant Fraction (RF) <30% 30–49% ≥50%
Effective Regurgitant Orifice Area (EROA) <0.20 cm² 0.20–0.39 cm² ≥0.40 cm²
Vena Contracta Width (VCW) <0.3 cm 0.3–0.69 cm ≥0.7 cm
Supportive Criteria for Severe MR
LA enlargement — in absence of other causes (AF, other valve disease)
LV enlargement/dysfunction — in chronic primary (degenerative) MR
Pulmonary hypertension — elevated PASP on echo
Dense, triangular CW Doppler jet — early peaking suggests severe, acute regurgitation
Systolic flow reversal in pulmonary veins — specific for severe MR
Flail leaflet / ruptured chordae on 2D imaging — structural marker of severity
Clinical Correlation
Symptoms — dyspnea, fatigue, orthopnea, palpitations (often from AF)
Auscultation — holosystolic apical murmur radiating to the axilla
Widely split S2 — due to earlier aortic valve closure
S3 gallop — may indicate volume overload/severe MR
ECG — LA enlargement (P mitrale), atrial fibrillation
CXR — LA/LV enlargement, pulmonary venous congestion
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Management

1. Acute MR (Medical Emergency)

  • Urgent cardiology and cardiothoracic surgery consultation

  • Urgent mitral valve repair or valve replacement (for acute primary MR)

  • Stabilize the patient while awaiting surgery:

    • Diuretics (for pulmonary edema)

    • Vasodilators (e.g., nitrates, nitroprusside) to reduce afterload

    • Inotropes/vasopressors if cardiogenic shock develops

  • If secondary MR, treat the underlying cause (e.g., revascularization for ischemic MR).

 

2. Chronic MR

Medical Management

  • Treat the underlying cause.

  • Manage heart failure with:

    • Diuretics

    • ACE inhibitors

    • Beta-blockers

  • Manage associated atrial fibrillation if present.

 

-Definitive Treatment

  • Mitral valve repair is the preferred treatment.

  • Mitral valve replacement if repair is not possible.

  • Transcatheter mitral valve repair (e.g., clip device) may be considered in selected patients who are not suitable for surgery.

Complications

    • Heart failure
    • Pulmonary edema
    • Cardiogenic shock (especially acute MR)
    • Atrial fibrillation
      • Increased risk of stroke and other thromboembolic events
    • Pulmonary hypertension
    • Infective endocarditis

Prognosis

  • Acute MR has a poor prognosis if not treated urgently.
  • Chronic MR may remain compensated for years but gradually progresses to left ventricular dysfunction and heart failure.
  • Early diagnosis and timely valve repair improve long-term outcomes.
  • Prognosis depends on the cause, severity, and timing of intervention.

Key Points / Clinical Pearls

    • MR = blood leaks from the LV back into the LA during systole.
    • Gold-standard investigation: Transthoracic echocardiography (TTE).
    • Classic murmur: Holosystolic (pansystolic) murmur at the apex radiating to the left axilla.
    • Acute MR is a medical and surgical emergency.
    • Mitral valve repair is preferred over replacement when feasible.
    • Common complications: heart failure, atrial fibrillation, pulmonary edema, pulmonary hypertension, and cardiogenic shock.