MITRAL REGURGITATION

✓ Medically ReviewedDISEASEID: MDBT0158🚨 TRIAGE: URGENTICD-10: I34.0

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Definition

CLINICAL DEFINITION

Mitral regurgitation is a valvular heart disease characterised by the retrograde flow of blood from the left ventricle into the left atrium during systole due to incomplete coaptation or structural failure of the mitral valve apparatus. It is classified as primary (organic) when caused by intrinsic structural abnormalities of the valve leaflets or chordae, and secondary (functional) when resulting from left ventricular dilation or dysfunction with structurally normal leaflets.

IN PLAIN ENGLISH

Mitral regurgitation occurs when the heart's mitral valve does not close tightly, allowing blood to flow backward into the upper left chamber of the heart instead of being pumped out to the body. Over time, this backward flow forces the heart to work harder and can lead to heart failure or irregular heart rhythms.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Mitral regurgitation is NOT mitral stenosis, which involves a narrowed valve opening that restricts forward blood flow. It is also distinct from tricuspid regurgitation, which affects the right side of the heart, and physiological trace regurgitation, which is a normal, benign finding on echocardiography in many healthy individuals.

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Word Breakdown

re-

=back, again (from Latin 're-')

gurgit-

=whirlpool (from Latin 'gurgitem'); 'mitral' from Latin 'mitra' (bishop's hat)

-ation

=process or condition (from Latin '-ation')

Literal Meaning: The process of flowing backward through the mitral valve

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Abbreviations

MR=Mitral Regurgitation — standard clinical abbreviation for the valvular disorder

MVR=Mitral Valve Replacement or Repair — surgical interventions for MR

EROA=Effective Regurgitant Orifice Area — key echocardiographic parameter for MR severity

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Synonyms & Variants

Mitral Insufficiency›Mitral Incompetence›

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Category-Specific Context

As a Disease, mitral regurgitation encompasses a spectrum from acute, life-threatening haemodynamic collapse to chronic, compensated volume overload. It is classified pathophysiologically into primary (organic) and secondary (functional) mechanisms, which dictate distinct diagnostic and therapeutic pathways according to current cardiology guidelines.

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Clinical Context & Usage

CLINICAL SETTINGS

Cardiology Outpatient ClinicEchocardiography LaboratoryCoronary Care UnitCardiothoracic Operating TheatreGeneral Medicine Ward

USAGE & DOCUMENTATION NOTES

Documented as "MR" in clinical notes and echo reports. Severity is typically graded as mild, moderate, or severe based on echocardiographic parameters (e.g., EROA, regurgitant volume). Clinicians often specify "primary MR" or "secondary MR" to guide management. Acute MR is frequently documented in the context of acute coronary syndrome or endocarditis.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

In primary mitral regurgitation, intrinsic structural damage to the valve apparatus—such as leaflet prolapse, flail leaflet, rheumatic thickening, or endocarditis-induced perforation—prevents adequate systolic coaptation. In secondary mitral regurgitation, the valve leaflets are structurally normal, but left ventricular dilation, remodelling, or regional wall motion abnormalities displace the papillary muscles, causing apical tethering and incomplete leaflet closure. In both forms, systolic retrograde flow into the left atrium causes left atrial volume and pressure overload. In acute MR, the non-compliant left atrium cannot accommodate the sudden volume load, leading to a rapid rise in pulmonary venous pressure and acute pulmonary oedema. In chronic MR, the left atrium and left ventricle undergo eccentric hypertrophy and dilation to accommodate the regurgitant volume, maintaining forward cardiac output for years until compensatory mechanisms fail and left ventricular systolic dysfunction ensues.

PRIMARY CAUSES

Mitral Valve Prolapse (Myxomatous Degeneration)

Excessive connective tissue proliferation causes leaflet redundancy and chordal elongation or rupture, leading to systolic prolapse into the left atrium.

Rheumatic Heart Disease

Autoimmune cross-reactivity causes leaflet thickening, commissural fusion, and chordal shortening, resulting in restricted leaflet motion and mixed stenosis/regurgitation.

Ischaemic Heart Disease (Papillary Muscle Rupture or Dysfunction)

Acute myocardial infarction can cause papillary muscle rupture (acute severe MR) or chronic ischaemic remodelling displaces papillary muscles, causing leaflet tethering (secondary MR).

Infective Endocarditis

Valvular vegetations cause leaflet perforation or chordal destruction, creating an acute regurgitant orifice.

Left Ventricular Dilated Cardiomyopathy

Global left ventricular dilation displaces papillary muscles and dilates the mitral annulus, preventing leaflet coaptation despite normal leaflet morphology (secondary MR).

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Drug-Induced Causes

💊 Ergot-derived dopamine agonists (Cabergoline, Pergolide) ↗

Mechanism: Stimulation of 5-HT2B receptors on cardiac valves promotes fibroblast proliferation and fibrotic valvulopathy, leading to restrictive leaflet motion and regurgitation.

→ Discontinue the offending agent; perform baseline and periodic echocardiographic screening for patients on long-term therapy.

💊 Fenfluramine and Dexfenfluramine (withdrawn) ↗

Mechanism: Metabolites activate 5-HT2B receptors, causing plaque-like fibrous tissue deposition on valve leaflets and chordae, resulting in retraction and regurgitation.

→ Historical context; these agents are withdrawn from the market. Patients with prior exposure require echocardiographic surveillance.

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Epidemiology

Prevalence:Mitral regurgitation is the most common valvular abnormality in developed countries, affecting approximately 1.7% to 2.5% of the general population. Prevalence increases significantly with age, affecting over 10% of individuals aged 75 years and older.

Age Group:Primary MR due to mitral valve prolapse often presents in young to middle-aged adults, while degenerative, ischaemic, and secondary MR predominantly affect older adults (typically >65 years). Rheumatic MR presents in younger populations in endemic regions.

Sex Predilection:Equal

Geographic Distribution:Rheumatic mitral regurgitation remains highly prevalent in low- and middle-income countries (e.g., Sub-Saharan Africa, South Asia, Oceania) due to inadequate treatment of streptococcal pharyngitis. Degenerative and ischaemic MR predominate in high-income countries with aging populations.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 URGENT

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Acute severe MR complicating acute myocardial infarction — consider papillary muscle rupture; requires urgent echocardiography and emergency surgical evaluation, as medical management alone carries extremely high mortality.
Flail leaflet in a patient with new-onset pulmonary oedema — suggests acute severe primary MR requiring rapid afterload reduction and urgent surgical or transcatheter intervention.

URGENT EVALUATION TRIGGERS

New-onset dyspnoea at rest or orthopnoea in a patient with known MR — suggests progression to decompensated heart failure.
New atrial fibrillation with rapid ventricular response — can acutely worsen MR severity and precipitate pulmonary oedema.
Syncope or presyncope — may indicate severe pulmonary hypertension or low forward cardiac output.

Contraindications & Precautions

CONTRAINDICATIONS

Vasodilators in acute severe MR with hypotension — may precipitate cardiovascular collapse by reducing systemic vascular resistance without improving forward stroke volume.

SPECIAL PRECAUTIONS

Avoid excessive bradycardia — prolonged diastole increases the regurgitant volume per beat in chronic MR; maintain normal to slightly elevated heart rates.
Endocarditis prophylaxis — indicated only for high-risk patients (e.g.
prior endocarditis
prosthetic valves) undergoing specific dental procedures
not for native valve MR alone according to current AHA/ESC guidelines.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Atrial Fibrillation — left atrial dilation and structural remodelling disrupt normal electrical conduction pathways.
Heart Failure — chronic volume overload eventually exceeds left ventricular compensatory mechanisms
leading to reduced forward cardiac output and pulmonary congestion.
Pulmonary Hypertension — chronic elevation of left atrial pressure transmits backward into the pulmonary vasculature
causing reactive vasoconstriction and vascular remodelling.
Infective Endocarditis — structurally abnormal or regurgitant valves create turbulent jets that damage the endothelium
predisposing to bacterial seeding.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Mitral Stenosis

Both are mitral valve disorders, but stenosis involves restricted opening and diastolic murmurs, whereas regurgitation involves incomplete closure and systolic murmurs.

Aortic Stenosis

Both can present with systolic murmurs and heart failure symptoms; aortic stenosis radiates to the carotids, while MR radiates to the axilla.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

Tricuspid Regurgitation

Key Distinguishing Feature: Holosystolic murmur best heard at the lower left sternal border that increases with inspiration (Carvallo's sign), unlike MR which is best heard at the apex and does not increase with inspiration.

Ventricular Septal Defect

Key Distinguishing Feature: Harsh holosystolic murmur at the lower left sternal border often accompanied by a palpable thrill; echocardiography confirms left-to-right shunting at the ventricular level rather than valvular regurgitation.

Aortic Stenosis

Key Distinguishing Feature: Crescendo-decrescendo systolic murmur radiating to the carotids with a delayed and diminished carotid upstroke (pulsus parvus et tardus), unlike the holosystolic apical murmur of MR.

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Clinical Pearls

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The murmur of chronic MR is typically holosystolic and loudest at the apex, radiating to the axilla. However, in acute severe MR, the murmur may be early systolic or decrescendo and softer due to rapid equalisation of left ventricular and left atrial pressures.

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Echocardiographic assessment of MR severity must integrate multiple parameters (vena contracta width, EROA, regurgitant volume, and pulmonary vein flow reversal) rather than relying solely on colour flow jet area, which is highly dependent on haemodynamic conditions and machine settings.

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Left ventricular ejection fraction (LVEF) overestimates true myocardial performance in severe MR because the ventricle ejects into the low-impedance left atrium. An LVEF <60% in severe MR often indicates early latent left ventricular systolic dysfunction and is a trigger for surgical intervention.

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Surgical mitral valve repair is strongly preferred over replacement for primary MR when anatomically feasible, as it preserves the subvalvular apparatus, maintains better left ventricular geometry, and avoids the long-term risks of prosthetic valves.

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Example Usage & SOAP

CLINICAL SENTENCE

"Transthoracic echocardiogram demonstrates severe primary mitral regurgitation secondary to posterior leaflet prolapse with a flail segment, associated with left atrial dilation and preserved left ventricular systolic function (LVEF 62%)."

IN A SOAP NOTE

S: 68-year-old male reports progressive exertional dyspnoea and orthopnoea over the past 3 months. O: BP 128/78 mmHg, HR 88 bpm irregularly irregular. JVP not elevated. Auscultation reveals a grade 3/6 holosystolic murmur at the apex radiating to the axilla, and bibasilar crackles. ECG shows atrial fibrillation. TTE shows severe MR with EROA 0.45 cm² and LVEF 55%. A: Severe primary mitral regurgitation with new-onset atrial fibrillation and early heart failure symptoms. P: Refer to cardiothoracic surgery for mitral valve repair evaluation. Initiate rate control with bisoprolol and anticoagulation with apixaban. Start furosemide 20 mg daily for symptom relief.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for a holosystolic murmur at the apex: (1) Mitral Regurgitation — radiates to axilla, increases with handgrip, associated with apical thrill or displaced PMI in chronic cases; (2) Tricuspid Regurgitation — lower left sternal border, increases with inspiration (Carvallo's sign), prominent v waves in JVP; (3) Ventricular Septal Defect — harsh murmur at left sternal border, often with palpable thrill, confirmed by step-up in oxygen saturation in the right ventricle.

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Classifications & Scoring

GRADING SYSTEM

ESC/EACTS MR Severity Grading

Classifies MR severity into mild, moderate, and severe based on echocardiographic parameters including vena contracta width, effective regurgitant orifice area (EROA), regurgitant volume, and pulmonary vein systolic flow reversal.

View Reference ↗

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Prognosis

SHORT-TERM OUTCOME

Acute severe MR (e.g., from papillary muscle rupture or endocarditis) carries a high short-term mortality without urgent surgical or percutaneous intervention due to rapid cardiogenic shock and pulmonary oedema.

LONG-TERM PROGNOSIS

Chronic severe primary MR has a prolonged asymptomatic phase, but once symptoms or left ventricular dysfunction develop, prognosis declines rapidly without intervention. Successful surgical repair is associated with excellent long-term survival and preservation of left ventricular function, whereas untreated severe symptomatic MR carries a high 5-year mortality.

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References & Coding

ICD-10 DIAGNOSTIC CODE

I34.0

LITERATURE CITATIONS & GUIDELINES

[1]Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2021;77(4):e25-e197.

[2]Vahanian A, Van Overscheldee N, Delgado V, et al. 2021 ESC/EACTS Guidelines for the management of valvular heart disease. Eur Heart J. 2022;43(7):561-632.

[3]Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease. J Am Coll Cardiol. 2017;70(2):252-289.

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