Key Facts

Mitral regurgitation (MR) is the backward flow of blood from the left ventricle into the left atrium during systole through an incompetent mitral valve. It is classified as primary (intrinsic valve disease) or secondary/functional (due to LV remodelling).

Epidemiology

• Most common valvular lesion: affects ~2-3% of the population
• Prevalence increases significantly with age
• Degenerative MR is the most common cause in developed countries
• Secondary MR occurs in ~30-50% of patients with heart failure and reduced EF

Aetiology

Primary MR:

• Myxomatous degeneration/mitral valve prolapse (most common in developed countries)
• Rheumatic heart disease (most common worldwide)
• Infective endocarditis (leaflet destruction)
• Connective tissue disorders: Marfan, Ehlers-Danlos
• Radiation, drugs (ergotamine, fenfluramine)

Secondary MR:

• Ischaemic heart disease (papillary muscle dysfunction, LV remodelling)
• Dilated cardiomyopathy (annular dilatation)
• Hypertrophic cardiomyopathy (SAM of mitral valve)

Acute MR:

• Acute MI (papillary muscle rupture — usually posteromedial)
• Chordal rupture (myxomatous disease, endocarditis)
• Endocarditis (leaflet perforation)
• Trauma

Pathophysiology

Chronic MR:

• Volume overload → LV dilatation (eccentric hypertrophy) → increased stroke volume to maintain forward cardiac output
• LA dilatation accommodates regurgitant volume at lower pressure (chronic compensation)
• Eventually: LV contractile failure, pulmonary hypertension, right heart failure

Acute MR:

• Non-compliant LA cannot accommodate sudden regurgitant volume
• Dramatic rise in LA pressure → flash pulmonary oedema
• Reduced forward cardiac output → cardiogenic shock

Chronic MR

• Asymptomatic for years (compensated phase)
• Progressive exertional dyspnoea, fatigue
• Palpitations (AF from LA dilatation)
• Eventually: orthopnoea, PND, peripheral oedema (decompensated)

Acute MR

• Sudden severe dyspnoea, flash pulmonary oedema
• Cardiogenic shock (hypotension, tachycardia, oliguria)
• May follow acute MI (papillary muscle rupture — typically day 2-7)

Examination Findings

• Pansystolic murmur at apex, radiating to axilla (classically)
  • Posterior leaflet prolapse: jet directed anteriorly → radiates to aortic area
  • Anterior leaflet prolapse: jet directed posteriorly → radiates to axilla/back
• Soft S1, widely split S2, S3 (volume overload)
• Displaced, hyperdynamic apex (volume-loaded LV)
• AF may be present
• In acute MR: murmur may be short and soft (rapid equalisation of pressures)

Red Flags

• Acute severe MR: pulmonary oedema + shock
• Declining LV function on serial echo in chronic MR
• New murmur post-MI (papillary muscle rupture)
• Endocarditis with worsening MR
• Progressive symptoms despite medical therapy

Bedside

• ECG: P mitrale, AF, LVH; in acute MI — ischaemic changes
• CXR: cardiomegaly, LA enlargement, pulmonary oedema

Bloods

• BNP/NT-proBNP: heart failure assessment
• Blood cultures: if endocarditis suspected
• Troponin: if ischaemia suspected
• FBC, U&Es, coagulation: preoperative

Imaging

• TTE: severity assessment (EROA, regurgitant volume, vena contracta), mechanism (leaflet prolapse, tethering), LV function and dimensions, LA size, pulmonary pressure
• TOE: detailed valve anatomy, pre-surgical planning, intraoperative guidance
• Cardiac MRI: gold standard for regurgitant fraction; myocardial fibrosis assessment
• Coronary angiography: preoperative coronary assessment

Severity Grading

Non-pharmacological

• Serial echocardiographic monitoring: 6-12 monthly in moderate-severe MR
• Moderate exercise generally safe in chronic compensated MR

Pharmacological

• ACEi/ARBs: afterload reduction in secondary MR and heart failure
• Beta-blockers: heart failure management, rate control in AF
• Diuretics: for pulmonary and systemic congestion
• Anticoagulation: warfarin for AF; DOACs increasingly used in non-valvular AF with MR (but warfarin for mechanical prosthesis)
• Acute severe MR: IV vasodilators (nitroprusside), inotropes (dobutamine), IABP as bridge to surgery

Surgical/Interventional

• Mitral valve repair (preferred over replacement):
  • Better long-term outcomes, preserves LV function, avoids anticoagulation
  • Success rate >90% in experienced centres for degenerative MR
• Mitral valve replacement: when repair not feasible
  • Mechanical: lifelong warfarin
  • Bioprosthetic: limited durability
• Indications (NICE NG208): symptomatic severe primary MR; asymptomatic with LVEF ≤60% or LVESD ≥40 mm; new AF or PASP >50 mmHg
• MitraClip (TEER — transcatheter edge-to-edge repair): for high-risk surgical patients
  • COAPT trial: MitraClip + GDMT superior to GDMT alone for secondary MR with HF
  • MITRA-FR trial: no benefit (different patient selection)
• Acute MR: emergency surgery (repair or replacement)

Referral Criteria

• Symptomatic severe MR: surgical assessment
• Asymptomatic severe MR with LV changes approaching thresholds: cardiology referral
• Acute severe MR: emergency admission and surgery
• Secondary MR in heart failure: consider TEER referral

• Asymptomatic severe MR with normal LV function: ~3-5% per year become symptomatic or develop LV dysfunction
• Symptomatic severe MR without surgery: 5-year survival ~30-40%
• Post-mitral valve repair: 10-year survival ~80-90%
• Post-mitral valve replacement: 10-year survival ~60-70%
• Acute severe MR (papillary rupture post-MI): without surgery mortality >75%
• Secondary MR in HFrEF: associated with ~2-fold increase in mortality
• MitraClip in selected patients: reduces HF hospitalisations and mortality (COAPT)

Primary vs Secondary MR

Causes of Acute Severe MR