Mitral regurgitation

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Chronic MR creates LV and LA volume overload. The compliant LA may mask pulmonary symptoms for years while the LV dilates; AF, pulmonary hypertension and LV dysfunction mark progression. In acute MR, a non-compliant LA develops severe pressure abruptly, causing oedema and shock.

Mechanism determines treatment. Primary degenerative disease is corrected at the valve, ideally by durable repair; secondary MR is initially a ventricular/atrial disease treated by optimising the underlying heart failure, rhythm and coronary substrate.

Echo uses anatomy, vena contracta, pulmonary-vein flow, EROA/regurgitant volume and chamber response. Eccentric or multiple jets and dynamic secondary MR can defeat single measurements, so TOE, 3D echo, exercise echo or CMR may be needed.

Key points

Primary MR is a disease of leaflets/chordae, commonly prolapse or flail; secondary MR results from LV or atrial remodelling with initially normal leaflets.
A pansystolic apical murmur radiating to the axilla is typical, but acute severe MR can have a short or quiet murmur because LA pressure rises rapidly.
Severe primary MR is supported by an integrated echo assessment, often including EROA at least 0.40 cm2 or regurgitant volume at least 60 mL/beat.
In chronic primary MR, LVEF 60% or less or LVESD 40 mm or more already signals LV dysfunction and is a surgical trigger even without symptoms.
Durable surgical repair is preferred to replacement for suitable degenerative primary MR and should be performed in an experienced valve centre.
For secondary MR, first optimise guideline-directed heart-failure treatment, revascularisation when indicated and CRT when eligible; reassess MR after optimisation.
Transcatheter edge-to-edge repair can be offered to selected symptomatic patients with severe MR and suitable anatomy when surgery is unsuitable or in selected secondary MR after optimal therapy.
Acute severe MR is a mechanical emergency: medical stabilisation is a bridge to urgent surgery, not definitive care.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Degenerative primary valve disease

Myxomatous leaflet prolapse, flail segments or chordal degeneration prevent normal leaflet coaptation. The valve apparatus itself is abnormal, and regurgitation may progress as chordae stretch or rupture.

Ventricular secondary regurgitation

Ischaemic scar or dilated cardiomyopathy displaces papillary muscles and tethers otherwise normal leaflets. Ventricular and annular enlargement then widen the gap during systole.

Atrial functional regurgitation

Long-standing atrial fibrillation or marked left-atrial enlargement can dilate the mitral annulus without primary leaflet destruction. Loss of coordinated atrial and annular function worsens closure.

Acute coaptation failure

Papillary-muscle rupture or ischaemic dysfunction after myocardial infarction, acute chordal rupture, or infective endocarditis can abruptly compromise leaflet support or coaptation. Severe regurgitation may then develop before the atrium and ventricle can adapt.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Systolic backward flow
Incomplete leaflet closure allows blood to pass from the left ventricle into the left atrium during systole, reducing effective forward stroke volume.
2
Chronic volume loading
In chronic disease, the left atrium becomes compliant and the ventricle receives increased diastolic volume. This can preserve forward output while concealing early haemodynamic deterioration.
3
Chamber remodelling
Persistent volume overload causes left-atrial enlargement and eccentric ventricular dilatation. Annular enlargement and papillary displacement can intensify regurgitation, creating a self-reinforcing cycle.
4
Pulmonary and ventricular decompensation
Rising left-atrial pressure transmits backwards into pulmonary veins, while prolonged ventricular stress impairs contractility. Breathlessness, pulmonary hypertension and reduced forward output follow.
5
Acute pressure overload
When regurgitation begins suddenly, a non-compliant left atrium cannot buffer the returning volume. Pulmonary venous pressure rises sharply, causing oedema, hypotension or cardiogenic shock.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Chronic primary MR

A displaced hyperdynamic apex, apical pansystolic murmur radiating to the axilla and a soft S1 may accompany prolapse or flail leaflet.

Mitral valve prolapse

A mid-systolic click with a late systolic murmur can move earlier with reduced LV volume; echo confirms anatomy and any regurgitation.

Acute severe MRRed flag

Abrupt breathlessness, pulmonary oedema, hypotension or shock after MI, endocarditis or chordal rupture may occur with a unimpressive murmur.

Chronic decompensation

Falling exercise capacity, orthopnoea, AF, pulmonary hypertension or oedema suggests loss of compensation.

Secondary MR phenotype

HFrEF, ischaemic scar or marked atrial enlargement causes leaflet tethering or annular dilatation without primary leaflet destruction.

Endocarditis or embolic context

Fever, bacteraemia, a new regurgitant murmur, emboli or conduction change requires urgent endocarditis imaging and microbiology.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Transthoracic echocardiographyFirst step
Why
Define mechanism, severity, LV/LA size, LVEF, pulmonary pressure and other valve disease.
Interpretation and limitations
Integrate measures; in primary MR, EROA at least 0.40 cm2 and regurgitant volume at least 60 mL support severe disease, but loading and jet geometry matter.
02
Transoesophageal and 3D echocardiography
Why
Clarify flail/prolapse segments, endocarditis, acute MR and repair or TEER suitability.
Interpretation and limitations
Provides surgical-quality anatomy and procedural planning; use urgently when TTE is inadequate in an unstable patient.
03
Cardiac MRI
Why
Quantify LV volumes and regurgitant fraction when echo measurements are discordant.
Interpretation and limitations
Useful for eccentric/multiple jets; decisions still integrate symptoms, anatomy and serial ventricular response.
04
Exercise testing or stress echocardiography
Why
Objectify equivocal symptoms and dynamic MR or pulmonary-pressure response.
Interpretation and limitations
Helpful in stable discordant cases, not acute oedema or clearly symptomatic severe MR.
05
ECG and ambulatory rhythm monitoring
Why
Detect AF, conduction disease and ventricular arrhythmia when symptoms suggest it.
Interpretation and limitations
New AF in severe primary MR is an adverse marker and may strengthen intervention timing.
06
Coronary angiography/CT and blood cultures when indicated
Why
Assess ischaemic mechanism before intervention and investigate suspected endocarditis.
Interpretation and limitations
Papillary-muscle rupture after MI requires emergency surgery; positive cultures alter antimicrobial and operative planning.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Aortic stenosis

Both can produce exertional breathlessness and a systolic murmur. The aortic-stenosis murmur is typically ejection-shaped, loudest at the right upper sternal edge and radiates towards the carotids.

Tricuspid regurgitation

Tricuspid regurgitation produces a pansystolic murmur nearer the lower sternal edge that usually intensifies with inspiration. Raised venous pressure and right-sided chamber enlargement support this diagnosis.

Ventricular septal defect

A septal defect can cause a harsh pansystolic murmur, usually loudest at the lower left sternal edge. Echocardiography demonstrates shunting rather than backward flow through the mitral valve.

Hypertrophic obstructive cardiomyopathy

Dynamic outflow obstruction causes an ejection systolic murmur that changes with loading manoeuvres. Echocardiography shows ventricular hypertrophy and outflow obstruction, sometimes with associated secondary mitral regurgitation.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01acuteAcute severe mitral regurgitationFirst stepAbrupt severe MR causes pulmonary oedema, hypotension or shock.

1Use ABCDE care, continuous monitoring and oxygen/ventilatory support for hypoxaemia; call cardiology, critical care and cardiac surgery immediately.
2Obtain urgent TTE and usually TOE, while investigating MI, papillary-muscle/chordal rupture and endocarditis; take cultures promptly when infection is possible.
3Use IV diuresis and specialist afterload/perfusion support as a bridge, tailored to BP; revascularise an acute coronary culprit when indicated.
4Proceed to emergency or urgent mitral surgery when the mechanical lesion is confirmed; do not rely on apparent improvement with medical therapy.

02primaryChronic severe primary MRDegenerative or other primary MR is severe.

1Confirm symptoms, mechanism, repair anatomy, LVEF and LVESD with expert imaging; use exercise testing or CMR when discordant.
2Offer surgery for attributable symptoms when operative benefit is expected, and refer even if asymptomatic when LVEF is 60% or less or LVESD is 40 mm or more.
3Also consider earlier repair at an expert centre when new AF, resting pulmonary pressure at least 50 mmHg or marked LA dilatation signals progression and durable repair is highly likely.
4Prefer durable surgical repair over replacement; if severe symptomatic MR persists but surgery is unsuitable and anatomy fits, consider transcatheter edge-to-edge repair.

03secondarySevere secondary MRMR results from LV/atrial remodelling and the patient remains symptomatic.

1Optimise evidence-based HFrEF medicines, volume status, rhythm/rate management and revascularisation; provide CRT when the electrical criteria are met.
2Repeat expert echo after optimisation because severity is dynamic and may improve with reverse remodelling.
3If severe symptoms and MR persist, discuss in a heart-failure/valve multidisciplinary team; consider TEER when anatomy and ventricular profile predict benefit and surgery is unsuitable.
4If CABG or another cardiac operation is required, assess concomitant mitral surgery; consider advanced heart-failure therapies when ventricular disease dominates.

04surveillanceAsymptomatic surveillanceSevere MR is present but an intervention trigger is not yet established.

1Review clinical status and TTE about every 6 months for severe primary MR with preserved LVEF above 60% and LVESD below 40 mm.
2Use serial measurements from comparable imaging and watch for falling LVEF, rising LVESD, new AF, pulmonary hypertension or progressive LA enlargement.
3Ask about real activity and consider supervised exercise testing if symptoms are uncertain.
4Bring valve-team review forward immediately when a trigger emerges; do not wait for overt heart failure.

Key medicines and prescribing safety2 treatments · regimens, roles and cautions

Relieves congestion in acute or chronic MR while cause-directed treatment is arranged.

Furosemide

For chronic oedema, 40 mg orally in the morning is a usual initial adult dose; maintenance is often 20 mg daily or 40 mg on alternate days. For acute oedema, the injection SmPC gives 20–50 mg IV initially, at no faster than 4 mg/min.

Monitor BP, renal function, sodium, potassium, urine output and weight. Diuresis does not repair MR and must not delay urgent surgery in acute severe disease.

Part of underlying HFrEF or hypertension treatment in secondary MR; not a disease-modifying substitute for repair of primary MR.

Ramipril

For stable symptomatic heart failure, start 1.25 mg orally once daily and double at 1–2-week intervals as tolerated to a maximum 10 mg/day, preferably in two divided doses; for hypertension, a usual start is 2.5 mg once daily.

Check BP, creatinine and potassium before and after titration; avoid in pregnancy, previous ACE-inhibitor angioedema and use caution with renal-artery stenosis.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Left-sided heart failure

Progressive volume overload eventually raises filling pressures and reduces effective output. Exertional breathlessness can advance to orthopnoea, pulmonary oedema and low-output symptoms.

Atrial fibrillation and embolism

Left-atrial enlargement and pressure promote atrial fibrillation. Loss of atrial contraction worsens filling and symptoms, while atrial stasis increases systemic thromboembolic risk.

Pulmonary hypertension and right failure

Sustained pulmonary venous hypertension can remodel the pulmonary circulation. The right ventricle then faces increased afterload, leading to tricuspid regurgitation, oedema and hepatic congestion.

Irreversible left-ventricular dysfunction

Total ejection can appear preserved because it includes regurgitant flow. Continued overload may therefore cause occult myocardial damage before conventional ejection fraction becomes clearly reduced.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

For asymptomatic severe primary MR without a trigger, perform clinical review and echo about every 6 months.
Trend LVEF, LVESD, LV/LA volumes, pulmonary pressure and MR severity using comparable studies.
Check rhythm for new AF and investigate palpitations or syncope with ambulatory monitoring when needed.
In secondary MR, reassess after HFrEF treatment, revascularisation and CRT optimisation before procedural decisions.
After repair, replacement or TEER, monitor residual/recurrent MR, transmitral gradient, LV remodelling and device/prosthesis complications.
With ACE inhibitor or diuretic treatment, monitor BP, renal function and electrolytes after initiation and dose changes.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

An EF of 60% is not reassuring

In chronic severe MR, forward and regurgitant ejection can preserve total LVEF. A value at or below 60% already indicates LV systolic dysfunction.

Acute MR can be quiet

Rapid LA pressure equalisation shortens the systolic gradient, so murmur intensity can underestimate catastrophic regurgitation.

Mechanism precedes device

A prolapsing leaflet, tethered secondary valve and annular atrial MR can all look severe but require different treatment sequences.

Repair quality is centre-dependent

Early surgery in asymptomatic primary MR makes sense only when durable repair is very likely with very low procedural risk at an experienced centre.

Secondary MR is dynamic

Loading, BP, ischaemia and resynchronisation alter severity; quantify after optimal therapy, not only during an overloaded admission.

Eccentric jets deceive

Wall-hugging Coanda jets may look small on colour Doppler. Quantitative measures, pulmonary-vein flow, 3D imaging or CMR prevent undercalling them.

11Common pitfallsFrequent interpretation and management errors.

01
Using LVEF below 50% as the trigger in chronic primary MR; waiting that long is too late.
02
Assuming a quiet murmur excludes acute severe MR after MI.
03
Sending secondary MR straight to a valve procedure before optimising HFrEF, revascularisation and CRT.
04
Grading an eccentric jet by colour area alone.
05
Treating symptom relief from diuresis as definitive management of severe primary MR.