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OverviewAetiologyPathophysiologyClinical features and red flagsInvestigationsDifferential diagnosisManagementComplicationsMonitoring and follow-upSpecial situationsCommon pitfallsQuestionsSources
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Educational draft · awaiting clinical reviewThe full textbook explains uncertainty but does not replace live national or local guidance, specialist advice, or current prescribing information.

Mitral stenosis

Cardiology · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

RapidFull
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Time-critical presentation

Call 999 for acute pulmonary oedema, hypoxaemia, shock, ongoing chest pain or a rapid arrhythmia with haemodynamic compromise. In unstable AF, use synchronised electrical cardioversion; pulmonary congestion and a very fast rate can sharply worsen transmitral obstruction.

Overview

Recognise clinically significant mitral stenosis, manage congestion and atrial fibrillation safely, and select transcatheter commissurotomy versus surgery.

Mitral narrowing obstructs LV filling, raising left-atrial pressure and eventually causing pulmonary hypertension, right-heart failure, AF and systemic embolism. Tachycardia shortens diastole, so symptoms can worsen disproportionately with fever, pregnancy, anaemia or AF.

Echo confirms valve area, gradient, leaflet/commissural anatomy, MR and pulmonary consequences. Valve area by planimetry is relatively flow-independent; the gradient is useful but changes with rate and output.

Medicines relieve congestion, slow an excessive ventricular rate and prevent embolism; none opens a fused valve. Intervention timing and the choice between balloon commissurotomy and surgery depend on symptoms, anatomy, thrombus, MR and associated valve/coronary disease.

Key points

  • Rheumatic commissural fusion is the classic cause; degenerative mitral-annular calcification is increasingly important in older adults and is not treated like pliable rheumatic disease.
  • Exertional dyspnoea, orthopnoea, haemoptysis and declining exercise tolerance reflect raised left-atrial and pulmonary pressure.
  • An opening snap followed by a low-pitched mid-diastolic apical rumble is typical; a longer murmur and shorter A2-to-opening-snap interval suggest greater severity.
  • Clinically significant stenosis is generally a mitral valve area 1.5 cm2 or less; mean gradient varies with heart rate and flow and must be reported with them.
  • AF removes atrial contribution, accelerates filling and increases embolic risk; new AF can abruptly unmask severe symptoms.
  • Use a vitamin K antagonist for AF with moderate-to-severe rheumatic mitral stenosis; direct oral anticoagulants are not the recommended substitute.
  • Percutaneous transcatheter commissurotomy is preferred for symptomatic rheumatic stenosis with favourable anatomy, no left-atrial thrombus and no more than mild MR.
  • Surgery is used when anatomy is unsuitable for commissurotomy, significant MR or other surgical disease coexists, or the percutaneous result is inadequate.

Aetiology

01

Rheumatic valve disease

Previous rheumatic inflammation causes commissural fusion, leaflet thickening and shortened chordae. Progressive scarring narrows the valve and may become symptomatic years after the original illness.

02

Degenerative annular calcification

In older adults, heavy calcium around the mitral annulus can extend towards the leaflet bases and restrict opening. Unlike rheumatic disease, fused pliable commissures are usually absent.

Pathophysiology

  1. 1
    Obstructed diastolic filling

    A narrowed mitral orifice impedes blood flow from the left atrium to the left ventricle during diastole, creating a persistent pressure gradient.

  2. 2
    Raised left-atrial pressure

    The left atrium dilates and pressure transmits to the pulmonary veins. Tachycardia shortens diastole, so fever, pregnancy or rapid atrial fibrillation can abruptly worsen congestion.

  3. 3
    Pulmonary vascular consequences

    Chronic venous hypertension causes pulmonary oedema and eventually pulmonary arterial remodelling. Rising pulmonary resistance increases right-ventricular afterload and may lead to right-sided failure.

  4. 4
    Atrial stasis and arrhythmia

    Atrial enlargement disrupts electrical conduction and encourages atrial fibrillation. Reduced atrial contraction and slow appendage flow promote thrombus formation and systemic embolism.

Clinical features and red flags

Pulmonary-pressure symptoms

Progressive exertional dyspnoea, orthopnoea, nocturnal dyspnoea, cough or haemoptysis are common; acute oedema may follow rapid AF, infection or pregnancy.

Auscultatory pattern

Loud S1, an opening snap and a low-pitched apical mid-diastolic rumble heard with the bell in the left lateral position support rheumatic MS.

Atrial fibrillation

An irregular pulse, palpitations or sudden functional decline may mark AF; loss of presystolic accentuation occurs when sinus rhythm is lost.

Pulmonary hypertension and right failure

A loud P2, parasternal heave, raised JVP, hepatomegaly or oedema indicates advanced haemodynamic consequences.

Systemic embolismRed flag

Focal neurological deficit, limb ischaemia or organ infarction can arise from left-atrial thrombus and requires emergency assessment.

Degenerative MS

Older adults with heavy annular calcification often lack commissural fusion; balloon commissurotomy is usually ineffective and intervention can be technically high risk.

Investigations

  1. 01
    Transthoracic echocardiographyFirst step
    Why
    Measure valve area, mean gradient at the recorded heart rate, MR, LA size, RV function and pulmonary pressure.
    Interpretation and limitations
    Valve area 1.5 cm2 or less is clinically significant; planimetry is the reference when measures disagree, while gradient rises with tachycardia and flow.
  2. 02
    Transoesophageal echocardiography
    Why
    Exclude left-atrial/appendage thrombus and define valve anatomy before commissurotomy or selected cardioversion.
    Interpretation and limitations
    LA thrombus is a major contraindication to immediate percutaneous commissurotomy and changes anticoagulation and procedural timing.
  3. 03
    12-lead ECG and ambulatory monitoring
    Why
    Detect AF, atrial enlargement, right-heart strain and intermittent arrhythmia.
    Interpretation and limitations
    AF changes anticoagulation and rate-control management even if paroxysmal.
  4. 04
    Exercise testing or stress echocardiography
    Why
    Clarify equivocal symptoms or discordance between symptoms and resting severity.
    Interpretation and limitations
    Provoked symptoms, a marked gradient rise or pulmonary-pressure response supports haemodynamic importance; avoid in unstable or clearly symptomatic severe disease.

Differential diagnosis

01

Mitral regurgitation

Mitral regurgitation causes a systolic rather than mid-diastolic apical murmur. Doppler echocardiography demonstrates backward systolic flow instead of anatomical obstruction to diastolic filling.

02

Left-atrial myxoma

A mobile atrial tumour can intermittently obstruct the mitral orifice and cause positional symptoms or a variable diastolic sound. Echocardiography directly identifies the mass.

03

Heart failure with preserved ejection fraction

Both disorders cause exertional dyspnoea, atrial enlargement and pulmonary congestion. In preserved-ejection-fraction heart failure, echocardiography shows raised filling pressure without a narrowed mitral valve.

04

Chronic pulmonary disease

Lung disease can explain breathlessness, pulmonary hypertension and right-sided signs. Respiratory examination and testing reveal a pulmonary cause, while echocardiography shows no significant transmitral obstruction.

Management

01acuteAcute pulmonary oedema or unstable AFFirst stepMS presents with respiratory failure, hypotension, ischaemia, syncope or shock.+
  1. 1Use ABCDE care, monitoring, IV access and oxygen for hypoxaemia; call cardiology/critical care urgently.
  2. 2If tachyarrhythmia is causing life-threatening compromise, perform synchronised electrical cardioversion with sedation/anaesthesia support when feasible.
  3. 3Treat congestion with an IV loop diuretic while monitoring BP, renal function and electrolytes; identify infection, anaemia or other precipitants.
  4. 4After stabilisation, evaluate urgently for valve intervention and institute stroke prevention appropriate to rheumatic MS and AF.
02commissurotomySymptomatic rheumatic MS with favourable anatomyValve area is 1.5 cm2 or less, symptoms are attributable to MS and commissural fusion is suitable.+
  1. 1

Complications

01

Pulmonary oedema

A sudden rise in left-atrial pressure, particularly during rapid atrial fibrillation, infection or pregnancy, can flood pulmonary interstitium and alveoli and cause acute respiratory compromise.

02

Atrial fibrillation

Progressive atrial stretch creates an arrhythmic substrate. The faster, irregular rhythm shortens filling time, removes atrial contribution and can cause abrupt symptomatic deterioration.

03

Systemic thromboembolism

Blood stasis in the enlarged atrium, especially its appendage and during atrial fibrillation, promotes thrombus. Emboli may cause stroke, limb ischaemia or organ infarction.

04

Pulmonary hypertension and right failure

Long-standing pulmonary venous pressure can produce fixed pulmonary vascular changes. Right-ventricular strain then causes functional tricuspid regurgitation, venous congestion and peripheral oedema.

Monitoring and follow-up

  • For mild asymptomatic MS, NICE suggests echo every 3–5 years; use shorter specialist intervals for clinically significant disease or changing symptoms.
  • Track mitral valve area, mean gradient with heart rate, MR, LA size, pulmonary pressure and RV function.
  • Check rhythm and rate at every review and investigate new palpitations, exercise decline or embolic symptoms promptly.
  • For warfarin, monitor INR closely during initiation and interactions, then at an interval appropriate to stability; review bleeding and adherence.
  • After commissurotomy, repeat echo for residual gradient, valve area and new/worsened MR, then continue long-term surveillance.
  • During diuretic or rate-control changes, monitor BP, renal function/electrolytes and bradycardia.

Special situations

Heart rate changes the gradient

Tachycardia shortens diastole and raises transmitral gradient. Always interpret the mean gradient with heart rate and flow, not as a fixed anatomical severity measure.

Planimetry anchors valve area

Direct measurement of the smallest orifice is relatively flow-independent and is the reference when Doppler-derived measures disagree.

Commissural fusion matters

Balloon commissurotomy splits fused commissures; heavily calcified degenerative annular stenosis lacks that target and needs a different Heart Team strategy.

TOE is procedural protection

A large LA can hide appendage thrombus. TOE before commissurotomy or selected cardioversion changes an apparently straightforward plan.

Severe MS makes AF different

Stroke prevention uses a vitamin K antagonist rather than the DOAC pathway used for most non-valvular AF.

Pregnancy increases flow

Rising blood volume and heart rate can unmask MS. Pre-pregnancy valve review is ideal; refractory symptomatic severe rheumatic MS may require expert commissurotomy during pregnancy.

Common pitfalls

  1. 01

    Using a DOAC for AF with moderate-to-severe rheumatic mitral stenosis.

  2. 02

    Calling MS severe from mean gradient without recording heart rate and flow conditions.

  3. 03

    Performing balloon commissurotomy without excluding LA thrombus and significant MR.

  4. 04

    Expecting cardioversion to remain successful while severe obstruction is untreated.

  5. 05

    Offering balloon treatment for calcific annular stenosis as though it were pliable commissural fusion.

Practice

Two practice questions

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Question 1 of 2
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CardiologyOriginal SBA

Anticoagulation in rheumatic MS

A patient with valve area 1.2 cm2 from rheumatic MS develops persistent AF. Which stroke-prevention approach is appropriate?

Choose one answer, then submit
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Sources and review status6 sources · checked 27 Aug 2026 · clinical review pending+
Sources

Sources and review status

National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

  • NICE NG208: Heart valve disease presenting in adultsUK transcatheter valvotomy, referral and monitoring recommendations.
  • ESC/EACTS 2025 valvular heart disease guidelineCurrent valve intervention and antithrombotic principles.
  • ESC: Expert review of mitral valve diseaseCommissurotomy selection and AF considerations.
  • ESC: Echocardiographic haemodynamics in mitral diseaseValve-area and gradient interpretation.
  • eMC: Warfarin SmPCINR-guided dosing and typical maintenance range.
  • eMC: Bisoprolol SmPCAdult dose range and contraindications.

Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem ·

05
Chest radiograph
Why
Assess pulmonary oedema, LA enlargement, pulmonary arteries and valve calcification.
Interpretation and limitations
Supports complications but cannot grade the valve or exclude significant disease.
  • 06
    CT and pre-intervention coronary assessment
    Why
    Define annular calcification and identify coronary/other surgical disease when intervention is considered.
    Interpretation and limitations
    Extensive commissural or annular calcification predicts a poor balloon result and may make surgery or transcatheter alternatives complex.
    • Use expert TTE to score leaflet mobility, thickening, calcification and subvalvular disease; quantify coexisting MR.
  • 2Perform TOE to exclude LA thrombus and review embolic history, pulmonary pressure, pregnancy status and procedural risk.
  • 3If there is no LA thrombus, no more than mild MR and anatomy is favourable, offer transcatheter mitral commissurotomy at an experienced valve centre.
  • 4Recheck valve area, gradient and MR after the procedure; arrange surgery if the anatomy was unsuitable or the result/complication requires it.
    • 03surgeryWhen surgery is preferredPreferredSymptomatic clinically significant MS is unsuitable for balloon commissurotomy.+
    1. 1Identify contraindications or poor-result features: LA thrombus, more than mild MR, absent commissural fusion, severe calcification or important associated valve/coronary disease.
    2. 2Discuss mitral replacement or selected repair/commissurotomy in the multidisciplinary valve team, incorporating frailty and pulmonary vascular disease.
    3. 3If other cardiac surgery is needed, plan combined treatment rather than an isolated balloon procedure.
    4. 4Continue symptom and thromboembolism treatment while awaiting surgery and reassess rapidly if pulmonary oedema or right failure develops.
    04afAF and embolic prevention in rheumatic MSPersistent or paroxysmal AF, LA thrombus or prior systemic embolism accompanies rheumatic MS.+
    1. 1Start a vitamin K antagonist unless contraindicated and individualise warfarin to an INR target generally 2.0–3.0; do not substitute a DOAC for moderate-to-severe rheumatic MS.
    2. 2Control an excessive ventricular rate with a beta blocker or another specialist-selected agent, balancing hypotension, conduction disease and heart failure.
    3. 3Do not expect cardioversion before relief of severe obstruction to remain durable; if recent-onset AF and LA enlargement is limited, consider cardioversion after successful intervention and adequate anticoagulation.
    4. 4Arrange structured INR, bleeding and rhythm follow-up and educate about stroke warning signs.
    Key medicines and prescribing safety3 treatments · regimens, roles and cautions+
    Prevents systemic embolism in AF with moderate-to-severe rheumatic MS, and in LA thrombus or prior embolism when indicated.

    Warfarin

    Dose orally once daily and adjust to INR; typical maintenance is 3–9 mg once daily, but the exact dose is individual. For AF with rheumatic MS, the usual INR target is 2.0–3.0.

    Check baseline and frequent INR, interactions, adherence and bleeding. Pregnancy requires specialist anticoagulation planning. A fixed tablet dose without INR adjustment is unsafe; DOACs are not the recommended alternative in moderate-to-severe rheumatic MS.

    Slows ventricular rate in AF or sinus tachycardia, lengthening diastolic filling; use is clinician-directed and rate control in AF is an off-label context for some products.

    Bisoprolol

    A common adult starting dose is 2.5–5 mg orally once daily, titrated to symptoms and ventricular rate; the SmPC hypertension/angina usual dose is 10 mg once daily and maximum 20 mg/day.

    Avoid or reduce in bradycardia, high-grade AV block, hypotension or acute decompensated heart failure; use caution in asthma and do not stop abruptly.

    Relieves pulmonary or peripheral congestion but does not alter the valve obstruction.

    Furosemide

    For 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, adjusted to response.

    Monitor weight, BP, renal function, sodium and potassium; avoid over-diuresis and reassess the need for definitive valve treatment.

    Content changes
    Authoring stateComplete draftClinical stateAwaiting reviewJurisdictionUnited Kingdom