Valvular heart disease

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

Valve disease ranges from incidental mild lesions to time-critical obstruction or regurgitation. Symptoms, ventricular response and haemodynamic severity—not murmur loudness alone—drive decisions.

Echocardiography defines valve anatomy, severity, ventricular consequences and pulmonary pressure. Serial comparison matters because an apparently asymptomatic ventricle may begin to decompensate before obvious symptoms.

Drug therapy treats congestion, hypertension, arrhythmia or thromboembolic risk. Definitive treatment is repair, replacement or transcatheter intervention when guideline thresholds are met.

Key points

Offer echocardiography when a murmur is accompanied by oedema, angina, breathlessness or an abnormal ECG, or when an ejection systolic murmur has a reduced second heart sound.
A systolic murmur plus exertional syncope requires urgent specialist assessment including echocardiography, or urgent echo, within 2 weeks.
After echo, offer specialist referral for any moderate or severe valve disease and for bicuspid aortic valve of any severity.
Offer intervention for symptomatic severe valve disease when suitable; tablets do not reverse a severe mechanical lesion.
In asymptomatic severe aortic stenosis, intervention assessment is triggered by Vmax above 5 m/s, valve area below 0.6 cm², LVEF below 55%, natriuretic peptide above twice the upper reference limit, or symptoms on exercise testing.
Asymptomatic severe aortic regurgitation needs intervention assessment when LVEF is below 55%, LV end-systolic diameter above 50 mm or indexed diameter above 24 mm/m².
Asymptomatic severe primary mitral regurgitation needs intervention assessment when LVEF is below 60%, LV end-systolic diameter above 45 mm/indexed above 22 mm/m², or exercise pulmonary artery systolic pressure exceeds 60 mmHg.
TAVI versus SAVR must be a valve-MDT decision using age, anatomy, bicuspid status, surgical risk, durability, access and preference. NHS England's September 2023 interim commissioning position permits TAVI as an alternative for selected lower-risk patients in England; it is not a UK-wide NICE default and must be rechecked before use.

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

Degenerative and congenital disease

Age-related calcification commonly narrows the aortic valve, while a bicuspid valve develops abnormal stress earlier. Myxomatous degeneration can weaken mitral leaflets and chordae, causing prolapse.

Rheumatic valve disease

Immune-mediated scarring after rheumatic fever thickens and fuses valve leaflets and commissures. The mitral valve is often narrowed, sometimes with additional regurgitation or aortic involvement.

Infection or acute structural injury

Endocarditis can perforate a leaflet or rupture supporting tissue. Myocardial infarction, chordal rupture or aortic-root disruption can likewise produce abrupt severe regurgitation.

Functional regurgitation

Ventricular or atrial enlargement can stretch an annulus and/or displace supporting structures, preventing normal leaflet coaptation even when the valve tissue itself is not primarily diseased.

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

1
Mechanical valve lesion
Leaflet narrowing obstructs forward flow, whereas failed coaptation permits backward flow. The chamber upstream of a stenosis faces a pressure load, while regurgitation imposes additional volume on one or more chambers.
2
Compensatory remodelling
Chronic ventricular pressure load may cause concentric hypertrophy, while chronic volume load may cause dilatation and eccentric remodelling; atria enlarge when upstream pressure or volume persists. These adaptations can initially preserve output but increase filling pressures and wall stress.
3
Upstream pressure rise
Mitral lesions and left-ventricular failure elevate left-atrial and pulmonary venous pressure, causing breathlessness and pulmonary oedema; chronic elevation may drive pulmonary hypertension.
4
Electrical and vascular effects
Atrial enlargement promotes atrial fibrillation, while hypertrophied myocardium may develop supply–demand ischaemia. Fixed outflow obstruction can prevent adequate cardiac-output augmentation during exertion.
5
Decompensation
Progressive fibrosis and chamber dysfunction may ultimately reduce forward flow and produce heart failure. An acute severe regurgitant lesion allows little time for adaptation and can cause pulmonary oedema in a left-sided lesion or haemodynamic shock.

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

Aortic stenosis

Ejection systolic murmur radiating to carotids, slow-rising pulse and reduced/absent A2; exertional breathlessness, angina or syncope signals important disease.

Aortic regurgitation

Early diastolic murmur, wide pulse pressure and displaced hyperdynamic apex; acute AR may have a short soft murmur with shock or pulmonary oedema.

Mitral regurgitation

Pansystolic apical murmur radiating to axilla, displaced apex and AF/HF signs; acute MR after MI, chordal rupture or endocarditis can cause sudden oedema and shock.

Mitral stenosis

Loud S1, opening snap and low-pitched mid-diastolic apical murmur; breathlessness, AF, haemoptysis or embolic events may dominate.

Decompensated valve diseaseRed flag

Rest/minimal-exertion breathlessness, severe angina, exertional syncope, pulmonary oedema, hypotension or new rapid AF needs urgent assessment; a murmur may be quiet when output is low.

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
History, examination and 12-lead ECGFirst step
Why
Link symptoms to the lesion, identify AF/LVH/conduction disease and assess urgency.
Interpretation and limitations
Exertional syncope with systolic murmur or severe rest symptoms prompts a 2-week urgent pathway; shock/pulmonary oedema is an emergency.
02
Transthoracic echocardiographyFirst line
Why
First-line assessment of valve morphology and severity, LV/RV size and function, pulmonary pressure and associated aortic disease.
Interpretation and limitations
Moderate/severe disease or any bicuspid aortic valve requires specialist referral. Use serial measurements, not a single value in isolation.
03
Transoesophageal echocardiography
Why
Define mitral repair anatomy, prosthetic dysfunction, endocarditis or a lesion inadequately seen on TTE.
Interpretation and limitations
Provides procedural anatomy and detects vegetations, dehiscence or peri-annular complications.
04
Exercise testing in apparently asymptomatic severe disease
Why
Unmask symptoms or abnormal physiology, especially in severe AS.
Interpretation and limitations
Symptoms on exercise in severe AS are a referral threshold for intervention; do not exercise-test a clearly symptomatic severe-AS patient.
05
Dobutamine stress echo or CT calcium scoring in low-gradient AS
Why
Distinguish true severe from pseudo-severe AS when flow/gradient is discordant.
Interpretation and limitations
With LVEF below 50%, severe AS is supported when mean gradient rises above 40 mmHg while valve area remains below 1.0 cm²; CT calcium assists when uncertainty persists.
06
Pre-intervention work-up
Why
Coronary assessment, CT annular/aortic/access anatomy for TAVI, frailty, renal/lung function, dental/infection review and surgical-risk estimation.
Interpretation and limitations
Valve MDT integrates anatomy, life expectancy, recovery, durability and preference; a numerical risk score does not decide alone.

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

Innocent or flow murmur

A soft systolic murmur may arise from increased flow during anaemia, pregnancy or fever. Normal valve anatomy and no chamber consequences on echocardiography are reassuring.

Hypertrophic cardiomyopathy

Dynamic outflow obstruction produces a systolic murmur that typically intensifies when ventricular filling falls, whereas aortic stenosis commonly radiates to the carotids and has fixed valve narrowing.

Primary cardiomyopathy

Ventricular dysfunction can cause breathlessness and secondary regurgitation without a primary valve lesion. Imaging shows whether myocardial disease or valve anatomy is the dominant abnormality.

Atrial septal defect

A pulmonary flow murmur and right-heart enlargement may mimic valve disease. Fixed splitting of the second sound and direct demonstration of an interatrial shunt discriminate it.

Acute coronary syndrome

Angina, dyspnoea or pulmonary oedema may be ischaemic rather than valvular. ECG, serial troponin and regional wall-motion findings help, although infarction can cause acute mitral regurgitation.

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

01ReferralFrom murmur to specialist reviewFirst stepMurmur or imaging suggests valve disease.

1Offer echo for murmur plus oedema, angina, breathlessness or abnormal ECG, or ejection systolic murmur plus reduced S2; consider echo for an isolated murmur when age, family history, AF or clinical features raise suspicion.
2Systolic murmur plus exertional syncope: urgent specialist assessment including echo, or urgent echo, within 2 weeks.
3Murmur plus severe angina or breathlessness on minimal exertion/at rest: consider urgent specialist assessment or echo within 2 weeks; emergency physiology overrides this outpatient window.
4Offer specialist referral after echo for moderate/severe valve disease or bicuspid aortic valve at any severity.

02AorticSevere aortic valve diseaseSevere AS or AR confirmed.

1Offer intervention to suitable symptomatic severe AS/AR patients; do not wait for irreversible ventricular failure.
2Asymptomatic severe AS: refer for intervention assessment if Vmax is above 5 m/s, valve area below 0.6 cm², LVEF below 55%, BNP/NT-proBNP above twice ULN, or exercise testing produces symptoms.
3Asymptomatic severe AR: refer if LVEF is below 55%, LVESD above 50 mm or LVESDi above 24 mm/m².
4Use the valve MDT for SAVR versus TAVI. NICE favours SAVR in low/intermediate surgical risk and TAVI when high risk or unsuitable for surgery. NHS England's September 2023 interim position additionally permits TAVI for selected intermediate/low-risk adults in England—commonly age 80 or older, or age 70 or older with recovery-limiting comorbidity—after MDT assessment; verify that interim policy before applying it.

03MitralSevere mitral valve diseaseSevere primary/secondary MR or rheumatic MS confirmed.

1Offer intervention for symptomatic severe primary MR; prefer surgical repair when durable repair is feasible.
2Asymptomatic severe primary MR: refer if LVEF below 60%, LVESD above 45 mm or LVESDi above 22 mm/m², or exercise pulmonary artery systolic pressure above 60 mmHg; also weigh new AF, resting pulmonary pressure and repair likelihood.
3Severe secondary MR: optimise HFrEF and CRT first; consider surgery with another cardiac operation or transcatheter edge-to-edge repair when symptoms persist and surgery is unsuitable after MDT selection.
4Severe rheumatic MS: use transcatheter balloon valvotomy when anatomy is suitable; otherwise surgical replacement. Manage AF and thromboembolic risk concurrently.

04Follow-upSurveillance and post-intervention careNo current intervention indication or valve already treated.

1If intervention would be suitable, review asymptomatic severe valve disease with clinical assessment and echo every 6–12 months; review mild AS or mild MS with echo every 3–5 years, sooner if symptoms change.
2Give explicit return advice for breathlessness, angina, syncope, declining exercise capacity or palpitations.
3After valve intervention document prosthesis type, antithrombotic plan, target INR where relevant, dental prevention advice and echo baseline.
4Mechanical valves require lifelong vitamin-K-antagonist anticoagulation; DOACs are not substitutes. Antithrombotic therapy after bioprosthesis/TAVI is indication- and procedure-specific.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Temporary relief of pulmonary/peripheral congestion while definitive valve planning proceeds.

Furosemide — licensed symptomatic example

A common oral start for oedema is 40 mg in the morning, then titrate to the lowest dose maintaining euvolaemia; smaller maintenance doses or specialist higher/divided doses may be needed.

Does not correct stenosis or regurgitation. Avoid excessive preload reduction, especially in severe AS, MS, HCM or restrictive physiology; monitor weight, BP, renal function, sodium and potassium.

Lifelong thrombosis prevention for mechanical prosthetic valves and selected valve-related indications.

Warfarin or another vitamin-K antagonist — guideline requirement for mechanical valves

No safe fixed adult dose: dose to the prosthesis- and position-specific INR target set by the valve/anticoagulation team, with regular INR testing.

DOACs are not an alternative for mechanical valves; dabigatran is specifically contraindicated. Check bleeding, interactions, diet consistency, pregnancy planning and bridging requirements for procedures.

NICE says consider aspirin after TAVI, or clopidogrel if aspirin is not tolerated; do not routinely add anticoagulation without another indication.

Aspirin — licensed low-dose example after TAVI when selected

75 mg by mouth once daily is a common single-antiplatelet dose; duration and whether it is needed must follow the TAVI team's plan and competing anticoagulation/ACS indications.

Assess bleeding, ulcer disease, anaemia and concomitant anticoagulation. Antithrombotic plans differ after TAVI, surgical bioprosthesis and mechanical replacement.

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

Heart failure

Chronic pressure or volume overload can impair ventricular filling or contraction, producing pulmonary or systemic congestion and low output; left-sided disease may later cause pulmonary hypertension and secondary right-heart failure.

Atrial fibrillation

Raised atrial pressure and enlargement disrupt atrial conduction. The resulting rapid or irregular rhythm can worsen filling, precipitate congestion and increase thromboembolic risk.

Systemic embolism

Blood stasis in an enlarged fibrillating atrium, particularly with mitral stenosis, favours thrombus formation that may embolise to the brain or other systemic arteries.

Infective endocarditis

Abnormal or prosthetic valve surfaces can support infected vegetations. Valve destruction, abscess, systemic emboli or conduction disturbance may cause rapid clinical deterioration.

Syncope, shock or sudden death

Severe outflow obstruction may limit exertional cardiac output and provoke syncope or malignant arrhythmia, while an acute regurgitant lesion can abruptly cause cardiogenic shock.

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

At every review ask specifically about exertional dyspnoea, angina, syncope, palpitations and objective decline; symptoms reset referral urgency.
Asymptomatic severe disease suitable for intervention: clinical review plus echo every 6–12 months; mild AS/MS: echo every 3–5 years unless symptoms or measurements change sooner.
Track lesion-specific ventricular thresholds: AS LVEF/Vmax/area/peptide; AR LVEF and LVESD/LVESDi; MR LVEF, LVESD/LVESDi and pulmonary pressure.
With diuretics monitor weight, BP, U&E/eGFR and avoid dehydration/preload depletion.
Mechanical valve: regular INR, bleeding/thrombosis review and interaction checks; urgent assessment for new dyspnoea, embolus, muffled/changed valve sounds or subtherapeutic INR.
After TAVI/SAVR/repair follow the valve team's echo and antithrombotic schedule and maintain excellent oral health.

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

A quiet murmur can be severe

Low cardiac output, obesity or acute regurgitation can make auscultation deceptively unimpressive.

Symptoms beat labels

An apparently asymptomatic patient may have unconsciously reduced activity; exercise testing can expose symptoms in severe AS when safe.

Preserved EF may already represent dysfunction

The referral thresholds are higher than the conventional 50% boundary: below 55% in severe AR and below 60% in severe primary MR.

TAVI is not simply an age cut-off

Bicuspid anatomy, vascular access, coronary anatomy, durability, need for other surgery, frailty and preference require MDT integration.

Prosthesis determines anticoagulation

Mechanical valves require a VKA and an individual INR target; a fixed warfarin dose or a DOAC substitution is unsafe.

11Common pitfallsFrequent interpretation and management errors.

01
Reassuring a patient with exertional syncope and a systolic murmur rather than arranging urgent assessment within 2 weeks.
02
Waiting for LVEF to fall below 50% in severe AR or primary MR before referring.
03
Using diuretics as definitive therapy for severe symptomatic valve disease.
04
Calling TAVI the default for every older adult without valve-MDT assessment.
05
Prescribing a DOAC for a mechanical prosthetic valve or using a fixed warfarin dose without an INR target.