Valvular Heart Disease (Complete)

Understanding valvular heart disease

• Definition: Disease of one or more cardiac valves producing obstruction (stenosis), backward flow (regurgitation) or a combination. Valve dysfunction can be primary (abnormal leaflets, chords or annulus) or secondary (distortion caused by chamber remodelling).
• Physiological consequences: Stenosis produces an upstream pressure burden; regurgitation produces volume loading of the receiving and ejecting chambers. Chronic compensation eventually gives way to raised filling pressures, atrial enlargement, pulmonary hypertension, heart failure or arrhythmia.
• Major lesions: Aortic stenosis (AS), aortic regurgitation (AR), mitral stenosis (MS), mitral regurgitation (MR), tricuspid regurgitation (TR), tricuspid stenosis (TS), pulmonary stenosis (PS) and pulmonary regurgitation (PR).
• Clinical objectives: Identify the lesion, establish severity and mechanism, assess symptoms and ventricular consequences, identify the need and timing of intervention, and choose repair, replacement or transcatheter treatment with a specialist Heart Team.
• Warning: Symptoms, physical findings and valve area or gradients can disagree. Management depends on an integrated clinical and imaging assessment, not a murmur grade alone.

💡 Clinical Pearl: A patient may have severe valvular disease before symptoms become obvious. Conversely, a loud murmur need not imply a severe lesion; flow, cardiac output and acoustic transmission determine murmur intensity.

Valve anatomy and the cardiac cycle

• Aortic and pulmonary valves: Semilunar valves open during ventricular systole and close in diastole. AS causes a systolic ejection murmur; AR causes an early diastolic murmur.
• Mitral and tricuspid valves: Atrioventricular valves open during diastolic ventricular filling and close during systole. MR and TR are usually systolic; MS and TS are diastolic.
• Valve apparatus: Leaflets, annulus, chordae tendineae, papillary muscles and ventricular geometry work together. Dysfunction in any component can cause regurgitation without an intrinsic leaflet defect.
• Heart sounds: S1 reflects closure of AV valves; S2 reflects closure of aortic and pulmonary valves. A2 may be soft in severe AS. An opening snap follows S2 in mobile rheumatic MS; an ejection click may accompany a bicuspid aortic valve.
• Murmur timing: Determine whether the murmur occurs between S1 and S2 (systole) or S2 and the next S1 (diastole). Carotid pulsation coincides with systole.

Pressure overload, volume overload and remodelling

• Pressure overload: AS or hypertension increases LV systolic wall stress, provoking concentric hypertrophy, impaired relaxation, fibrosis and eventual systolic dysfunction.
• Volume overload: AR or chronic MR increases LV end-diastolic volume and often produces eccentric enlargement. Stroke volume may remain high for years even as myocardial contractile reserve declines.
• Atrial consequences: MS increases left atrial pressure directly; MR increases left atrial volume and pressure. Both predispose to AF and pulmonary venous hypertension.
• Pulmonary vascular effects: Persistent left-sided filling pressure elevation can lead to secondary pulmonary hypertension and RV dysfunction; significant TR may follow.
• Acute versus chronic: Acute severe MR or AR produces abrupt pressure elevation in an unadapted chamber and can cause pulmonary oedema or shock despite apparently normal chamber size. Chronic severe disease permits remodelling before decompensation.

Aetiology and risk factors

• Degenerative/calcific: Calcific AS, mitral annular calcification and age-related valve degeneration; increasingly common with older age, CKD and cardiovascular risk factors.
• Congenital: Bicuspid aortic valve, congenital pulmonary stenosis, mitral clefts and Ebstein anomaly.
• Rheumatic: Predominantly MS, often with MR, AR or mixed disease; linked to previous rheumatic fever and remains important in migrant and global populations.
• Infective: Endocarditis may cause leaflet destruction, perforation, abscess, acute regurgitation and emboli.
• Functional/secondary: LV dilatation and papillary displacement cause ventricular secondary MR; atrial/annular dilatation in AF causes atrial functional MR or TR; RV dilatation causes TR.
• Other: Aortic root aneurysm, dissection, Marfan/other heritable aortopathies, carcinoid syndrome, prior thoracic radiation, drug-related leaflet disease, connective tissue disease and cardiac device leads.

Clinical assessment and symptoms

• Symptoms: Exertional dyspnoea, declining exercise tolerance, fatigue, angina, exertional presyncope/syncope, orthopnoea, PND, peripheral oedema and palpitations. Ask about subtle activity avoidance and progressive reduction in walking distance.
• History: Childhood/congenital disease, rheumatic fever, previous endocarditis, AF, prior MI, radiotherapy, valve surgery, family history, dental infection, pregnancy plans and anticoagulation.
• Examination: Pulse rate/rhythm, blood pressure and pulse pressure, carotid contour, JVP, peripheral perfusion, apex location/character, thrills, S1/S2 and additional sounds, murmurs by timing/quality/radiation, lung bases, oedema and hepatomegaly.
• Assess severity and consequences: Symptoms attributable to the valve, HF signs, AF, pulmonary hypertension, LV/RV changes and end-organ dysfunction. A seemingly asymptomatic patient may have adapted to a restricted lifestyle.
• Red flags: Exertional syncope with a systolic murmur, angina or breathlessness at minimal exertion, acute pulmonary oedema, hypotension, fever with new regurgitant murmur, or sudden chest/back pain suggesting dissection.

How to describe and distinguish murmurs

• Sequence: State timing → location of maximal intensity → quality/pitch → radiation → grade/thrill → changes with respiration/posture → relevant heart sounds and pulse character.
• Aortic stenosis: Harsh crescendo-decrescendo ejection systolic murmur at right upper sternal edge, often radiating to carotids; delayed carotid upstroke and soft A2 with advanced disease.
• Aortic regurgitation: High-pitched early diastolic decrescendo murmur, usually at left sternal border, best heard leaning forward in expiration; wide pulse pressure in chronic severe AR.
• Mitral regurgitation: Blowing apical pansystolic murmur radiating towards axilla (direction varies with leaflet lesion); S3 may indicate significant volume loading.
• Mitral stenosis: Loud S1 early in mobile disease, opening snap and low-pitched mid-diastolic rumble at apex, best with bell in left lateral position.
• Tricuspid regurgitation: Lower left sternal pansystolic murmur that often becomes louder on inspiration (Carvallo sign), with prominent JVP V waves.
• Pulmonary stenosis: Left upper sternal ejection systolic murmur; may have ejection click and RV heave. Pulmonary regurgitation: Early diastolic murmur at left upper sternal edge, e.g. Graham Steell murmur with pulmonary hypertension.

💡 MRCP Pearl: Always distinguish a systolic from a diastolic murmur by palpating the carotid pulse. A diastolic murmur is pathological until shown otherwise, whereas a soft systolic flow murmur can be physiological.

Dynamic manoeuvres and bedside interpretation

• Inspiration: Usually increases right-sided venous return and right-sided murmurs, especially TR (Carvallo sign); do not interpret a single manoeuvre in isolation.
• Handgrip: Increases systemic afterload, tending to accentuate MR and AR; often reduces dynamic LVOT obstruction murmur of HCM.
• Standing/Valsalva strain: Reduces preload; classically increases HCM outflow murmur and brings the MVP click earlier, often reducing AS murmur.
• Squatting/leg raise: Increases preload (and squatting increases afterload); tends to reduce HCM murmur and delay MVP click; may augment AS flow murmur.
• Posture: Left lateral decubitus accentuates the low-pitched MS rumble; sitting forward in expiration helps reveal AR.
• Limitations: Murmur responses are variable with complex disease, low output, obesity and prior intervention; echocardiography determines anatomy and severity.

Investigations and multimodality imaging

• ECG: AF, chamber enlargement, LVH/RVH, conduction disease, previous infarction or signs of strain; a normal ECG cannot rule out major valve disease.
• Blood tests: FBC, U&E/eGFR, LFT, NT-proBNP when HF suspected, CRP/cultures if infection, troponin if ACS or acute injury; add coagulation testing when anticoagulated or operative planning.
• Chest X-ray: Chamber enlargement, pulmonary congestion, oedema or pleural effusion; not sufficient to quantify valve severity.
• Transthoracic echo (TTE): First-line assessment of mechanism, leaflet mobility, velocities, gradients, valve area, regurgitation, chamber size/function and pulmonary pressure.
• Transoesophageal echo (TOE): Clarifies MR mechanism, prosthetic valves, endocarditis, abscess, suspected LA thrombus and intervention planning.
• Cardiac CT: TAVI annular/access planning, aortic root measurements, calcification and uncertain AS severity; CMR: regurgitant volume/fraction and precise ventricular volumes where echo is discordant.
• Stress testing: Specialist-supervised exercise testing may reveal occult symptoms in apparently asymptomatic severe AS; avoid exercise testing in symptomatic severe AS. Dobutamine stress echo helps selected low-flow AS cases.

Echocardiographic severity: principles

• Integration: Use more than one variable: morphology, Doppler gradients and velocity, quantitative regurgitation measures, forward stroke volume, ventricular response and clinical context.
• Gradient: Doppler gradients depend on transvalvular flow; a low gradient does not automatically imply mild AS or MS in low-flow states.
• Regurgitation: Jet colour area alone is unreliable, especially with eccentric wall-hugging jets. Evaluate vena contracta, flow convergence, EROA, regurgitant volume/fraction, pulmonary/hepatic venous flow and chamber adaptation.
• Measurements: Indexed chamber dimensions are important in smaller patients; compare serial studies when the lesion is chronic.
• Mixed lesions: Significant regurgitation raises transvalvular forward flow and can increase an apparent stenotic gradient. Low stroke volume may mask severe obstruction.

UK referral, surveillance and the Heart Team

• NICE NG208 echocardiography: Offer TTE when a suspected valve-related murmur accompanies symptoms/signs or abnormal ECG, or when an ejection systolic murmur has a reduced S2; consider TTE for other suspicious murmurs depending on history and risk.
• Urgent referral: Systolic murmur with exertional syncope → specialist assessment including echo within 2 weeks; also consider within 2 weeks for a murmur with severe breathlessness or angina at rest/minimal exertion.
• Intervention: NICE recommends offering intervention in symptomatic severe valve disease when appropriate; asymptomatic severe lesions can need earlier intervention if LV changes or high-risk features occur.
• Follow-up: Asymptomatic severe disease suitable for intervention generally requires clinical review and TTE every 6–12 months. Mild aortic or mitral stenosis may be reassessed echocardiographically every 3–5 years (adjust for progression and symptoms).
• Heart Team: Cardiologists, imaging specialists, surgeons and interventionists balance anatomy, operative risk, frailty, life expectancy, concomitant coronary disease, durability and patient priorities.

⚠️ Clinical Pearl: New symptoms in someone with known severe stenosis are a reason for prompt reassessment, not simply a reason to advance a routine annual echocardiogram.

Aortic stenosis: causes and pathophysiology

• Causes: Degenerative calcific AS is commonest in older adults; bicuspid AV causes earlier disease; rheumatic fusion and radiation-related changes are less common.
• Mechanism: Progressive leaflet thickening and calcification reduce effective orifice area, increasing LV systolic pressure, afterload and myocardial oxygen demand.
• Compensation: Concentric LV hypertrophy initially maintains systolic performance, but impairs diastolic relaxation and raises filling pressure. Later fibrosis, myocardial ischaemia and LV dysfunction may develop.
• Symptoms: Exertional dyspnoea, angina, exertional presyncope/syncope and heart failure. Chest pain may result from supply–demand mismatch even without obstructive coronary disease.
• Syncope mechanism: Fixed obstruction limits augmentation of output during exercise, while peripheral vasodilatation may reduce blood pressure; arrhythmia can also contribute.

Aortic stenosis: clinical signs and ECG

• Pulse: Slow-rising and often reduced-amplitude carotid pulse (pulsus parvus et tardus); may be less apparent with coexistent hypertension or arterial stiffness.
• Auscultation: Harsh ejection systolic murmur at right upper sternal border, radiating to neck/carotids; late peaking suggests more severe obstruction, but low-output severe AS may be quiet.
• Heart sounds: Soft/absent A2 in advanced calcific AS, possible paradoxical S2 splitting and S4 from a stiff LV; ejection click can occur with a mobile bicuspid valve.
• Examination: Sustained/heaving apex, LVH; pulmonary congestion or low-output signs in advanced cases.
• ECG: LVH with strain, LA enlargement, conduction disease or AF; no ECG finding accurately grades AS.
• Differentials: Aortic sclerosis (murmur without major obstruction), HCM (dynamic murmur, different manoeuvres), pulmonary stenosis and flow murmurs.

Aortic stenosis: Doppler severity and low-flow states

• Severe high-gradient AS: Peak aortic velocity (Vmax) ≥4.0 m/s, mean gradient ≥40 mmHg and usually AV area ≤1.0 cm² (indexed ≤0.6 cm²/m²). Interpret the parameters together, not as isolated cut-offs.
• Very severe/high-risk AS: Vmax >5 m/s and/or very small AV area indicate higher risk; additional markers include adverse BNP, exercise symptoms and reduced LV function.
• Dimensionless velocity index: Ratio of LVOT to aortic valve Doppler velocities; <0.25 supports severe AS when other measurements are uncertain.
• Low-flow, low-gradient AS: Valve area ≤1 cm², mean gradient <40 mmHg, stroke-volume index ≤35 mL/m²; may occur with reduced EF (classical) or preserved EF (paradoxical).
• Low-flow work-up: Confirm LVOT measurement/Doppler alignment, BP and loading conditions; use low-dose dobutamine stress echo in selected reduced-EF cases and CT calcium scoring when uncertainty persists.
• CT calcium: Sex-specific scoring helps adjudicate severe AS in discordant cases; thresholds of approximately >2,000 Agatston units in men or >1,200 in women support severity, but morphology and clinical context remain important.

💡 MRCP Pearl: A mean gradient of only 25 mmHg does not exclude severe AS in a patient with low stroke volume. First ask whether the ventricle can generate sufficient flow to produce a high gradient.

Aortic stenosis: management, SAVR and TAVI

• Symptomatic severe AS: Prompt Heart Team referral for aortic valve intervention; valve replacement is definitive treatment, not diuretics or vasodilators alone.
• Asymptomatic severe AS: Consider intervention if LV impairment, unmasked exercise symptoms, very severe haemodynamics, markedly abnormal natriuretic peptides or other high-risk features. NICE NG208 lists Vmax >5 m/s, AVA <0.6 cm², LVEF <55% and BNP/NT-proBNP >2× ULN among triggers for consideration.
• SAVR: Surgical replacement is particularly appropriate for many younger patients, bicuspid anatomy with relevant aortopathy, coexisting need for bypass or aortic surgery, or anatomy poorly suited to TAVI.
• TAVI: Transcatheter replacement commonly preferred in older patients with suitable anatomy; 2025 ESC guidance uses age ≥70 years as one consideration for suitable tricuspid AS, but UK pathways and individual lifetime plans differ.
• Medical treatment: Manage HF/AF, hypertension and coronary disease cautiously; diuretics can relieve congestion but excessive preload reduction may cause hypotension. No medicine reliably reverses established calcific valve stenosis.
• Balloon aortic valvuloplasty: Provides temporary haemodynamic improvement in selected unstable patients or as a bridge, not durable definitive therapy in most adults.

Aortic regurgitation: mechanism and causes

• Definition: Diastolic reflux from aorta to LV, causing combined LV volume loading and increased systolic stroke volume.
• Leaflet causes: Bicuspid valve, rheumatic disease, endocarditis, degenerative change and trauma.
• Root causes: Aortic root/ascending aortic dilatation, hypertension, bicuspid-associated aortopathy, connective tissue disease and acute aortic dissection.
• Chronic response: Eccentric LV dilatation preserves forward output initially; later rising LV end-diastolic pressure and systolic dysfunction develop.
• Acute severe AR: No time for LV enlargement; abrupt pressure rise causes pulmonary oedema, hypotension and shock. Causes include endocarditis and type A dissection.

Aortic regurgitation: symptoms and signs

• Symptoms: Often asymptomatic for years; later exertional dyspnoea, awareness of forceful heartbeat, orthopnoea, angina and reduced exercise capacity.
• Pulse/BP: Bounding or collapsing pulse and wide pulse pressure in chronic haemodynamically important AR; peripheral signs include head bobbing or capillary pulsation but are insensitive and nonspecific.
• Murmur: High-pitched, blowing early diastolic decrescendo, usually left sternal border; best sitting forward at end-expiration. An associated systolic flow murmur may be present.
• Austin Flint murmur: Apical low-pitched mid/late diastolic rumble in severe AR, due to regurgitant flow influencing mitral leaflet motion; distinguish from MS.
• LV: Displaced, hyperdynamic apex in chronic severe AR. Acute AR: Peripheral pulse signs and a loud murmur may be absent despite profound haemodynamic compromise.
• ECG: LVH and, in chronic advanced disease, changes of LV enlargement; ECG cannot quantify regurgitation.

Aortic regurgitation: assessment and intervention

• Echo: Assess leaflet/root anatomy, regurgitant flow, vena contracta, pressure half-time (supportive only), diastolic flow reversal in descending aorta, LV volumes and LVEF; TOE or CMR may clarify discordant findings.
• Severe AR indicators: Vena contracta width >6 mm, effective regurgitant orifice area ≥0.30 cm², regurgitant volume ≥60 mL/beat or regurgitant fraction ≥50%, with supporting holodiastolic aortic flow reversal and LV enlargement; use integrated grading.
• Symptomatic severe AR: Usually indication for valve surgery if feasible, regardless of resting EF. Aortic root disease may also require root intervention.
• Asymptomatic severe AR: NICE suggests considering intervention with LVEF <55%, LV end-systolic dimension >50 mm or indexed >24 mm/m². ESC 2025 distinguishes established triggers from selected earlier intervention in low-risk patients; discuss threshold differences at the valve MDT.
• Medical care: Treat hypertension and HF while awaiting definitive treatment; vasodilators may help associated hypertension but do not replace surgery when indicated.
• Acute severe AR: Surgical emergency. Urgent echo, cardiothoracic assessment and stabilisation; avoid delaying definitive treatment. Intra-aortic balloon counterpulsation is contraindicated because it worsens diastolic regurgitation.

Bicuspid aortic valve and thoracic aortopathy

• Prevalence: Common congenital aortic valve variation with two functional cusps; predisposes to calcific AS, AR, endocarditis and progressive aortic dilatation.
• Clinical assessment: Listen for ejection click/murmur; TTE should evaluate valve severity and aortic root/ascending aortic size. CT/CMR can assess the thoracic aorta if echo is incomplete.
• Associated lesions: Coarctation of the aorta and familial aortopathy may coexist; consider screening first-degree relatives according to specialist practice.
• Intervention: Valve replacement decisions consider age, aortic dimensions, rate of growth, family history, genetic disease and any need for concomitant root/ascending aortic repair.
• Follow-up: Lifelong surveillance of both valve and aorta is important, including after valve intervention.

Mitral stenosis: aetiology and haemodynamics

• Causes: Rheumatic leaflet fusion remains the classical cause; degenerative mitral annular calcification causes non-rheumatic obstruction, especially in older adults or CKD.
• Mechanism: Narrowed valve obstructs LA-to-LV flow during diastole; LA pressure rises, leading to pulmonary venous hypertension and eventually pulmonary arterial hypertension/RV failure.
• Consequences: LA enlargement, AF, atrial thrombus and systemic embolism; resting forward cardiac output can be low even when LV EF is preserved.
• Worsening factors: Tachycardia shortens diastolic filling time, sharply increasing transmitral pressure gradient and breathlessness; pregnancy increases cardiac output and may unmask MS.
• Symptoms: Exertional dyspnoea, orthopnoea, haemoptysis, palpitations/AF, fatigue and, in advanced cases, right HF.

Mitral stenosis: murmur, investigations and treatment

• Examination: Tapping apex, loud S1 when leaflets remain mobile, opening snap after S2 and a low-pitched apical mid-diastolic rumble (best with bell in left lateral position). A shorter S2-to-snap interval may indicate higher LA pressure in classic rheumatic disease.
• Echo: Rheumatic commissural fusion/dom­ing, valve area, mean transmitral gradient (strongly heart-rate dependent), LA size, pulmonary pressures, MR severity, valve calcification and LA thrombus when intervention considered.
• Clinically significant rheumatic MS: Valve area ≤1.5 cm² is a key threshold for considering intervention; mean gradients alone should not grade severity without heart rate and flow.
• Medical: Diuretics for congestion, rate control for AF or sinus tachycardia; anticoagulate with warfarin (VKA) for AF associated with moderate/severe rheumatic MS, not a DOAC. LA thrombus or prior embolism also affects anticoagulation decisions.
• Balloon mitral commissurotomy: Preferred in suitable symptomatic rheumatic MS with pliable valve anatomy, without LA thrombus or more-than-mild MR; surgical repair/replacement if anatomy is unfavourable or balloon procedure contraindicated.
• Degenerative MS: Extensive annular calcification creates different anatomy and intervention risks; specialist valve-centre review is important.

💡 MRCP Pearl: A patient with rheumatic MS who develops AF can deteriorate rapidly because tachycardia shortens the already compromised diastolic filling period. Rate control often produces striking symptomatic improvement.

Mitral regurgitation: causes and mechanisms

• Primary (degenerative) MR: Intrinsic leaflet or chordal pathology including prolapse, flail leaflet, chordal rupture, fibroelastic deficiency, Barlow disease, rheumatic change or endocarditis.
• Ventricular secondary MR: LV enlargement/ischaemic remodelling displaces papillary muscles and tethers otherwise structurally near-normal leaflets; annular dilatation worsens coaptation.
• Atrial secondary MR: Chronic AF/LA enlargement and annular dilatation cause MR despite relatively preserved LV size and systolic function.
• Chronic physiology: Blood ejects into LA during systole, causing LA and LV volume loading, eventually AF, pulmonary hypertension and ventricular dysfunction.
• Acute severe MR: Chordal or papillary muscle rupture, endocarditis and acute ischaemic dysfunction can rapidly increase LA pressure, causing pulmonary oedema and shock with a non-dilated LA/LV.

Mitral regurgitation: presentation and examination

• Symptoms: Dyspnoea, exercise intolerance, palpitations/AF, orthopnoea and fatigue; chronic compensated MR may be asymptomatic despite substantial regurgitation.
• Murmur: Usually blowing apical pansystolic, frequently radiates to axilla; posterior leaflet pathology may radiate anteriorly, so direction is not absolute.
• Other signs: Displaced hyperdynamic apex, S3 with substantial volume loading, AF, pulmonary crackles and secondary pulmonary hypertension in advanced disease.
• Acute MR: May produce a short or relatively soft murmur because LA and LV pressures rapidly equalise; severity cannot be excluded because the murmur is unimpressive.
• Differentiate: TR increases with inspiration and has systemic venous findings; VSD can produce a harsh left sternal pansystolic murmur with thrill.

Mitral regurgitation: echocardiographic assessment

• Assess mechanism: Prolapse/flail (primary), tethered leaflets from LV disease (ventricular secondary), or annular dilatation from AF (atrial secondary). 3D TOE helps assess repair feasibility.
• Severity: Integrated quantitative assessment including effective regurgitant orifice area (EROA), regurgitant volume/fraction, vena contracta, pulmonary vein systolic flow reversal, LV/LA size and pulmonary pressures.
• Typical severe primary MR markers: EROA ≥0.40 cm², regurgitant volume ≥60 mL/beat, vena contracta ≥7 mm (supportive); secondary MR has different haemodynamic interpretation and should not rely on one rigid cut-off.
• LV function: EF may appear preserved or hyperdynamic because ejection into the lower-resistance LA is included. LVEF of 60% can already indicate declining contractile reserve in chronic severe primary MR.
• Uncertain severity: Exercise/stress echo, TOE or CMR can resolve discordance or evaluate dynamic change during exertion.

Primary mitral regurgitation: timing of repair

• Symptomatic severe primary MR: Refer for intervention if suitable; mitral valve repair is generally preferable to replacement when durable repair is likely.
• Asymptomatic severe primary MR: NICE NG208 suggests considering referral for intervention with LVEF <60%, LV end-systolic dimension >45 mm or indexed >22 mm/m², or exercise pulmonary systolic pressure >60 mmHg.
• Guideline differences: ESC 2025 gives greater emphasis to earlier intervention in selected asymptomatic patients with durable repair options, including smaller LV end-systolic dimensions (around ≥40 mm) and other risk features. Do not silently merge NICE and ESC thresholds.
• Other triggers: New AF, pulmonary hypertension, progressive LV/LA enlargement, and increasing symptoms influence timing.
• Surgery: Repair often involves leaflet repair, chordal replacement and annuloplasty. Replacement if repair unlikely to be durable; mechanical versus biological choice is individualised.
• Transcatheter edge-to-edge repair (mitral TEER): Option for selected symptomatic patients at high/prohibitive surgical risk with appropriate anatomy after Heart Team review.

💡 MRCP Pearl: Normal-looking EF in chronic severe MR is not necessarily reassuring: the LV ejects both into the aorta and backwards into the LA. An EF below 60% may already represent significant systolic impairment.

Secondary mitral regurgitation: HF treatment and TEER

• Mechanism first: Secondary MR is a consequence of ventricular or atrial disease; severity and treatment can change with loading conditions, rhythm and heart failure therapy.
• Ventricular secondary MR: Optimise guideline-directed HFrEF therapy (renin-angiotensin treatment/ARNI where appropriate, beta blocker, MRA, SGLT2 inhibitor and diuretics) and assess suitability for CRT or coronary revascularisation.
• Atrial secondary MR: Manage AF, rhythm/rate and volume status; intervention may be appropriate when significant symptomatic regurgitation persists.
• Mitral TEER: Consider in selected patients with persistent severe symptomatic secondary MR despite optimised treatment, suitable anatomy and appropriate ventricular dimensions/function; selection is specialist-led.
• Surgery: Particularly considered when concomitant CABG or other cardiac surgery is necessary; prognosis depends strongly on underlying myocardial disease.
• Clinical implication: Do not treat an echo colour jet without first optimising HF treatment and assessing the mechanism.

Mitral prolapse and mitral annular calcification

• Mitral valve prolapse (MVP): Systolic displacement of leaflet tissue into LA, often with a midsystolic click followed by a late systolic murmur; severe MR may develop with chordal rupture or flail leaflet.
• Manoeuvres: Standing/Valsalva reduces LV volume and can bring click/murmur earlier; squatting increases chamber volume and often delays click.
• Complications: MR, AF and uncommon ventricular arrhythmias; most uncomplicated MVP does not require intervention beyond indicated monitoring.
• Mitral annular calcification: Common in older adults and CKD; may cause MR, degenerative MS or both and complicate surgical/transcatheter intervention.
• Management: Echocardiographic follow-up guided by severity, symptoms and chamber changes; refer progressive significant regurgitation or obstruction to specialist teams.

Tricuspid regurgitation

• Causes: Usually secondary to RV or right atrial/annular dilatation from left-sided heart disease, pulmonary hypertension or AF; primary causes include endocarditis, carcinoid, Ebstein anomaly, rheumatic disease and pacemaker/ICD leads.
• Symptoms: Fatigue, peripheral oedema, ascites, abdominal fullness/early satiety, hepatomegaly and reduced exercise tolerance; important TR may coexist with other valve lesions.
• Examination: Raised JVP with giant systolic V waves, pulsatile liver, RV heave and lower left sternal pansystolic murmur increasing on inspiration (Carvallo sign); severe wide-open TR may be quiet.
• Echo: RV size/function, annular dilatation, leaflet tethering, device-lead interference, pulmonary pressure, hepatic vein systolic flow reversal and quantitative regurgitation (e.g., vena contracta ≥7 mm, EROA ≥0.40 cm² in severe TR).
• Management: Treat the underlying cause, optimise diuresis and HF/AF care. Refer significant symptomatic TR before irreversible RV dysfunction, renal impairment or advanced liver disease develops.
• Procedures: Surgical repair often at the time of left-sided valve surgery; isolated surgery for suitable patients and transcatheter TEER/replacement for selected high-risk symptomatic severe TR in expert centres.

💡 Clinical Pearl: A very large JVP V wave and systolic hepatic pulsation strongly suggest important TR, but they are not specific enough to replace echocardiography.

Tricuspid stenosis

• Causes: Rare; rheumatic disease, carcinoid syndrome, congenital abnormalities and occasionally infiltrative/metabolic disease.
• Pathophysiology: Obstructed RA-to-RV diastolic filling raises RA/systemic venous pressure and limits forward cardiac output.
• Features: Fatigue, oedema, hepatomegaly/ascites, raised JVP with prominent A waves in sinus rhythm, and low-pitched diastolic murmur near lower left sternal edge that may increase on inspiration.
• Investigation: Echo valve morphology, area/gradient and associated lesions; gradients vary with heart rate and venous flow.
• Treatment: Diuretics for congestion and management of rhythm; symptomatic severe TS usually requires valve intervention, most often surgical in appropriate candidates.

Pulmonary stenosis and pulmonary regurgitation

• Pulmonary stenosis: Usually congenital; may occur in Noonan syndrome or carcinoid disease. Causes RV pressure overload, RVH and eventually RV failure.
• PS murmur: Ejection systolic at left upper sternal edge, often louder with inspiration; RV heave and delayed P2 in advanced disease. Echo estimates peak velocity/gradient and RV response.
• PS treatment: Balloon pulmonary valvuloplasty for suitable significant valvular PS; surgery for dysplastic/complex anatomy or associated lesions.
• Pulmonary regurgitation: Often occurs after congenital RV outflow tract repair, with pulmonary hypertension or after endocarditis. Produces RV volume overload and progressive enlargement.
• PR murmur: Early diastolic at left upper sternal border; high-pitched Graham Steell murmur may occur in pulmonary hypertension.
• PR treatment: Treat cause and monitor RV size/function (often with CMR). Pulmonary valve replacement may be appropriate before irreversible RV dilatation or arrhythmias in selected congenital populations.

Carcinoid heart disease and unusual valve causes

• Carcinoid heart disease: Serotonin-driven plaque-like fibrosis predominantly affects right-sided valves, causing TR and pulmonary stenosis/regurgitation; left-sided disease is less common.
• Clinical clues: Flushing, diarrhoea, bronchospasm, elevated urinary 5-HIAA and right HF in a patient with neuroendocrine tumour.
• Assessment: TTE shows thickened/retracted leaflets with reduced mobility; coordinate with neuroendocrine/cardiology teams.
• Management: Control hormone secretion (e.g., somatostatin analogue), treat congestion and consider valve surgery in selected patients.
• Radiation/medication-related disease: Fibrotic or calcific multivalve disease can appear many years after mediastinal radiotherapy; historical serotonergic medications also caused valve thickening.
• Endocarditis: Leaflet perforation or destruction may cause acute severe regurgitation; see the dedicated emergency section.

31. Mixed and multiple-valve disease

• Mixed disease: Stenosis and regurgitation affect the same valve; each alters forward flow and may distort the other's severity estimate.
• Multiple-valve disease: Rheumatic disease commonly affects mitral and aortic valves; degenerative disease or prior radiation can involve several valves.
• Haemodynamics: Severe MR can lower forward aortic flow and hence the AS gradient; AR can increase systolic flow across a stenotic aortic valve. MS may lower forward flow and conceal severe concomitant AS.
• Assessment: Integrate symptoms, gradients, quantitative regurgitation, stroke-volume index, ventricular and pulmonary pressure responses and multimodality imaging.
• Management: Valve MDT prioritises the lesion producing symptoms/haemodynamic compromise, considers staged versus combined procedures and weighs intervention burden in frailty.

Acute valve emergencies

• Acute severe MR: Papillary muscle rupture after MI, chordal rupture or endocarditis. Acute pulmonary oedema/shock may occur with relatively normal chamber size and a quiet murmur; urgent TOE/TTE and cardiothoracic input.
• Acute severe AR: Type A aortic dissection or endocarditis; hypotension, pulmonary oedema, short/soft diastolic murmur. Urgent imaging and emergency surgery evaluation; avoid IABP.
• Prosthetic valve thrombosis: Acute valve obstruction or regurgitation, pulmonary oedema or embolic events, especially with subtherapeutic anticoagulation; urgent echo/fluoroscopy/CT as appropriate and valve centre management.
• Infective endocarditis: Fever, bacteremia, new murmur, embolic or heart failure features; obtain appropriate blood cultures before antibiotics whenever safe and expedite echo/specialist treatment.
• Severe symptomatic AS with decompensation: Shock or pulmonary oedema requires senior cardiology input and urgent consideration of definitive intervention or bridge valvuloplasty.
• General actions: ABCDE, ECG/monitoring, oxygen if hypoxaemic, IV access, bloods, early urgent echocardiography; avoid indiscriminate fluid loading or vasoactive medication without defining haemodynamics.

⚠️ Safety Pearl: A sudden pulmonary oedema episode with a new murmur after MI is a mechanical complication until excluded. In acute severe regurgitation the murmur may be deceptively short or soft because pressures equalise rapidly.

Surgical replacement versus transcatheter treatment

• SAVR: Open surgical aortic valve replacement; allows concomitant CABG, other valve procedures and aortic root repair. Durable mechanical valves are often considered in younger patients who can take VKA safely.
• TAVI: Catheter-delivered aortic bioprosthesis; avoids sternotomy and generally allows faster recovery, but vascular access, annular anatomy, coronary access, paravalvular leak, pacemaker requirement and long-term durability matter.
• ESC 2025: Greater use of TAVI in suitable patients ≥70 years with tricuspid AS, while recognising surgical indications in younger patients, bicuspid anatomy, aortopathy or need for associated surgery.
• Mitral intervention: Repair preferred for suitably repairable primary MR; mitral TEER for selected high-risk primary or persistent secondary MR. Balloon commissurotomy for favourable rheumatic MS.
• Tricuspid intervention: Early repair in selected operable patients; transcatheter therapy may improve symptoms/quality of life in high-risk severe TR without advanced RV failure.
• Decision: Heart Team reviews frailty, comorbidity, expected valve longevity, endocarditis risk, coronary anatomy, future procedures, patient preferences and feasibility of anticoagulation.

Mechanical and biological valve prostheses

• Mechanical prosthesis: Very durable but thrombogenic; requires lifelong vitamin-K antagonist (usually warfarin) with valve-specific INR target and regular monitoring.
• Bioprosthetic valve: Less thrombogenic, generally avoids lifelong VKA unless AF/other indication exists, but can degenerate over time; durability influenced by age, CKD and valve position.
• Transcatheter bioprostheses: Also subject to thrombosis, paravalvular regurgitation, structural deterioration and late prosthetic infection; follow-up imaging is important.
• Valve choice: Consider patient age, pregnancy plans, bleeding risks, anticoagulation adherence, occupation, preferred activity, future valve-in-valve feasibility and personal priorities.
• After repair: An annuloplasty ring or other repair may still require short-term antithrombotic treatment according to procedure and specialist protocol.

Antithrombotic treatment after valve intervention

• Mechanical valves: Lifelong warfarin/VKA; DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) must not replace VKA for mechanical valves. INR targets depend on valve type/position and thromboembolic risk (many mechanical aortic targets around 2.5; mitral often around 3.0, but use the exact cardiology plan).
• Rheumatic moderate/severe MS with AF: Warfarin/VKA rather than DOAC. Non-rheumatic native valve disease with AF is generally managed by usual AF anticoagulation indications unless a specific contraindication applies.
• Bioprosthetic SAVR/MVR: Early VKA or antiplatelet treatment depends on position, rhythm, local policy and bleeding risk; long-term anticoagulation if independent indication (e.g. AF).
• TAVI without OAC indication: Single antiplatelet therapy, commonly low-dose aspirin, is often preferred; routine dual antiplatelet treatment is not generally necessary.
• TAVI with AF/OAC indication: Continue indicated anticoagulant; avoid unnecessary added antiplatelet therapy unless recent PCI or other indication justifies it.
• Monitoring: Educate about bleeding and thrombosis, interactions, dental procedures, pregnancy, perioperative bridging decisions and what to do with missed doses; never stop mechanical-valve anticoagulation without an individual plan.

💡 MRCP Pearl: Mechanical valve + DOAC is a dangerous prescribing error. Mechanical valves require a vitamin-K antagonist even if a patient has been taking a DOAC for atrial fibrillation.

Prosthetic valve dysfunction and complications

• Thrombosis: Obstruction (high gradient, poor leaflet motion) or regurgitation; may cause acute dyspnoea, shock or embolism. Investigate INR history in mechanical valves.
• Pannus: Fibrous tissue overgrowth causing more gradual mechanical obstruction; differentiation from thrombus may need TOE, CT or fluoroscopy.
• Structural valve deterioration: Progressive stenosis or regurgitation from leaflet degeneration, particularly in bioprosthetic valves.
• Paravalvular leak: Regurgitation around sewing ring/device; can cause HF or haemolytic anaemia. Severe new leak raises concern for endocarditis or dehiscence.
• Prosthetic endocarditis: High-risk infection with abscess, dehiscence or emboli; needs specialist endocarditis team and often surgical assessment.
• Investigations: Compare with postoperative baseline TTE; TOE/3D echo, gated CT, fluoroscopy and blood cultures as indicated.

Infective endocarditis prevention and recognition

• High-risk patients: Prosthetic valves (including TAVI), prior endocarditis and some congenital heart disorders have particularly important IE risk; maintain meticulous oral and dental health.
• Clinical suspicion: Fever, positive blood cultures, new/changing regurgitation, heart failure, embolic phenomena, back pain or stroke in a patient with native/prosthetic valve disease.
• Urgent work-up: Obtain multiple properly collected blood culture sets before antimicrobials if clinically safe; request TTE and often TOE, particularly with prostheses or suspected complications.
• Antibiotic prophylaxis: NICE CG64 states that antibiotic prophylaxis is not recommended routinely for dental procedures. Individual high-risk decisions should follow current UK implementation advice and multidisciplinary/shared assessment, not an automatic blanket rule.
• Advice: Prompt evaluation of unexplained persistent fever, oral hygiene, management of skin/dental infection and discussion before invasive procedures.
• Do not confuse: Prevention advice is separate from urgent treatment of established endocarditis, which requires specialist IV antimicrobial and surgical evaluation as appropriate.

38. Valvular disease in pregnancy

• Physiological stress: Pregnancy increases plasma volume, heart rate and cardiac output; labour/postpartum fluid shifts can precipitate decompensation in severe valve disease.
• High-risk lesions: Severe symptomatic MS or AS, severe pulmonary hypertension, advanced RV dysfunction, symptomatic severe regurgitation with LV dysfunction and mechanical prostheses.
• Preconception: Cardiology/obstetric MDT review before pregnancy, including valve severity, aortic dimensions, medication safety and intervention where indicated.
• Rheumatic MS: Worsens with tachycardia and increased flow; beta blockers and diuretics may help selectively, with balloon commissurotomy considered for suitable severe disease.
• Mechanical valves: Pregnancy anticoagulation is complex: warfarin exposure carries fetal risks, but interruption can endanger the mother; specialist anticoagulation planning is essential.
• Medication caution: ACE inhibitors, ARBs, ARNIs and certain other agents are contraindicated during pregnancy; check individual drug and gestational guidance.

Non-cardiac surgery and anaesthetic risk

• Assess: Severity, symptoms, LV/RV function, pulmonary hypertension, urgency of surgery, procedure stress and anticoagulation status.
• Severe symptomatic AS: Particularly high risk of hypotension and ischaemia during anaesthesia; valve treatment may be required before elective major surgery where feasible.
• MS: Tachycardia and fluid loading worsen LA pressure; preserve appropriate rate control and avoid pulmonary oedema.
• Regurgitation: Anaesthetic goals differ from stenosis and depend on whether disease is acute/chronic and on ventricular function.
• Mechanical valve: Perioperative anticoagulation interruption and bridging are specialist risk decisions balancing valve thrombosis and bleeding.
• Practical: Document lesion, recent echo, functional class, anticoagulation and a cardiology/anaesthetic plan rather than simply listing 'heart murmur'.

AF, heart failure and medical treatment principles

• Valvular HF: Diuretics reduce congestion and guideline-directed HF therapy treats ventricular dysfunction, but a severe mechanical valve lesion often requires intervention.
• AF: Common with MS/MR/TR and LA enlargement. Rate control may relieve symptoms, especially MS; anticoagulation depends on valve lesion and AF risk assessment.
• AS: Treat hypertension and congestion carefully without causing abrupt hypotension; do not assume nitrates/vasodilators are absolutely prohibited in every patient, but individual haemodynamics matter.
• AR/MR: Treat afterload and HF when indicated, but do not mistake symptomatic improvement for reversal of an anatomically severe regurgitant lesion.
• Endocarditis: Antibiotics treat infection but urgent surgery may be required for acute severe regurgitation, abscess, uncontrolled infection or selected embolic risks.
• Shared decisions: Consider quality of life, frailty, expected benefit, treatment burden and patient preferences; the Heart Team should identify potential futility without denying appropriate intervention solely because of age.

Surveillance, follow-up and NHS pathways

• Asymptomatic severe disease: NICE advises clinical review and TTE every 6–12 months if an intervention is appropriate but not yet indicated; earlier with new symptoms or changing measurements.
• Mild stenosis: Consider TTE every 3–5 years for mild AS or MS, adjusting for progression rate, morphology and risk factors.
• After intervention: Record type/size/date of prosthesis, postoperative baseline echo, anticoagulation/antiplatelet plan, endocarditis advice, and follow-up in appropriate valve clinic.
• Postoperative symptoms: New breathlessness, fever, embolic symptoms, unexplained anaemia or a new murmur prompt earlier echo and evaluation for prosthetic dysfunction or infection.
• UK referral: Severe symptoms and exertional syncope with a systolic murmur merit urgent specialist assessment; Heart Valve Centres manage complex multivalve, redo surgery and transcatheter treatment decisions.
• Patient counselling: Explain which symptoms should prompt urgent contact, anticoagulation interactions, dental hygiene and exercise advice appropriate to lesion severity.

Common medicines and adult doses

These are illustrative usual adult doses used to treat symptoms, AF, hypertension or HF in patients with valve disease. They do not correct severe anatomical stenosis/regurgitation and must be individualised to renal function, heart rate, blood pressure, pregnancy and local protocols.

⚠️ Safety: Avoid DOACs with mechanical valves. Warfarin dosing is INR-led, not a standard daily dose. Beta blockers/rate-limiting agents can cause bradycardia or hypotension. Diuretics and RAAS blockers require biochemical monitoring. All prescription decisions must use up-to-date BNF and local guidance.

43. Rapid pattern recognition: lesion, murmur and pulse

• AS: Ejection systolic at right upper sternal edge → carotids; slow-rising pulse, soft A2, heaving apex; triad of exertional angina/syncope/dyspnoea.
• AR: Early diastolic at left sternal edge; bounding/collapsing pulse and wide pulse pressure in chronic severe disease; Austin Flint rumble sometimes.
• MS: Opening snap + apical mid-diastolic rumble; AF, pulmonary hypertension, haemoptysis and possible embolism; tachycardia makes symptoms worse.
• MR: Apical pansystolic → axilla; displaced hyperdynamic apex, S3, AF or pulmonary congestion; acute severe MR may have a quiet murmur.
• TR: Left lower sternal pansystolic louder with inspiration; giant JVP V waves, pulsatile liver, ascites and oedema.
• PS: Left upper sternal ejection systolic with RV heave; often congenital. PR: Early diastolic left upper sternal murmur with RV volume loading.
• VSD: Harsh pansystolic at lower left sternal edge; HCM: dynamic systolic murmur increases with standing/Valsalva; consider in murmur differential.

MRCP traps and higher-level reasoning

• 1. Murmur intensity: Severe AS or acute severe MR can have a deceptively quiet murmur because flow is low or pressures equalise.
• 2. Echo gradients: Low gradient does not exclude severe stenosis in a low-flow state; always inspect stroke volume, EF and integrated valve measurements.
• 3. MR ejection fraction: An LVEF below 60% in severe chronic primary MR may already indicate LV impairment.
• 4. Tachycardia in MS: Shortens filling time and increases LA pressure; rate control is an important symptomatic intervention.
• 5. AS treatment: Symptomatic severe AS needs valve intervention assessment; medical therapy cannot remove a calcified obstruction.
• 6. Chronic versus acute: Chamber enlargement supports chronic volume loading; lack of enlargement does not rule out acute severe AR/MR.
• 7. Anticoagulation: Mechanical valve → lifelong VKA; rheumatic moderate/severe MS with AF → VKA; DOAC contraindicated for mechanical valves.
• 8. Valve choice: Biological avoids routine lifelong VKA but may degenerate; mechanical is durable but requires warfarin.
• 9. Right heart: Massive TR may have little murmur yet severe organ congestion; refer before advanced RV, hepatic or renal damage.
• 10. Endocarditis: NICE does not recommend routine antibiotic prophylaxis for all dental work, while good oral health and individual high-risk planning remain important.
• 11. Follow-up: New exertional syncope and suspicious systolic murmur requires urgent echo/specialist assessment, not routine outpatient waiting.
• 12. Multiple lesions: MR can reduce forward stroke volume and mask aortic gradients; evaluate the circulation, not each Doppler measurement in isolation.

Clinical teaching commentary

Valvular heart disease becomes easier to understand when each lesion is linked to the phase of the cardiac cycle in which flow is abnormal. A stenotic valve obstructs forward flow when it should be open, while a regurgitant valve leaks when it should be closed. This predicts whether the murmur is systolic or diastolic and which chamber experiences pressure or volume loading.

• At the bedside: Identify murmur timing relative to the carotid pulse, then use location, radiation, pulse character, JVP and chamber signs to propose the lesion.
• With echocardiography: Establish the mechanism, quantify severity, identify ventricular and pulmonary vascular consequences, and watch trends across serial studies.
• With management: Separate symptom-relieving treatment from definitive correction. Diuretics relieve congestion, but progressive severe structural lesions require appropriately timed intervention.
• At MRCP level: Understand why acute regurgitation can be life-threatening without chamber dilatation, why low-output AS has a low gradient, why MR distorts the interpretation of EF, and why a mechanical valve mandates VKA anticoagulation.

46. NICE, ESC and clinical references

• NICE NG208 — Heart valve disease presenting in adults: referral, intervention criteria, surveillance and treatment decisions.
• 2025 ESC/EACTS Valvular Heart Disease Guidelines: contemporary imaging, Heart Team and surgical/transcatheter management.
• NICE CG64 — Prophylaxis against infective endocarditis: UK prevention and dental guidance.
• SDCEP — Infective endocarditis implementation advice: UK high-risk dental shared decision-making.
• NICE NG106 — Chronic heart failure: medical therapy for coexisting ventricular dysfunction.
• NICE NG196 — Atrial fibrillation: rate/rhythm control and thromboembolic risk assessment.
• BNF: verify prescribing, renal adjustments, interactions and contraindications.

📌 Guideline note (October 2026): NICE NG208 provides UK service/referral guidance, while the 2025 ESC/EACTS document supplies more recent European procedural recommendations. They are not interchangeable where numerical thresholds or TAVI selection pathways differ.