🫀 Valvular heart disease means one or more heart valves either fails to open properly (stenosis, an obstruction) or fails to close properly (regurgitation, a leak). The heart compensates for years, often silently, until it eventually fails.
Your four questions for every patient: Which valve, and is it stenosis or regurgitation? What caused it? How severe is it? Has it started to damage the heart, and does it need fixing?
4.01 What Is Valve Disease?
The four heart valves keep blood moving in one direction. Disease takes one of two forms:
- Stenosis: The valve is narrowed and will not open fully. The chamber behind it must generate a higher pressure to push blood through — a pressure load.
- Regurgitation (incompetence): The valve leaks when it should be closed, so blood flows backwards. The heart has to pump the same blood twice — a volume load.
A valve can be both stenosed and leaky (mixed disease), and several valves can be affected at once.
Primary versus secondary disease. In primary disease the valve itself is abnormal (e.g. calcified, prolapsing or infected). In secondary (functional) disease the valve leaflets are normal, but the surrounding chamber has enlarged and pulled them apart so they no longer meet — for example, MR from a dilated left ventricle. This distinction matters because secondary disease is treated mainly by treating the underlying heart.
The goals of management:
- 1. Identify the lesion.
- 2. Establish its cause and severity.
- 3. Detect damage to the heart.
- 4. Decide when to repair or replace the valve — before irreversible damage, but not unnecessarily early.
💡 Clinical Pearl: Murmur loudness does not reliably reflect severity. Severe AS with a failing ventricle and acute severe MR can both have quiet murmurs, because loudness depends on flow.
4.02 Valves and the Cardiac Cycle
Working out when in the cardiac cycle blood flows across each valve lets you predict the timing of every murmur.
- Aortic and pulmonary valves (semilunar) open in systole and close in diastole.
- Stenosis obstructs flow in systole → ejection systolic murmur (AS, PS).
- Regurgitation leaks in diastole → early diastolic murmur (AR, PR).
- Mitral and tricuspid valves (atrioventricular) open in diastole and close in systole.
- Stenosis obstructs flow in diastole → mid-diastolic murmur (MS, TS).
- Regurgitation leaks in systole → pansystolic murmur (MR, TR).
- Heart sounds: S1 is closure of the mitral and tricuspid valves; S2 is closure of the aortic (A2) and pulmonary (P2) valves.
- Valve apparatus: The leaflets, annulus (ring), chordae tendineae, papillary muscles and the ventricle wall all work together. A fault in any part can cause a leak.
- Added sounds: An ejection click after S1 suggests a bicuspid aortic valve or pulmonary stenosis. An opening snap after S2 suggests mobile rheumatic MS.
💡 Clinical Pearl: Time every murmur against the carotid pulse. A murmur that coincides with the pulse is systolic; one between pulses is diastolic. A diastolic murmur is always pathological.
4.03 Pressure and Volume Overload
How the heart responds depends on whether the load is pressure or volume, and whether it develops slowly or suddenly.
- Pressure overload (AS, hypertension):
- The LV thickens with concentric hypertrophy to cope with the higher pressure.
- This keeps up output but makes the ventricle stiff, impairs filling and raises oxygen demand.
- Eventually fibrosis develops and the ventricle fails.
- Volume overload (AR, MR):
- The LV dilates (eccentric hypertrophy) to accommodate the extra volume.
- Patients may feel well for years while contractility slowly declines.
- This is why surgery is timed by ventricular size and function, not just symptoms.
- The atria: MS and MR raise left atrial pressure and size, causing AF and pulmonary congestion.
- The lungs and right heart: Long-standing high left-sided pressure causes pulmonary hypertension, then RV failure and secondary TR.
- Acute versus chronic:
- A sudden severe leak (acute MR or AR) hits a ventricle that has had no time to adapt. Pressure rises abruptly, causing pulmonary oedema and shock even though the heart looks a normal size.
- Chronic disease allows years of adaptation before decompensation.
4.04 Causes
- Degenerative / calcific: The commonest cause in the UK. Age-related calcification causes AS and mitral annular calcification; it is more common with CKD and cardiovascular risk factors.
- Congenital: Bicuspid aortic valve (1–2% of the population), pulmonary stenosis, Ebstein anomaly.
- Rheumatic: Follows rheumatic fever (an immune reaction to streptococcal throat infection) years earlier. It classically causes MS, often with MR or aortic disease. Now uncommon in UK-born patients but still important in people from countries where rheumatic fever is common.
- Infective endocarditis: Destroys or perforates leaflets, causing acute regurgitation, abscesses and emboli.
- Functional / secondary:
- LV dilatation pulls the mitral leaflets apart (secondary MR).
- AF enlarges the atria and valve rings (atrial functional MR and TR).
- RV dilatation causes TR.
- Aortic root disease: Aneurysm, Marfan syndrome and dissection stretch the root, causing AR.
- Other: Carcinoid syndrome, chest radiotherapy, drugs (historically ergot-derived dopamine agonists and fenfluramine), connective tissue disease and pacemaker leads crossing the tricuspid valve.
4.05 History and Examination
Symptoms:
- Exertional breathlessness, falling exercise tolerance and fatigue.
- Angina.
- Dizziness or blackouts on exertion.
- Orthopnoea, PND and ankle swelling.
- Palpitations.
Many older patients quietly reduce their activity to avoid symptoms, so ask specifically how far they can walk now compared with a year ago.
History:
- Rheumatic fever, congenital heart disease, previous endocarditis or valve surgery.
- Radiotherapy, AF, previous MI.
- Family history (bicuspid valve, aortopathy).
- Dental health, plans for pregnancy, current anticoagulation.
Examination: Work through the following systematically:
- Pulse rate, rhythm and character (slow-rising, collapsing).
- Blood pressure and pulse pressure.
- JVP.
- Apex position and character.
- Thrills and heaves.
- Heart sounds and added sounds.
- Murmurs.
- Lung bases, oedema and the liver.
Red flags needing urgent assessment:
- Exertional syncope with a systolic murmur.
- Angina or breathlessness on minimal exertion.
- Pulmonary oedema or hypotension.
- Fever with a new regurgitant murmur (endocarditis).
- Sudden chest or back pain with a diastolic murmur (aortic dissection).
4.06 Describing Murmurs
Describe every murmur in the same order: timing → site of maximal intensity → character → radiation → grade (and thrill) → effect of manoeuvres, then mention the heart sounds and pulse.
| Lesion | Murmur and associated signs |
|---|---|
| Aortic stenosis | Harsh ejection systolic, right upper sternal edge, radiating to the carotids. Slow-rising pulse, soft A2, heaving apex. |
| Aortic regurgitation | High-pitched early diastolic, left sternal edge, best heard sitting forward in expiration. Collapsing pulse, wide pulse pressure. |
| Mitral stenosis | Low-pitched mid-diastolic rumble at the apex, best with the bell in the left lateral position. Loud S1, opening snap, often AF. |
| Mitral regurgitation | Blowing pansystolic at the apex, radiating to the axilla. Displaced apex, S3. |
| Tricuspid regurgitation | Pansystolic at the lower left sternal edge, louder on inspiration. Giant V waves in the JVP, pulsatile liver. |
| Pulmonary stenosis | Ejection systolic at the upper left sternal edge, louder on inspiration. RV heave, ejection click. |
| Pulmonary regurgitation | Early diastolic at the upper left sternal edge (Graham Steell murmur in pulmonary hypertension). |
Grading: Systolic murmurs are graded 1–6.
- Grade 4 or above has a palpable thrill.
- Grade 6 is audible with the stethoscope just off the chest.
💡 MRCP Pearl: Right-sided murmurs get louder on inspiration and left-sided murmurs on expiration ("RILE"). It is a useful first clue to which side of the heart the lesion is on.
4.07 Dynamic Manoeuvres
Changing how much blood returns to the heart (preload) or the resistance it pumps against (afterload) changes murmurs in predictable ways.
- Inspiration: Increases venous return to the right heart, so right-sided murmurs get louder (e.g. TR — Carvallo's sign).
- Handgrip: Raises afterload, so MR and AR murmurs get louder; the HCM murmur gets quieter.
- Standing or Valsalva: Reduces preload. Most murmurs (including AS) get quieter. Two get louder or move: HCM gets louder, and the MVP click moves earlier.
- Squatting or leg raising: Increases preload. The AS murmur may get louder; the HCM murmur gets quieter; the MVP click moves later.
- Posture: Left lateral position for MS (with the bell); sitting forward in expiration for AR.
- Limitations: Responses are unreliable in complex disease, low cardiac output or obesity. Echo decides.
💡 Clinical Pearl: If a systolic murmur gets louder on standing, think HCM. Almost every other murmur gets quieter.
4.08 Investigations
- ECG: AF, LVH or RVH, left atrial enlargement (P mitrale), conduction disease. A normal ECG does not exclude severe valve disease.
- Bloods:
- FBC, U&E and LFTs.
- NT-proBNP if heart failure is suspected.
- CRP and blood cultures if infection is possible.
- Clotting if anticoagulated or before surgery.
- Chest X-ray: Heart size, pulmonary congestion, valve calcification. It cannot grade severity.
- Transthoracic echo (TTE): The key test. It shows the mechanism, leaflet motion, gradients, valve area, size of any leak, chamber size and function, and pulmonary pressure.
- Transoesophageal echo (TOE): Gives a close-up view from the oesophagus behind the heart. Used for:
- The mechanism of MR and planning repair.
- Prosthetic valves.
- Endocarditis and abscess.
- Left atrial thrombus before procedures.
- Cardiac CT:
- Planning TAVI: sizing the valve ring and checking the access arteries.
- Measuring the aorta.
- Calcium scoring when the severity of AS is uncertain.
- Cardiac MRI: Accurate ventricular volumes and regurgitant volumes when echo is inconclusive.
- Exercise testing: In apparently asymptomatic severe AS, a supervised exercise test can reveal hidden symptoms. Never exercise-test a patient with symptomatic severe AS.
- Dobutamine stress echo: For low-flow AS with reduced EF (see AS severity).
4.09 Grading Severity on Echo
Severity is never decided by one number. Echo combines several measurements with the clinical picture.
- Gradients depend on flow: The pressure gradient across a stenotic valve depends on how much blood goes through it. If the heart is weak and pumping little blood, a severely stenosed valve can show only a low gradient. Always check the stroke volume.
- Regurgitation: The size of the colour jet alone is misleading, especially for eccentric jets that hug the wall. Severity combines:
- Vena contracta (the width of the jet at its narrowest point).
- Effective regurgitant orifice area (EROA).
- Regurgitant volume and fraction.
- Flow reversal in the veins or aorta.
- Chamber size.
- Size the chambers for the patient: Index chamber sizes to body surface area, especially in smaller patients.
- Trends matter: Compare with previous scans; rapid progression changes management.
- Mixed lesions: A leak increases flow across the same valve and exaggerates a stenotic gradient. Conversely, low output can hide severe stenosis.
4.10 Referral, Surveillance and the Heart Team
NICE NG208 — who needs an echo?
- Offer TTE to anyone with a suspected valve murmur plus symptoms, signs or an abnormal ECG, or an ejection systolic murmur with a soft or absent S2.
- Urgent referral (within 2 weeks): A systolic murmur with exertional syncope. Also consider urgent referral for a murmur with severe breathlessness, or angina at rest or on minimal exertion.
When to intervene: Intervention is offered for symptomatic severe valve disease when appropriate. Asymptomatic severe disease may need earlier intervention if the ventricle starts to suffer or other high-risk features appear (thresholds are given under each valve).
Surveillance:
- Asymptomatic severe disease suitable for intervention: Clinical review and echo every 6–12 months.
- Moderate disease: Usually every 1–2 years.
- Mild AS or MS: Every 3–5 years.
- New symptoms at any stage mean prompt reassessment, not waiting for the next routine scan.
The Heart Team: Cardiologists, imaging specialists, cardiac surgeons and interventionists decide together. They weigh anatomy, operative risk, frailty, life expectancy, coronary disease, valve durability and — crucially — what the patient wants.
⚠️ Clinical Pearl: New symptoms in a patient with known severe stenosis are an indication for urgent review, not for bringing forward the annual echo.
4.11 Aortic Stenosis
Mechanism: The aortic valve narrows, so the LV must generate a higher pressure to eject blood. It responds with concentric hypertrophy, which preserves output for years. However, the thick muscle is stiff, fills poorly and needs more oxygen than the coronary arteries can supply. Eventually fibrosis develops and the ventricle fails. The commonest valve disease requiring intervention in the UK.
Causes:
- Degenerative calcification: Most cases over 70.
- Bicuspid valve: Presents earlier, typically at 50–70.
- Rheumatic disease: Usually with mitral disease.
- Radiation.
Clinical pattern — the classic triad:
- Exertional breathlessness: The stiff ventricle raises filling pressures.
- Angina: The thick muscle needs more oxygen than the coronaries can deliver, even when they are normal.
- Exertional syncope: The fixed obstruction prevents cardiac output rising during exercise while muscle blood vessels dilate, so blood pressure falls. Arrhythmias can also contribute.
Once symptoms appear, average survival without valve replacement is only 2–3 years.
Signs:
- Pulse: Slow-rising, low-volume (pulsus parvus et tardus).
- Blood pressure: Narrow pulse pressure.
- Apex: Heaving, undisplaced.
- Murmur: Harsh ejection systolic at the right upper sternal edge, radiating to the carotids. A late-peaking murmur suggests more severe disease.
- Heart sounds: Soft or absent A2, possibly an S4. An ejection click suggests a mobile bicuspid valve.
- Low output: In severe AS with a failing ventricle, the murmur may become quieter.
ECG: LVH with strain, left atrial enlargement, conduction disease or AF.
Differentials:
- Aortic sclerosis: Thickened valve with a murmur but no obstruction; normal pulse and normal A2.
- HCM: The murmur gets louder on standing.
- Pulmonary stenosis and flow murmurs.
💡 Clinical Pearl: A soft A2 and a slow-rising pulse indicate severe AS. A loud murmur with a normal A2 is more often aortic sclerosis.
4.12 AS: Severity and Low-flow States
| Severity | Echo findings |
|---|---|
| Mild | Peak velocity 2.6–2.9 m/s; mean gradient <20 mmHg; valve area >1.5 cm² |
| Moderate | Peak velocity 3.0–3.9 m/s; mean gradient 20–39 mmHg; valve area 1.0–1.5 cm² |
| Severe | Peak velocity ≥4.0 m/s; mean gradient ≥40 mmHg; valve area ≤1.0 cm² (indexed ≤0.6 cm²/m²) |
| Very severe | Peak velocity >5 m/s — higher risk even without symptoms |
Dimensionless index: The ratio of the velocity just below the valve to the velocity across it. A value below 0.25 supports severe AS when other measurements are uncertain.
Low-flow, low-gradient AS — an MRCP favourite: The valve area is ≤1.0 cm², but the mean gradient is below 40 mmHg because the heart is pumping too little blood (stroke volume index ≤35 mL/m²). There are two forms:
- Classical (reduced EF): A weak LV cannot generate a high gradient.
- Low-dose dobutamine stress echo increases flow.
- If the gradient rises to severe levels while the valve area stays small, the AS is truly severe.
- If the valve area increases, it was "pseudo-severe" — the valve only looked tight because flow was low.
- Paradoxical (preserved EF): A small, thick-walled ventricle ejects a low stroke volume despite a normal EF. It is common in older women and hypertensive patients.
- CT calcium score: Helps when uncertainty remains. Roughly >2,000 Agatston units in men or >1,200 in women supports severe AS.
- Check the basics first: Confirm the measurements are technically correct (outflow tract diameter, Doppler alignment) and that blood pressure was controlled at the time of the scan.
💡 MRCP Pearl: A mean gradient of 25 mmHg does not exclude severe AS if the stroke volume is low. Ask first whether the ventricle can generate enough flow to produce a high gradient.
4.13 AS: Management, SAVR and TAVI
No drug reverses a calcified stenosis. Valve replacement is the only definitive treatment.
- Symptomatic severe AS: Prompt Heart Team referral for valve replacement.
- Asymptomatic severe AS: Consider intervention if high-risk features are present. NICE NG208 lists:
- Peak velocity above 5 m/s.
- Valve area below 0.6 cm².
- LVEF below 55%.
- BNP or NT-proBNP more than twice the upper limit of normal.
- Surgical aortic valve replacement (SAVR): Open surgery. Generally preferred for:
- Younger patients.
- Bicuspid valves with a dilated aorta.
- Patients who also need bypass grafting or aortic surgery.
- Anatomy unsuitable for TAVI.
- Transcatheter aortic valve implantation (TAVI):
- How it works: A biological valve on a stent is passed up from the femoral artery and expanded inside the old valve. There is no sternotomy and recovery is quick.
- Who: Increasingly the default for older patients with suitable anatomy. ESC 2025 uses age 70 or over as one factor for tricuspid-valve AS; UK pathways individualise.
- Drawbacks: Pacemaker requirement, leak around the valve (paravalvular leak), vascular complications and uncertain long-term durability.
- Medical care while waiting:
- Treat heart failure, AF, hypertension and coronary disease cautiously.
- Diuretics relieve congestion, but too much preload reduction can cause hypotension.
- Vasodilators are not absolutely forbidden but need care.
- Balloon aortic valvuloplasty: A temporary bridge in unstable patients, not a lasting treatment.
💡 Clinical Pearl: Unexplained heart failure in an older patient with a soft ejection systolic murmur may be severe low-flow AS — request an echo before calling it "just a flow murmur".
4.14 Aortic Regurgitation
Mechanism: Blood leaks back from the aorta into the LV in diastole. The LV then has to pump both the normal return from the lungs and the leaked blood. It dilates to cope and ejects a large stroke volume. This big volume ejected into the aorta, followed by rapid backflow, explains the wide pulse pressure and collapsing pulse.
Causes:
- Leaflet disease: Bicuspid valve, rheumatic disease, endocarditis, degeneration.
- Aortic root dilatation: Hypertension, bicuspid-associated aortopathy, Marfan syndrome, ankylosing spondylitis, syphilis (historical), aortic dissection.
Chronic AR: Often asymptomatic for years. Patients may notice a pounding heartbeat; later breathlessness, orthopnoea and angina develop.
Acute severe AR (endocarditis, type A dissection): The LV has had no time to dilate, so pressure rises abruptly, causing pulmonary oedema and shock. The classic peripheral signs and even the murmur may be absent. This is a surgical emergency.
Signs of chronic severe AR:
- Pulse: Collapsing (water-hammer) pulse.
- Blood pressure: Wide pulse pressure, e.g. 170/40.
- Apex: Displaced and hyperdynamic.
- Murmur: High-pitched early diastolic at the left sternal edge, best heard sitting forward in expiration. Often accompanied by a systolic flow murmur from the large stroke volume.
- Austin Flint murmur: A mid-diastolic rumble at the apex. The regurgitant jet hits the mitral valve and partly closes it; it can be mistaken for MS.
- Eponymous signs: Nodding head (de Musset), visible nail-bed pulsation (Quincke), pistol-shot femoral pulses. Classic, but neither sensitive nor specific.
ECG: LVH.
💡 Clinical Pearl: Chest pain radiating to the back with a new early diastolic murmur is aortic dissection until proven otherwise. Do not give anticoagulants or thrombolysis.
4.15 AR: Assessment and Management
Echo: Shows the leaflets and aortic root, the size of the leak, LV size and EF. TOE or cardiac MRI help if the findings are unclear.
Signs of severe AR on echo:
- Vena contracta >6 mm.
- EROA ≥0.30 cm².
- Regurgitant volume ≥60 mL per beat, or regurgitant fraction ≥50%.
- Reversed flow throughout diastole in the descending aorta.
- A dilated LV.
Management:
- Symptomatic severe AR: Valve surgery, whatever the EF. The aortic root is repaired at the same time if dilated.
- Asymptomatic severe AR (NICE NG208): Consider intervention if any of the following, which show the ventricle is starting to fail:
- LVEF below 55%.
- LV end-systolic diameter above 50 mm.
- Indexed end-systolic diameter above 24 mm/m².
- Medical treatment: Treat hypertension (vasodilators such as ACE inhibitors or dihydropyridines) and heart failure while awaiting surgery. Drugs do not replace surgery when it is indicated.
- Acute severe AR: Emergency echo and cardiothoracic surgery. An intra-aortic balloon pump is contraindicated, because it inflates in diastole and pushes more blood back through the leaking valve.
💡 Clinical Pearl: In chronic AR, surgery is timed by LV size and function, not just symptoms. Waiting for symptoms risks irreversible LV damage.
4.16 Bicuspid Aortic Valve
Mechanism: The commonest congenital heart abnormality (1–2% of people). The aortic valve has two cusps instead of three. The abnormal flow wears the valve out faster, so AS develops 10–20 years earlier than in a normal valve, and AR can also occur. The aortic wall itself is often weak too.
Associations:
- Dilatation of the ascending aorta (aortopathy), with a risk of dissection.
- Coarctation of the aorta.
- Turner syndrome.
- Endocarditis.
Clinical pattern: An ejection click followed by a systolic murmur in a younger adult; AS presenting in the 50s–60s.
Assessment: Echo for the valve and the aorta, with CT or MRI if the aorta is not well seen. Consider screening first-degree relatives.
Management: The timing and type of valve replacement depends on age, aortic size and growth rate, and family history. Aortic surgery is sometimes needed at the same time. Lifelong surveillance of both the valve and the aorta is needed, even after valve replacement.
💡 Clinical Pearl: In a young adult with AS, look for coarctation: check for radio-femoral delay and measure blood pressure in both arms.
4.17 Mitral Stenosis
Mechanism: The narrowed mitral valve obstructs flow from the left atrium to the LV in diastole. Pressure builds up in the left atrium and then the lungs, causing breathlessness and eventually pulmonary hypertension and right heart failure. The LV itself is usually normal and underfilled.
Causes:
- Rheumatic heart disease: The classic cause — the commissures fuse and the leaflets thicken.
- Mitral annular calcification: A non-rheumatic cause in older people and those with CKD.
Why heart rate matters so much: Blood can only cross the narrow valve during diastole. A fast heart rate shortens diastole, so left atrial pressure rises steeply. This is why AF, exercise, fever and pregnancy often unmask or worsen MS.
Clinical pattern:
- Exertional breathlessness, orthopnoea and fatigue.
- Palpitations from AF.
- Haemoptysis from ruptured bronchial veins.
- Embolic stroke from left atrial thrombus.
- Right heart failure in advanced disease.
- Malar flush (purplish cheeks) in severe, longstanding disease.
Signs:
- Irregularly irregular pulse (AF).
- Tapping apex beat (a palpable loud S1).
- Loud S1 while the leaflets are still mobile.
- Opening snap after S2 — the closer to S2, the more severe.
- Low-pitched mid-diastolic rumble at the apex.
- Signs of pulmonary hypertension: loud P2, RV heave, TR.
💡 MRCP Pearl: When a patient with MS develops AF, symptoms can worsen dramatically. Rate control alone often brings striking improvement.
4.18 MS: Assessment and Management
Echo:
- Commissural fusion and doming leaflets in rheumatic disease.
- Valve area.
- Mean gradient — strongly dependent on heart rate, so record the rate.
- Left atrial size and pulmonary pressure.
- Any MR and calcification.
- Left atrial thrombus, on TOE before any procedure.
Severity: A valve area of 1.5 cm² or less is clinically significant MS and the threshold for considering intervention. A normal valve is 4–6 cm².
Medical treatment:
- Diuretics: For congestion.
- Rate control: Beta blockers or rate-limiting CCBs, to lengthen diastole for AF or sinus tachycardia.
- Anticoagulation: Use warfarin (a vitamin K antagonist) — not a DOAC — for AF with moderate or severe rheumatic MS. Also anticoagulate for left atrial thrombus or previous embolism.
Intervention:
- Percutaneous balloon mitral commissurotomy: A balloon is passed across the atrial septum and inflated to split the fused commissures. Preferred for symptomatic rheumatic MS with pliable, non-calcified leaflets, no left atrial thrombus and no more than mild MR.
- Surgical repair or replacement: If the anatomy is unsuitable for balloon treatment.
- Degenerative MS (annular calcification): Behaves differently — balloon treatment does not work. Needs specialist valve-centre review.
4.19 Mitral Regurgitation
Mechanism: Blood leaks back into the left atrium in systole. The LV dilates to pump the extra volume, and the left atrium enlarges, leading to AF and pulmonary hypertension. Because the LV can empty easily into the low-pressure atrium, the EF looks higher than the true muscle function.
Three types — the distinction drives treatment:
- Primary (degenerative) MR: The valve itself is abnormal — prolapse, a flail leaflet, chordal rupture, rheumatic disease or endocarditis. Fix the valve.
- Ventricular secondary MR: A dilated or infarcted LV pulls the papillary muscles apart, so normal leaflets cannot meet. Treat the heart failure first.
- Atrial secondary MR: Long-standing AF stretches the left atrium and the valve ring, even though the LV is normal. Treat the AF.
Acute severe MR (papillary muscle rupture after MI, chordal rupture, endocarditis):
- A sudden leak into a small, non-compliant atrium causes flash pulmonary oedema and shock.
- The murmur may be short or quiet because the pressures equalise quickly.
Clinical pattern: Chronic MR may cause no symptoms for years despite a big leak. Eventually breathlessness, fatigue and AF develop.
Signs:
- Blowing pansystolic murmur at the apex radiating to the axilla. Posterior leaflet disease may radiate anteriorly instead.
- Displaced, hyperdynamic apex.
- Soft S1.
- S3, reflecting large-volume filling.
- AF.
- Pulmonary crackles.
Differentials:
- TR: Louder on inspiration, with giant V waves in the JVP.
- VSD: Harsh pansystolic murmur at the lower left sternal edge, often with a thrill.
4.20 MR: Echo Assessment
- Mechanism first: Is the MR primary (prolapse or flail), ventricular secondary (tethered leaflets) or atrial secondary (dilated ring)? 3D TOE shows whether the valve can be repaired.
- Severe primary MR:
- EROA ≥0.40 cm².
- Regurgitant volume ≥60 mL per beat.
- Vena contracta ≥7 mm.
- Supported by reversed systolic flow in the pulmonary veins and an enlarged LA and LV.
- Reading the EF in MR: The LV ejects both forwards into the aorta and backwards into the atrium, so the EF overestimates true function. An EF of 60% may already mean the ventricle is weakening.
- If severity is unclear: Exercise echo, TOE or cardiac MRI.
💡 MRCP Pearl: In chronic severe MR, a "normal" EF is not reassuring. An EF below 60% signals LV dysfunction and is a trigger for surgery.
4.21 Primary MR: Timing of Repair
- Symptomatic severe primary MR: Refer for intervention. Repair is preferred to replacement when a durable repair is likely; it preserves LV function and avoids the problems of a prosthetic valve.
- Asymptomatic severe primary MR (NICE NG208): Consider referral if any of the following:
- LVEF below 60%.
- LV end-systolic diameter above 45 mm (or indexed above 22 mm/m²).
- Pulmonary artery systolic pressure above 60 mmHg on exercise.
- Other triggers: New AF, pulmonary hypertension at rest, progressive enlargement of the LV or LA, rising symptoms.
- ESC 2025 supports earlier repair in selected asymptomatic patients at expert centres where a durable repair is very likely (e.g. LV end-systolic diameter around 40 mm). NICE and ESC thresholds differ — do not merge them silently.
- Surgery: Leaflet repair, artificial chords and an annuloplasty ring. Replacement (mechanical or biological) if repair is not feasible.
- Transcatheter edge-to-edge repair (TEER): A clip is delivered via the femoral vein to pinch the leaflets together. For selected symptomatic patients at high surgical risk, after Heart Team review.
4.22 Secondary MR
Secondary MR is a consequence of a diseased ventricle or atrium, so the first step is always to treat that underlying disease. The leak often improves when the heart failure is treated.
- Ventricular secondary MR:
- Optimise heart failure therapy first: ACE inhibitor or sacubitril/valsartan, beta blocker, MRA, SGLT2 inhibitor, and diuretics.
- Consider CRT if eligible, and coronary revascularisation if appropriate.
- Atrial secondary MR: Control the AF (rate or rhythm) and fluid status.
- Mitral TEER: Consider if severe symptomatic MR persists despite optimal therapy, with suitable anatomy and LV size and function. Selection is by specialists.
- Surgery: Usually only when other cardiac surgery (e.g. CABG) is being done.
- Prognosis: Depends mainly on the underlying heart muscle disease.
💡 Clinical Pearl: Never "fix" secondary MR before optimising heart failure treatment. The valve is the victim, not the cause.
4.23 Mitral Valve Prolapse
Mechanism: Floppy, thickened mitral leaflets (myxomatous degeneration) bulge back into the left atrium during systole. It is common (2–3% of people) and associated with Marfan and Ehlers–Danlos syndromes.
Clinical pattern: Often asymptomatic. The classic finding is a mid-systolic click followed by a late systolic murmur.
Manoeuvres: Standing or Valsalva makes the LV smaller, so the click comes earlier. Squatting delays it.
Complications:
- Progressive MR, or sudden severe MR from chordal rupture (flail leaflet).
- AF.
- Endocarditis.
- Rarely, ventricular arrhythmias.
Management: Uncomplicated MVP needs only echo follow-up. Treat significant MR as primary MR.
4.24 Mitral Annular Calcification
Mechanism: Calcium is deposited in the ring around the mitral valve. It is common in older people and in CKD.
Effects: MR, degenerative (non-rheumatic) MS, or both. It is also associated with AF, conduction disease and stroke.
Management: Echo surveillance. The heavy calcium makes surgery and transcatheter procedures technically difficult, so refer significant disease to a specialist valve centre.
4.25 Tricuspid Regurgitation
Mechanism: Blood leaks back from the RV into the right atrium in systole, raising venous pressure throughout the body. Most TR is secondary: the valve ring stretches because the right heart is enlarged by left-sided heart disease, pulmonary hypertension or AF.
Causes:
- Secondary: Left heart failure, MS or MR, pulmonary hypertension, AF, RV infarction.
- Primary: Infective endocarditis (especially in people who inject drugs), carcinoid syndrome, rheumatic disease, Ebstein anomaly, and pacemaker or ICD leads crossing the valve.
Clinical pattern: Right-sided congestion:
- Swollen legs, ascites and abdominal fullness.
- Early satiety and fatigue.
- A pulsatile, enlarged liver.
Signs:
- Raised JVP with giant V waves (a systolic pulsation).
- Pulsatile liver.
- RV heave.
- Pansystolic murmur at the lower left sternal edge that gets louder on inspiration (Carvallo's sign). Very severe "wide-open" TR may have almost no murmur.
Echo:
- RV size and function, and ring dilatation.
- Pacemaker lead interference.
- Pulmonary pressure.
- Severity: vena contracta ≥7 mm, EROA ≥0.40 cm², and reversed systolic flow in the hepatic veins in severe TR.
Management:
- Treat the cause; use diuretics for congestion; manage heart failure and AF.
- Refer before the RV, kidneys or liver are irreversibly damaged.
- Surgical repair is often done at the same time as left-sided valve surgery; isolated surgery in selected patients.
- Transcatheter repair or replacement for selected high-risk patients in expert centres.
💡 Clinical Pearl: Giant V waves and a pulsatile liver strongly suggest severe TR, but always confirm with echo.
4.26 Tricuspid Stenosis
Mechanism: Obstruction of flow from the right atrium to the RV in diastole raises systemic venous pressure and limits cardiac output. It is rare.
Causes: Rheumatic disease (almost always with mitral disease), carcinoid syndrome and congenital abnormalities.
Clinical pattern: Fatigue, oedema, an enlarged liver and ascites.
Signs:
- Raised JVP with giant A waves in sinus rhythm (the atrium contracts against the narrowed valve).
- A low-pitched mid-diastolic murmur at the lower left sternal edge, louder on inspiration.
Management: Diuretics and rhythm control. Symptomatic severe TS usually needs intervention, typically surgery.
4.27 Pulmonary Stenosis
Mechanism: Obstruction to RV outflow causes RV pressure overload, then RV hypertrophy, and eventually RV failure.
Causes: Usually congenital. Associated with Noonan syndrome, tetralogy of Fallot, congenital rubella and carcinoid disease.
Signs:
- Ejection systolic murmur at the upper left sternal edge, louder on inspiration.
- Ejection click.
- RV heave.
- Soft, delayed P2 in severe disease.
- Prominent A waves in the JVP.
Assessment: Echo measures the peak velocity and gradient, and the RV response.
Management: Balloon pulmonary valvuloplasty for significant valvular PS. Surgery for dysplastic valves or complex anatomy.
4.28 Pulmonary Regurgitation
Mechanism: A leaky pulmonary valve causes RV volume overload and progressive RV dilatation.
Causes:
- After surgical repair of tetralogy of Fallot (the commonest significant cause in adults).
- Pulmonary hypertension.
- Endocarditis.
- Carcinoid disease.
Signs: Early diastolic murmur at the upper left sternal edge. In pulmonary hypertension this high-pitched murmur is called the Graham Steell murmur.
Management: Treat the cause and monitor RV size and function, usually with cardiac MRI. Pulmonary valve replacement (surgical or transcatheter) before irreversible RV dilatation or arrhythmias, particularly after Fallot repair.
4.29 Carcinoid Heart Disease
Mechanism: Neuroendocrine (carcinoid) tumours that have spread to the liver release serotonin directly into the hepatic veins and on to the right heart. Serotonin causes plaque-like fibrosis of the right-sided valves, making them thick, retracted and stiff. The lungs inactivate serotonin, so left-sided valves are usually spared, unless there is a lung tumour or a patent foramen ovale.
Clinical pattern:
- Carcinoid syndrome: Flushing, diarrhoea and wheeze.
- Cardiac involvement: Right heart failure from TR and pulmonary stenosis.
Diagnosis:
- Raised urinary 5-HIAA.
- Echo shows thickened, immobile tricuspid and pulmonary leaflets.
Management:
- Control hormone release with somatostatin analogues (e.g. octreotide).
- Diuretics for congestion.
- Valve surgery in selected patients, coordinated with the neuroendocrine tumour team.
Other unusual causes of valve thickening:
- Radiotherapy: Multivalve fibrosis and calcification years after mediastinal radiotherapy (e.g. for Hodgkin lymphoma).
- Serotonergic drugs: Historically pergolide, cabergoline and fenfluramine.
💡 Clinical Pearl: Flushing and diarrhoea with right heart failure and a TR murmur is carcinoid heart disease.
4.30 Mixed and Multiple-valve Disease
- Mixed disease: Stenosis and regurgitation of the same valve, each distorting the measurement of the other.
- Multiple valves: Common in rheumatic disease (mitral plus aortic), and after radiation or with degenerative disease.
- How lesions mask each other:
- Severe MR reduces forward flow, lowering the AS gradient and making AS look milder.
- AR increases flow across a stenotic aortic valve, exaggerating the gradient.
- MS reduces forward flow and can hide coexisting severe AS.
- Assessment: Combine symptoms, gradients, leak volumes, stroke volume, ventricular and pulmonary responses, and multimodality imaging.
- Management: The Heart Team decides which lesion is causing the problem, whether to treat lesions together or in stages, and how much intervention is reasonable in frail patients.
4.31 Acute Valve Emergencies
General approach:
- ABCDE, ECG and monitoring, oxygen if hypoxic, IV access and bloods.
- Blood cultures if infection is possible.
- Urgent echo.
- Avoid giving large fluid volumes or vasoactive drugs until the haemodynamics are known.
Specific emergencies:
- Acute severe MR (papillary muscle rupture after MI, chordal rupture, endocarditis):
- Presentation: Flash pulmonary oedema and shock; the heart is a normal size and the murmur may be quiet.
- Management: Urgent echo and cardiothoracic referral; afterload reduction and mechanical support as a bridge to surgery.
- Acute severe AR (type A dissection, endocarditis):
- Presentation: Hypotension, pulmonary oedema and a short, soft diastolic murmur.
- Management: Emergency imaging and surgery. Avoid an intra-aortic balloon pump.
- Prosthetic valve thrombosis:
- Presentation: Acute breathlessness, shock or embolism. Often there is a history of low INR or missed warfarin; muffled prosthetic clicks may be noted.
- Management: Urgent echo, fluoroscopy or CT, and valve-centre management (surgery or thrombolysis).
- Infective endocarditis:
- Presentation: Fever, a new or changing murmur, emboli or heart failure.
- Management: Take three sets of blood cultures before antibiotics whenever it is safe to do so; urgent echo; endocarditis team.
- Decompensated severe AS (shock or pulmonary oedema):
- Management: Senior cardiology input; urgent TAVI, surgery or bridging balloon valvuloplasty.
⚠️ Safety Pearl: Sudden pulmonary oedema with a new murmur after MI is a mechanical complication until proven otherwise. In acute regurgitation the murmur can be deceptively quiet.
4.32 Surgery versus Transcatheter Treatment
| Valve | Options |
|---|---|
| Aortic stenosis | SAVR: Open surgery; allows bypass grafting, other valve or aortic root surgery at the same time; mechanical valve possible in younger patients. TAVI: No sternotomy, rapid recovery; consider pacemaker need, paravalvular leak, coronary access and durability. ESC 2025 favours TAVI for suitable tricuspid AS in patients aged 70 or over. |
| Mitral regurgitation | Surgical repair preferred for repairable primary MR. TEER (clip) for selected high-risk primary MR or persistent secondary MR. |
| Mitral stenosis | Balloon commissurotomy for favourable rheumatic anatomy; surgery otherwise. |
| Tricuspid regurgitation | Surgical repair (often with left-sided surgery); transcatheter repair or replacement for high-risk severe TR before advanced RV failure. |
| Pulmonary stenosis | Balloon valvuloplasty for valvular PS. |
The Heart Team's decision takes into account:
- Frailty and comorbidity.
- Expected valve lifespan versus patient life expectancy.
- Endocarditis risk and coronary anatomy.
- Whether future procedures (e.g. a valve-in-valve TAVI) will be possible.
- Whether the patient can take anticoagulation safely.
- The patient's own priorities.
4.33 Mechanical and Biological Valves
| Feature | Mechanical | Biological (tissue) |
|---|---|---|
| Durability | Lifelong | Degenerates, typically after 10–20 years (faster in the young and in CKD) |
| Anticoagulation | Lifelong warfarin (VKA) | Usually not needed long term unless there is another reason (e.g. AF) |
| Usually chosen for | Younger patients who can take warfarin safely | Older patients, women planning pregnancy, high bleeding risk, poor adherence |
| Examination | Audible metallic click | No click; normal heart sounds |
Other points:
- TAVI valves are biological. They can thrombose, leak around the edge, degenerate and become infected, so they need imaging follow-up.
- Choosing a valve also depends on occupation, lifestyle, bleeding risk and whether a later valve-in-valve procedure is feasible.
- After mitral repair with an annuloplasty ring, short-term antithrombotic treatment may be needed according to local protocol.
💡 Clinical Pearl: A muffled or absent mechanical valve click in a breathless patient suggests valve thrombosis — check the INR and arrange an urgent echo.
4.34 Anticoagulation and Valves
- Mechanical valves:
- Lifelong warfarin (VKA). DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) must never be used — they caused excess valve thrombosis and stroke in trials.
- INR target: Depends on valve type, position and patient risk. Typically about 2.5 for aortic and 3.0 for mitral mechanical valves; always use the target set by the cardiology team.
- Moderate or severe rheumatic MS with AF: Warfarin, not a DOAC.
- Other native valve disease with AF (including AS, MR and bioprosthetic valves after the early period): Anticoagulate as for ordinary AF; DOACs are acceptable.
- Surgical bioprosthetic valve: Early warfarin or antiplatelet therapy depending on valve position, rhythm, bleeding risk and local policy; long-term anticoagulation only if there is another indication such as AF.
- TAVI:
- No other indication for anticoagulation: Single antiplatelet therapy (usually aspirin 75 mg daily). Routine dual antiplatelet therapy is not needed.
- AF or another indication: Continue the anticoagulant alone; avoid adding antiplatelets unless there is a specific reason such as recent PCI.
- Patient education:
- Signs of bleeding and of valve thrombosis.
- Drug and food interactions with warfarin.
- Planning around dental work and surgery.
- Pregnancy planning.
- What to do about missed doses.
💡 MRCP Pearl: Mechanical valve + DOAC is a dangerous prescribing error. Even if the patient also has AF and was previously on a DOAC, a mechanical valve needs warfarin.
4.35 Prosthetic Valve Complications
- Valve thrombosis:
- Effect: Obstruction (high gradient, stuck leaflet) or leak; presents with acute breathlessness, shock or embolism.
- Action: Check the INR history.
- Pannus: Fibrous tissue slowly growing over a mechanical valve, causing gradual obstruction. TOE, CT or fluoroscopy distinguish it from thrombus.
- Structural valve deterioration: Biological valves gradually stiffen (stenosis) or tear (regurgitation).
- Paravalvular leak:
- Effect: A leak around the sewing ring causes heart failure or haemolytic anaemia (red cells shredded by the jet).
- Warning sign: A new severe leak suggests endocarditis or valve dehiscence.
- Prosthetic valve endocarditis: High risk of abscess, dehiscence and emboli. Managed by the endocarditis team, often with surgery.
- Investigations:
- Compare with the post-operative baseline echo.
- TOE or 3D echo, gated CT and fluoroscopy.
- Blood cultures, FBC, LDH and haptoglobin (for haemolysis).
4.36 Infective Endocarditis
High-risk patients:
- Prosthetic valves, including TAVI.
- Previous endocarditis.
- Some congenital heart disease.
Good dental and skin hygiene matters more than antibiotics before procedures.
When to suspect it:
- Fever with a new or changing murmur.
- Positive blood cultures.
- Heart failure.
- Embolic events (stroke, splinter haemorrhages, Janeway lesions).
- Immune phenomena (Osler nodes, Roth spots, haematuria).
- Back pain (discitis).
Work-up:
- Three sets of blood cultures from separate sites before antibiotics, if the patient is stable enough to wait.
- TTE, and usually TOE, especially with prosthetic valves or suspected complications.
- Diagnosis is made using the modified Duke criteria.
Antibiotic prophylaxis:
- NICE CG64: Antibiotic prophylaxis is not recommended routinely for dental or other procedures.
- High-risk patients: Individual decisions follow UK implementation advice (SDCEP) and shared decision-making, not a blanket rule.
Patient advice: Seek prompt review for unexplained persistent fever, keep good oral hygiene, and get dental and skin infections treated early.
Treatment: Prevention advice is different from treating established endocarditis, which needs prolonged IV antibiotics guided by cultures and early surgical assessment.
💡 Clinical Pearl: "Fever + murmur = endocarditis until proven otherwise." Do not give oral antibiotics to a febrile patient with a prosthetic valve before taking blood cultures.
4.37 Valve Disease in Pregnancy
Why pregnancy is a stress test: Blood volume rises by about 50%, heart rate and cardiac output rise, and there are large fluid shifts during labour and after delivery. Stenotic lesions tolerate this poorly; regurgitant lesions usually tolerate it better.
High-risk lesions:
- Severe symptomatic MS or AS.
- Severe pulmonary hypertension.
- Severe regurgitation with LV dysfunction.
- Mechanical valves.
Before conception: Joint cardiology and obstetric review, with valve intervention first where indicated.
Rheumatic MS: Worsened by the rising heart rate and volume. Beta blockers and diuretics help; balloon commissurotomy can be performed in pregnancy for severe disease.
Mechanical valves: The hardest problem.
- Warfarin crosses the placenta and can cause embryopathy, especially in weeks 6–12.
- Low-molecular-weight heparin carries a higher risk of valve thrombosis for the mother.
- Specialist anticoagulation planning throughout pregnancy is essential.
Drugs to avoid: ACE inhibitors, ARBs, ARNIs and others are contraindicated in pregnancy — check each drug.
4.38 Non-cardiac Surgery
- Assess before surgery:
- Valve severity, symptoms, LV and RV function, and pulmonary pressure.
- The urgency and size of the operation.
- Anticoagulation.
- Severe symptomatic AS: High risk of hypotension and ischaemia under anaesthesia; consider valve treatment before elective major surgery.
- MS: Avoid tachycardia and fluid overload, both of which raise left atrial pressure.
- Regurgitant lesions: Usually better tolerated. Anaesthetic goals depend on whether the lesion is acute or chronic and on ventricular function.
- Mechanical valves: Interrupting warfarin and bridging with heparin is a specialist decision, balancing valve thrombosis against bleeding.
- Practical: In the notes, record the lesion, the date of the most recent echo, functional class, the anticoagulation plan and the cardiology and anaesthetic plan — not just "murmur".
4.39 Medical Treatment: AF and Heart Failure
Drugs relieve symptoms and treat complications, but they do not fix a severe structural lesion. Intervention is usually needed.
- Heart failure: Diuretics for congestion; standard HFrEF therapy for a weak ventricle.
- AF: Common with MS, MR and TR. Rate control relieves symptoms, especially in MS. Anticoagulation depends on the valve lesion (warfarin for mechanical valves and moderate or severe rheumatic MS) and the usual AF risk assessment.
- AS: Treat hypertension and congestion gently, avoiding sudden drops in blood pressure.
- AR and MR: Vasodilators and heart failure drugs can help, but symptom relief does not mean the lesion has improved.
- Endocarditis: Antibiotics treat the infection, but urgent surgery may be needed for acute severe regurgitation, abscess, uncontrolled infection or a high embolic risk.
- Shared decisions: Consider quality of life, frailty and patient preferences. Age alone should not exclude a patient from intervention.
4.40 Drug Reference Table
These are typical adult doses for treating symptoms, AF, hypertension or heart failure in valve disease. They do not correct the valve lesion. Adjust for renal function, heart rate, blood pressure and pregnancy, and check the BNF.
| Drug | Usual adult dose / purpose |
|---|---|
| Furosemide (oral) | 20–40 mg once daily initially for congestion; titrate to response, renal function and electrolytes. |
| Furosemide (IV) | 20–40 mg IV if diuretic-naive in acute congestion; higher if already on a loop diuretic. Monitor BP, urine output and U&E. |
| Bumetanide | 0.5–1 mg orally daily initially; titrate to congestion. |
| Bisoprolol | Rate control or HFrEF: 1.25 mg daily initially in HFrEF, titrated to 10 mg daily if tolerated. |
| Digoxin | 62.5–125 micrograms daily (older or renally impaired patients) for AF rate control; monitor level and renal function. |
| Ramipril | Hypertension or HFrEF: 1.25–2.5 mg daily initially, titrated to 5 mg twice daily; check BP, potassium and creatinine. |
| Spironolactone | 12.5–25 mg daily for HFrEF or congestion; check potassium and renal function. |
| Dapagliflozin / empagliflozin | 10 mg once daily for eligible heart failure, with or without diabetes; sick-day rules. |
| Warfarin | No fixed dose — titrate to the individual INR target for mechanical valves or rheumatic MS with AF. |
| Apixaban | AF with non-mechanical valve disease: 5 mg twice daily; 2.5 mg twice daily only if two of: age ≥80, weight ≤60 kg, creatinine ≥133 µmol/L. Never for mechanical valves. |
| Aspirin | 75 mg daily as single antiplatelet therapy after TAVI if no anticoagulation is needed. |
| Amoxicillin | Not routine endocarditis prophylaxis. Any prophylaxis in high-risk patients follows individual assessment and UK implementation advice. |
⚠️ Safety: No DOACs with mechanical valves. Warfarin dosing is INR-led. Rate-limiting drugs can cause bradycardia and hypotension. Diuretics and RAAS blockers need blood monitoring.
4.41 Spot the Diagnosis
| Clue | Think of |
|---|---|
| Ejection systolic murmur to carotids, slow-rising pulse, soft A2 | Aortic stenosis |
| Exertional syncope in an older person with a systolic murmur | Severe AS — urgent echo |
| Early diastolic murmur, collapsing pulse, wide pulse pressure | Aortic regurgitation |
| Chest pain to the back plus new early diastolic murmur | Aortic dissection with AR |
| Loud S1, opening snap, mid-diastolic rumble, AF | Mitral stenosis (rheumatic) |
| Apical pansystolic murmur to axilla, displaced apex | Mitral regurgitation |
| Mid-systolic click and late systolic murmur | Mitral valve prolapse |
| Pansystolic murmur louder on inspiration, giant V waves | Tricuspid regurgitation |
| Systolic murmur louder on standing | HCM (not AS) |
| Young adult with AS, radio-femoral delay | Bicuspid valve with coarctation |
| Flushing, diarrhoea, TR and pulmonary stenosis | Carcinoid heart disease |
| Fever, new murmur, splinter haemorrhages | Infective endocarditis |
| Mechanical valve, breathless, muffled clicks, low INR | Prosthetic valve thrombosis |
| Anaemia with raised LDH after valve surgery | Paravalvular leak with haemolysis |
4.42 MRCP Traps
- 1. Murmur intensity: Severe AS with low output and acute severe MR or AR can have quiet murmurs.
- 2. Low gradient: Does not exclude severe AS in a low-flow state — check the stroke volume and EF.
- 3. EF in MR: An EF below 60% in chronic severe MR already means LV impairment.
- 4. Tachycardia in MS: Shortens filling time; rate control is a key treatment.
- 5. AS treatment: Symptomatic severe AS needs valve replacement; drugs cannot remove calcium.
- 6. Acute versus chronic: A normal-sized heart does not exclude acute severe regurgitation.
- 7. Anticoagulation: Mechanical valve → warfarin for life. Rheumatic MS with AF → warfarin. Never a DOAC with a mechanical valve.
- 8. Valve choice: Biological avoids warfarin but wears out; mechanical lasts but needs warfarin.
- 9. Right heart: Massive TR may have little murmur but severe congestion; refer before liver and kidney damage.
- 10. Endocarditis prophylaxis: Not routine for dental work (NICE CG64); good oral health matters most.
- 11. Exertional syncope with a systolic murmur: Urgent echo within 2 weeks, not a routine appointment.
- 12. Multiple lesions: MR can mask AS gradients — assess the whole circulation.
- 13. IABP: Contraindicated in significant AR.
4.43 Exam-style Scenarios
Decide your answer before reading on.
- 1. An 82-year-old man has two episodes of dizziness while walking uphill. He has an ejection systolic murmur radiating to the carotids and a soft S2. Answer: Likely severe AS with exertional syncope. Urgent echo and specialist referral within 2 weeks; if severe, Heart Team review for TAVI or SAVR. Do not exercise-test him.
- 2. A 74-year-old woman with heart failure and EF 30% has AS with a valve area of 0.8 cm² but a mean gradient of only 22 mmHg. Answer: Classical low-flow, low-gradient AS. Arrange a low-dose dobutamine stress echo to distinguish true severe from pseudo-severe AS; consider a CT calcium score.
- 3. A 32-year-old woman from Pakistan, 28 weeks pregnant, becomes increasingly breathless with new AF. There is a mid-diastolic rumble at the apex. Answer: Rheumatic MS unmasked by pregnancy and tachycardia. Rate control (beta blocker), cautious diuretics, anticoagulation with LMWH in pregnancy, and specialist review; balloon commissurotomy if severe and refractory.
- 4. A 55-year-old man with asymptomatic severe primary MR from a flail posterior leaflet has an EF of 58% and an LV end-systolic diameter of 47 mm. Answer: Refer for mitral valve repair: EF below 60% and LVESD above 45 mm both meet the NICE criteria despite no symptoms.
- 5. A patient with a mechanical mitral valve and AF asks to switch from warfarin to apixaban. Answer: No. DOACs are contraindicated with mechanical valves; continue warfarin to the target INR (typically about 3.0 for mitral).
- 6. A 45-year-old man develops sudden severe breathlessness and hypotension. He has had fever for 2 weeks. There is a short early diastolic murmur, but his pulse pressure is not wide. Answer: Acute severe AR from endocarditis. Blood cultures, urgent echo and emergency cardiothoracic referral. Avoid an intra-aortic balloon pump.
- 7. A man with liver metastases from a small-bowel tumour has flushing, ankle oedema and a pansystolic murmur louder on inspiration. Answer: Carcinoid heart disease with TR. Check urinary 5-HIAA and do an echo; start a somatostatin analogue; refer to the cardiac and neuroendocrine teams.
4.44 Key Points
- 1. Stenosis = pressure load (hypertrophy); regurgitation = volume load (dilatation).
- 2. Time every murmur against the carotid pulse; diastolic murmurs are always pathological.
- 3. AS triad: breathlessness, angina, exertional syncope. After symptoms appear, survival without replacement is 2–3 years.
- 4. Severe AS: peak velocity ≥4 m/s, mean gradient ≥40 mmHg, valve area ≤1.0 cm² — but watch for low-flow states.
- 5. TAVI is increasingly used for older patients; SAVR for younger patients, bicuspid valves and combined surgery.
- 6. Chronic AR and MR: operate on LV size and function, not just symptoms.
- 7. MS: heart rate is everything — rate control, warfarin for AF, balloon commissurotomy for suitable valves.
- 8. Primary MR: repair rather than replace; secondary MR: treat the heart failure first.
- 9. Right-sided murmurs get louder on inspiration.
- 10. Mechanical valve = lifelong warfarin; never a DOAC.
- 11. Fever + murmur = blood cultures before antibiotics.
- 12. Antibiotic prophylaxis for dental work is not routine (NICE CG64).
4.45 NICE and ESC Guidelines
- NICE NG208 — Heart valve disease presenting in adults: referral, intervention criteria and surveillance.
- 2025 ESC/EACTS Valvular Heart Disease Guidelines: imaging, Heart Team, surgical and transcatheter management.
- NICE CG64 — Prophylaxis against infective endocarditis.
- SDCEP — Infective endocarditis implementation advice: high-risk dental decision-making.
- NICE NG106 — Chronic heart failure.
- NICE NG196 — Atrial fibrillation.
- BNF: prescribing, renal adjustment and interactions.
📌 Guideline note: NICE NG208 sets UK referral and intervention thresholds; the 2025 ESC/EACTS guideline gives more recent European procedural advice. Where their numbers differ, follow local Heart Team policy.