Aortic regurgitation

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

AR results from leaflet failure, aortic-root dilatation or both. Chronic regurgitation allows adaptive LV enlargement and a large stroke volume; acute regurgitation abruptly raises LV diastolic pressure, impairing forward output and causing pulmonary oedema.

Assessment integrates mechanism, quantitative regurgitation, LV dimensions and function, aortic dimensions and symptoms. An apparently normal LVEF may already represent declining contractility in a volume-loaded ventricle, so trends matter.

Surgical repair or replacement is the definitive therapy for severe disease with symptoms or LV/aortic triggers. Transcatheter treatment is not the routine equivalent of TAVI for native pure AR and is reserved for selected inoperable patients at expert centres.

Key points

Chronic AR produces LV volume overload, eccentric dilatation and a wide pulse pressure; symptoms can appear late after prolonged compensation.
An early diastolic decrescendo murmur at the left sternal edge is typical; leaning forward in expiration can make it clearer.
Acute severe AR may have a short, soft murmur and normal pulse pressure because the LV has had no time to dilate.
Echo grades regurgitation using several measures; severe markers include vena contracta over 6 mm, regurgitant volume at least 60 mL/beat or EROA at least 0.30 cm2.
Symptomatic severe AR and severe AR with LV systolic impairment or excessive LV dilatation require valve-surgery assessment.
Measure the aortic root and ascending aorta: bicuspid valve, connective-tissue disease and dissection can determine the operation as much as the valve lesion.
Vasodilators treat coexisting hypertension or heart failure when surgery is not yet possible; they do not replace timely surgery in operable severe AR.
New dyspnoea, falling LVEF or rising LV end-systolic size during surveillance should trigger valve-team review before irreversible damage.

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

Primary leaflet disease

Bicuspid morphology, degenerative change, rheumatic disease or leaflet prolapse can prevent complete diastolic coaptation. Bicuspid disease also warrants assessment of the root and ascending aorta.

Aortic root dilatation

Hypertension, age-related aortic disease and heritable connective-tissue aortopathy can enlarge the annulus or root, pulling otherwise mobile leaflets apart and creating central regurgitation.

Infective endocarditis

Infection can perforate, tear or destroy a cusp and cause abrupt severe regurgitation. Fever, embolic features or positive cultures make this a time-critical cause rather than routine chronic valve disease.

Dissection, trauma or iatrogenic injury

An aortic dissection may disrupt commissural support, while trauma or a valve procedure can damage a leaflet. These causes often present acutely with pulmonary oedema or shock.

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

1
Diastolic backflow
Incomplete valve closure allows blood to return from the aorta into the LV during diastole. Severity depends on the regurgitant opening, pressure gradient and duration of diastole.
2
Chronic volume compensation
With gradual disease, the LV dilates eccentrically and increases total stroke volume to preserve forward flow. The large stroke volume and rapid diastolic run-off produce a wide pulse pressure.
3
Ventricular decompensation
Continuing volume load raises wall stress and eventually impairs contractility. Forward output falls while LV filling and pulmonary venous pressures rise, causing exertional limitation and heart failure.
4
Acute haemodynamic decompensation
In acute severe regurgitation, a non-dilated, relatively non-compliant LV cannot accommodate the sudden volume. Diastolic pressure rises sharply, may close the mitral valve early, and can cause pulmonary oedema, hypotension and shock.

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

Chronic compensated AR

A forceful displaced apex, collapsing pulse, wide pulse pressure and long early diastolic murmur reflect a large chronic regurgitant volume.

Chronic decompensation

Exertional breathlessness, reduced stamina, orthopnoea or angina indicates loss of compensation and prompts rapid reassessment.

Acute severe ARRed flag

Sudden pulmonary oedema, hypotension and tachycardia after endocarditis, dissection, trauma or iatrogenic injury may occur without classic peripheral signs.

Austin Flint murmur

A low-pitched mid-diastolic apical murmur can occur when a severe AR jet functionally impedes mitral inflow; it does not prove mitral stenosis.

Aortic disease cluesRed flag

Unequal pulses, tearing chest/back pain, connective-tissue phenotype or rapid aortic enlargement suggests associated aortopathy or dissection.

Endocarditis clues

Fever, new regurgitant murmur, embolic features or positive blood cultures require urgent endocarditis assessment and early surgical discussion.

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

Investigation order

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

01
Transthoracic echocardiographyFirst step
Why
Define mechanism, quantify AR, measure LV size/function and examine the aortic root.
Interpretation and limitations
Use an integrated assessment; severe features include vena contracta over 6 mm, regurgitant volume at least 60 mL, regurgitant fraction at least 50% or EROA at least 0.30 cm2.
02
Transoesophageal echocardiography
Why
Clarify mechanism, endocarditis, dissection complications or repair anatomy when TTE is limited.
Interpretation and limitations
Particularly valuable in acute severe AR, but should not delay emergency surgery when the diagnosis and instability are clear.
03
Cardiac MRI
Why
Quantify regurgitant fraction and LV volumes when echo is equivocal or discordant.
Interpretation and limitations
Serial CMR can provide reproducible ventricular volumes; interpret alongside symptoms and echo rather than as an isolated threshold.
04
ECG and chest radiograph
Why
Assess LV hypertrophy, rhythm, pulmonary oedema, cardiac size and aortic contour.
Interpretation and limitations
Chronic severe AR may show LV enlargement; acute severe AR can produce oedema without cardiomegaly.
05
CT or MR aortography
Why
Measure the thoracic aorta and diagnose suspected acute aortic syndrome.
Interpretation and limitations
An acute-dissection protocol is time-critical; aortic diameter, growth, genotype and family history guide combined aortic surgery.
06
Blood cultures and inflammatory tests when indicated
Why
Investigate infective endocarditis before antibiotics when the patient is stable enough for sampling.
Interpretation and limitations
Obtain multiple culture sets promptly; never delay antibiotics or surgery in septic shock for perfect sampling.

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

Pulmonary regurgitation

Its early diastolic murmur is usually loudest at the upper left sternal edge and may increase with inspiration. A high-pressure pulmonary regurgitation murmur can accompany pulmonary hypertension; echocardiography identifies the affected valve.

Mitral stenosis

A low-pitched apical mid-diastolic rumble with an opening snap supports mitral obstruction. An Austin Flint murmur from severe AR can mimic it, so valve imaging is decisive.

Patent ductus arteriosus

PDA produces a continuous, often machinery-like murmur around the left infraclavicular area rather than an isolated early diastolic murmur; Doppler demonstrates persistent aortopulmonary flow.

High-output or stiff-artery pulse pressure

Anaemia, thyrotoxicosis or marked arterial stiffness can widen pulse pressure and produce forceful pulses, but do not create holodiastolic aortic flow reversal or a regurgitant valve jet.

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

01acuteAcute severe aortic regurgitationFirst stepSudden severe AR causes pulmonary oedema, hypotension or shock.

1Use ABCDE care, continuous monitoring, urgent TTE/TOE and immediate cardiology, critical-care and cardiothoracic-surgical involvement.
2Search simultaneously for dissection, endocarditis, trauma or procedure complication; obtain blood cultures promptly if infection is plausible.
3Support oxygenation and perfusion in critical care; avoid reflex bradycardia and recognise that intra-aortic balloon counterpulsation is contraindicated because it worsens regurgitation.
4Proceed to emergency surgery when severe acute AR is confirmed and treat the cause; medical therapy is only a bridge.

02chronic-symptomaticSymptomatic chronic severe ARSevere AR is associated with breathlessness, reduced exercise tolerance, angina or heart failure.

1Confirm severity and LV/aortic measurements with expert echo, using CMR if quantification is discordant.
2Refer promptly to the valve team for surgery if operative benefit is expected; assess the coronary arteries and the entire thoracic aorta.
3Choose repair in selected expert-centre anatomy or valve replacement, adding root/ascending-aortic surgery when indicated.
4Use diuretics for congestion and treat hypertension while awaiting intervention, but do not let symptom relief postpone surgery.

03asymptomaticAsymptomatic severe AR surveillanceSevere AR is present without clear symptoms and LV function is preserved.

1Record baseline LVEF, LV end-systolic diameter and indexed size, LV volumes and aortic dimensions; ask about actual exercise capacity.
2EscalationUnder NICE NG208, consider referral for intervention when LVEF is less than 55%, LVESD is more than 50 mm or indexed LVESD is more than 24 mm/m2; also escalate for serial decline/dilatation or when the aorta itself meets an intervention threshold.
3If no trigger exists, monitor clinically and by echo every 6–12 months while intervention remains suitable; use the same measurement method where possible.
4Bring review forward for new symptoms, pregnancy planning, rapid aortic growth or a meaningful LV trend.

04hypertensionBlood-pressure and congestion managementDefinitiveChronic AR coexists with systolic hypertension or congestion while definitive timing is assessed.

1Measure BP accurately and treat persistent hypertension, generally with an ACE inhibitor/ARB or dihydropyridine calcium-channel blocker selected for the individual.
2If fluid overloaded, use a loop diuretic at the lowest effective dose and monitor renal function and electrolytes.
3Avoid deliberately slowing the heart excessively in severe AR because a long diastole can increase regurgitant volume; treat another compelling indication carefully.
4Reassess symptoms and LV response; medical control does not cancel a surgical trigger.

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

Treats coexisting hypertension or heart failure when appropriate; it does not correct the regurgitant valve.

Ramipril

For hypertension, usually 2.5 mg orally once daily initially; use 1.25 mg once daily when the renin–angiotensin system is strongly activated, then titrate at 2–4-week intervals to a maximum 10 mg/day.

Check creatinine and potassium before and 1–2 weeks after starting or titrating; avoid in pregnancy and previous ACE-inhibitor angioedema, and use caution in renal-artery stenosis.

Controls congestion while the cause and intervention timing are addressed.

Furosemide

For chronic oedema, 40 mg orally in the morning is a usual initial adult dose; maintenance may be 20 mg daily or 40 mg on alternate days, adjusted to response.

Monitor weight, BP, renal function, sodium and potassium; over-diuresis can cause hypotension and renal injury. It does not delay a surgical indication.

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

Progressive LV failure

Long-standing severe volume overload can cause increasing LV dilatation, fibrosis and systolic dysfunction. Symptoms and ejection-fraction decline may appear only after substantial remodelling, so serial trends matter.

Pulmonary oedema and shock

Acute severe AR abruptly raises LV and left-atrial pressure while reducing forward output, producing life-threatening pulmonary oedema, hypotension and multi-organ hypoperfusion.

Myocardial ischaemia and arrhythmia

Reduced aortic diastolic pressure can impair coronary perfusion while the enlarged LV has high oxygen demand. Angina may occur, and ventricular arrhythmia can complicate advanced LV dysfunction, although neither is specific to AR.

Progressive aortic disease

When root or ascending-aortic disease underlies regurgitation, continuing enlargement increases the risk of dissection or rupture and may determine the need for combined aortic surgery.

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

In asymptomatic severe AR suitable for intervention, review symptoms and repeat echocardiography every 6–12 months.
Trend LVEF and LV end-systolic diameter/index rather than acting on one borderline measurement.
Measure aortic root and ascending-aortic diameters consistently and shorten follow-up if growth accelerates.
Check BP at each review and renal function/electrolytes after ACE-inhibitor or diuretic initiation and dose changes.
Ask about exercise capacity, orthopnoea, nocturnal dyspnoea and angina; new symptoms override a previously reassuring schedule.
After intervention, monitor prosthetic or repaired-valve function, LV reverse remodelling and any residual aortic disease.

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

Acute AR looks different

Peripheral collapsing signs require time and a large stroke volume to develop. In acute severe AR the pulse pressure may be normal and the murmur short despite life-threatening haemodynamics.

LVEF can be misleadingly normal

Ejection into both aorta and low-pressure LV diastolic flow can preserve the percentage initially; serial LV end-systolic size helps identify failing compensation.

The aorta may drive treatment

Bicuspid valve and heritable aortopathy require systematic aortic measurement; combined aortic surgery may be indicated even when valve symptoms are modest.

IABP is harmful

Balloon inflation during diastole raises aortic diastolic pressure and can increase regurgitant flow, so it is contraindicated in significant AR.

Vasodilators are not definitive therapy

Afterload treatment is useful for hypertension or inoperable heart failure, but it has not replaced surgery for operable symptomatic severe disease.

Use more than jet area

Colour-jet appearance changes with gain, BP and direction; vena contracta, flow reversal, quantitative volume/fraction and ventricular response should agree.

11Common pitfallsFrequent interpretation and management errors.

01
Waiting for a wide pulse pressure before recognising acute severe AR.
02
Grading severity from colour-jet area alone.
03
Following LVEF without LV end-systolic size, serial trend or aortic dimensions.
04
Using symptom improvement on diuretics as a reason to postpone indicated surgery.
05
Using intra-aortic balloon counterpulsation in significant AR.