Aortic Regurgitation

Acute AR

Infective endocarditis

• Causes leaflet perforation, rupture, or paravalvular abscess formation.
• Vegetations can obstruct cusp closure, producing acute severe regurgitation.

Aortic dissection

• Impairs leaflet coaptation by dilating the sinuses of Valsalva, disrupting commissural support, extending into a leaflet base, or prolapsing into the left ventricular outflow tract.

Trauma

• Blunt chest injury or rapid deceleration may rupture valve leaflets.

Iatrogenic injury

• Occurs after balloon valvuloplasty, transcatheter aortic valve implantation (TAVI), or surgical interventions.

Congenital cusp rupture

• Rupture of congenitally fenestrated cusps can suddenly precipitate acute AR.

Prosthetic valve dysfunction

• Includes bioprosthetic degeneration, mechanical valve thrombosis or pannus formation, leaflet escape in older models, or paravalvular dehiscence, often secondary to endocarditis or connective tissue aortopathy.

Chronic AR

Valvular pathology

• Includes rheumatic heart disease, congenital malformations (commonly bicuspid valve, less often unicuspid or quadricuspid), myxomatous degeneration, and senile calcification.

Aortic root disorders

• Degenerative age-related dilation, systemic hypertension–related ectasia, Marfan syndrome, Ehlers–Danlos syndrome, bicuspid aortopathy, syphilitic aortitis, giant cell arteritis, Takayasu arteritis, and Behçet disease.

Systemic and autoimmune conditions

• Osteogenesis imperfecta, Crohn disease, Whipple disease, systemic lupus erythematosus, rheumatoid arthritis, psoriatic arthritis, relapsing polychondritis, and reactive arthritis.

Drug-induced valvulopathy

• Reported with dopamine agonists (e.g., bromocriptine) and ergot derivatives.

Hypertension

• Associated with aortic root enlargement at commissural attachment sites, although its causal role is debated.

Congenital and Genetic Associations

• Turner syndrome is linked with AR ranging from trivial to severe; observational data suggest up to 15% of patients may develop moderate to severe regurgitation.

Epidemiological Observations

• In surgical cohorts, chronic AR is most often caused by aortic enlargement of uncertain origin or bicuspid valve malformation.
• Acute AR requiring urgent valve replacement is usually due to infective endocarditis or aortic dissection.

Acute Aortic Regurgitation

• The left ventricle (LV) is suddenly subjected to an increased diastolic volume without time for compensatory dilation.
• End-diastolic pressure rises abruptly, leading to elevation of left atrial and pulmonary venous pressures, with pulmonary oedema as a frequent consequence.
• Forward stroke volume declines because the LV cannot acutely augment total output. This is further compounded by tachycardia and premature mitral valve closure, both of which reduce diastolic filling time.
• The clinical result is hypotension, cardiogenic shock, and in severe cases, acute heart failure with myocardial ischaemia due to impaired coronary perfusion.
• These haemodynamic changes are more pronounced in patients with small, non-compliant ventricles, such as those with pre-existing hypertrophy from systemic hypertension or prior aortic stenosis.
• Without urgent intervention, acute AR carries high mortality; surgical correction is particularly urgent in the setting of aortic dissection or prosthetic valve dysfunction.

Chronic Aortic Regurgitation

• Chronic AR produces a persistent volume overload, which drives both eccentric hypertrophy (sarcomere addition in series) and chamber dilation.
• According to Laplace’s law, wall tension rises with increasing ventricular pressure and radius; hypertrophy develops as a compensatory mechanism to normalise wall stress.
• The LV maintains a near-normal forward stroke volume for many years despite regurgitation, as chamber enlargement increases diastolic compliance and preserves ejection fraction in the early stages.
• Systolic hypertension often develops due to the increased stroke volume (sum of regurgitant and forward flow).
• Over time, progressive dilation and interstitial fibrosis reduce compliance, leading to a fall in ejection fraction, rise in LV end-systolic and end-diastolic volumes, and ultimately symptomatic heart failure.
• As end-diastolic pressure increases, coronary perfusion pressure falls, contributing to subendocardial ischaemia, myocardial necrosis, and apoptosis. Morphologically, the LV remodels from an elliptical to a spherical configuration.

Determinants of Severity

• The degree of regurgitation is governed by three main factors:
  • The effective regurgitant orifice area.
  • The diastolic pressure gradient between the aorta and LV.
  • The duration of diastole (which is shortened in tachycardia).
• Together, these variables determine regurgitant volume and subsequent haemodynamic burden.

Clinical Consequences

• In acute AR, haemodynamics deteriorate rapidly with pulmonary oedema and shock.
• In chronic AR, patients often remain asymptomatic for decades until the compensatory mechanisms fail, at which point heart failure symptoms and irreversible LV dysfunction emerge. The optimal timing of valve replacement is critical to prevent progression to permanent myocardial injury.

Prevalence in Population-Based Studies

• Aortic regurgitation (AR) is less common than aortic stenosis or mitral regurgitation. Its prevalence and severity vary by age, sex, geography, and underlying risk factors.
• In the Framingham Heart Study, the prevalence of AR of any severity was 13% in men and 8.5% in women.
• Moderate or severe AR was identified in about 0.5% of the general US population.
• Prevalence increases with age, peaking in the fifth and sixth decades, and reaching around 2% in people over 70 years.
• Severe AR remains uncommon, affecting less than 1% of the general population.

Sex and Racial Differences

• Men have a higher prevalence of AR than women, whereas women more frequently present with aortic stenosis when bicuspid valves are involved.
• African-American populations show a prevalence of approximately 15–16%, slightly higher than in white cohorts.
• Male predominance may be related to higher frequency of conditions such as bicuspid aortic valve and Marfan syndrome in men.

Aetiology and Geographic Variation

• In industrialised nations, congenital bicuspid valve and degenerative processes are the leading causes, with most cases identified between 40 and 60 years of age.
• In developing countries, rheumatic heart disease and infective endocarditis remain major contributors, and AR tends to occur in younger patients, often with a rapid clinical onset.

Age-Related Trends

• Chronic AR most commonly begins in the late 50s and is seen most frequently in patients over 80 years of age.
• While severe chronic AR is uncommon before age 70, patients with bicuspid aortic valve or connective tissue disorders such as Marfan syndrome may develop AR earlier in life.

Bicuspid Aortic Valve and Morphology

• Registry data suggest men and women have similar distributions of bicuspid valve morphology.
• Men more often develop moderate to severe AR, whereas women more commonly present with stenotic disease.

Impact of Transcatheter Aortic Valve Replacement (TAVR)

• Paravalvular AR is a recognised complication of TAVR.
• Some degree of regurgitation occurs in up to 70% of cases, with moderate or severe AR reported in approximately 15%.

Acute Aortic Regurgitation

• Presentation is typically abrupt, with severe dyspnoea, rapidly progressive pulmonary oedema, and acute left-sided heart failure.
• Chest pain may occur if coronary perfusion is compromised or in association with acute aortic dissection.
• Patients may also report cough, palpitations, orthopnoea, or paroxysmal nocturnal dyspnoea.
• Clinical deterioration is rapid and often progresses to hypotension or cardiogenic shock without urgent treatment.

Chronic Aortic Regurgitation

• Many patients remain asymptomatic for years because ventricular dilation and tachycardia maintain forward stroke volume.
• Left ventricular dysfunction can occur silently; up to 25% of patients may develop systolic impairment before symptoms.
• Once symptomatic, over one-quarter of patients with previously asymptomatic LV dysfunction progress within one year, with mortality exceeding 10% annually if untreated.

Symptoms of Chronic Severe AR

Palpitations

• Often described as “pounding” or “forceful” heartbeats due to widened pulse pressure and hyperdynamic circulation.

Awareness of heartbeat

• Frequently troublesome when lying down.

Exertional dyspnoea

• Early in the disease may be absent due to shortened diastole from tachycardia; later becomes more prominent as LV dysfunction advances.

Orthopnoea and paroxysmal nocturnal dyspnoea

• Reflect rising LV filling pressures and pulmonary congestion.

Chest pain

• Can occur even without coronary disease, caused by reduced coronary perfusion pressure; angina may worsen with exercise.

Fatigue and weakness

• Common late features of LV dysfunction.

Syncope

• An infrequent manifestation but recognised in advanced disease.

Sudden cardiac death

• Rare (<0.2% annually) in asymptomatic patients with preserved LV function, but risk rises once symptoms develop.

Risk Factors Elicited from the History

Bicuspid aortic valve

• Most common cause in developed countries.
• Associated with proximal aortic dilation and progressive worsening of AR.

Rheumatic fever

• Still a leading cause in developing regions.

Endocarditis

• May cause leaflet rupture, paravalvular leaks, or vegetations interfering with cusp closure.

Marfan syndrome and connective tissue disease

• Around 80% of patients present at a young age with AR; progressive aortic root dilation is the main mechanism.

Aortitis

• Causes include syphilis, Behçet’s disease, Takayasu arteritis, reactive arthritis, and ankylosing spondylitis, all of which weaken and dilate the aortic root.

Systemic hypertension

• Can contribute to aortic root dilation and impaired leaflet closure.

Older age

• Associated with degenerative valvular changes and increased prevalence of AR.

Acute Aortic Regurgitation

• Physical signs are often dominated by features of cardiogenic shock rather than classical findings of AR.
• Patients may appear gravely ill with profound hypotension, pallor, diaphoresis, tachycardia, cyanosis, and evidence of peripheral vasoconstriction.
• Pulmonary oedema is common, with basal lung crepitations and tachypnoea.
• Arterial pulse is rapid and of low amplitude; pulse pressure may be normal or reduced.
• The apex beat is usually not displaced and is not hyperdynamic.
• In cases caused by aortic dissection, there may be asymmetry of pulses and blood pressure between the arms, although this may not be detected in profound hypotension.

Heart Sounds and Murmurs in Acute AR

• S1 is often soft or absent, due to early closure of the mitral valve.
• A2 is diminished; P2 may be accentuated, reflecting pulmonary hypertension.
• An S3 gallop is common; S4 is typically absent.
• The diastolic murmur is low-pitched, early, and shorter than in chronic AR; best heard at the left sternal border with the patient leaning forward in expiration. It may be easily missed, particularly with a small diastolic gradient.
• A soft systolic murmur may accompany the diastolic murmur, creating a “to-and-fro” pattern at the cardiac base.
• An Austin Flint murmur may occasionally be heard, produced by regurgitant flow impinging on the mitral apparatus, though it is typically brief and lower pitched than in chronic AR.
• A murmur at the right sternal border is particularly suggestive of AR due to aortic dissection.

Chronic Aortic Regurgitation

• Findings are largely due to a widened pulse pressure, with systolic hypertension and a marked fall in diastolic pressure.
• Diastolic pressures often fall below 60 mmHg; pulse pressures may exceed 100 mmHg, especially in younger patients with compliant vessels.

Peripheral Signs of Chronic AR

Corrigan (Water-hammer) Pulse

• Rapid rise and sudden collapse of the arterial pulse, best felt in large arteries such as the carotids.

de Musset’s Sign

• Rhythmic head nodding in time with the heartbeat.

Quincke’s Sign

• Capillary pulsations visible in the nail beds or lips with light pressure.

Traube’s Sign

• “Pistol-shot” systolic and diastolic sounds over the femoral arteries.

Duroziez’s Sign

• Systolic and diastolic murmurs heard over the femoral artery with proximal and distal compression.

Müller’s Sign

• Visible pulsation of the uvula.

Becker’s Sign

• Retinal arteriolar pulsations.

Hill’s Sign

• Popliteal systolic pressure exceeding brachial systolic pressure by more than 40–60 mmHg.

Other Described Signs

• Landolfi’s sign (alternating pupillary constriction and dilatation).
• Rosenbach’s sign (systolic pulsations of the liver).
• Gerhardt’s sign (pulsatile spleen).
• Lincoln’s sign (pulsatile popliteal artery).
• Mayne’s sign (fall in diastolic BP >15 mmHg when the arm is raised).
• Lighthouse sign (alternating blanching and flushing of the forehead).
• Palmar click (systolic pulsations felt in the palms).
• Embolic phenomena (in endocarditis-related AR) or skeletal/connective tissue features (in Marfan syndrome, spondyloarthropathy) may provide clues to the underlying cause.

Cardiac Examination in Chronic AR

• The apical impulse is displaced laterally and inferiorly, and is often diffuse and hyperdynamic.
• Peripheral pulses are bounding.
• A high-pitched, decrescendo, blowing diastolic murmur is typically heard best at the left sternal border, with severity correlating to murmur duration.
• A systolic flow murmur may also be present due to increased stroke volume.
• An Austin Flint murmur may be audible at the apex in severe AR, mimicking mitral stenosis.
• Additional findings may include an S3 gallop from LV dysfunction or occasionally an S4 from LV hypertrophy.

Echocardiography

• First-line and diagnostic for both acute and chronic AR.
• Transthoracic echocardiography (TTE) confirms AR, quantifies severity, and evaluates LV size, systolic function, and aortic root anatomy.
• Colour Doppler demonstrates diastolic backflow across the valve. Findings suggestive of severe AR include:
  • Vena contracta width >6 mm.
  • Jet width ≥65% of LV outflow tract diameter (for central jets).
  • Holodiastolic flow reversal in the descending thoracic or abdominal aorta.
• Continuous-wave Doppler: severe AR produces a dense signal with steep deceleration slope, pressure half-time <200 msec, and rapid equalisation of LV and aortic diastolic pressures.
• Pulsed-wave Doppler: holodiastolic flow reversal in the descending aorta indicates severe regurgitation.
• M-mode/2D imaging: may show premature mitral valve closure (in severe acute AR), diastolic fluttering of the anterior mitral leaflet, or hyperdynamic interventricular septal motion.
• Transoesophageal echocardiography (TEE): superior to TTE for detecting vegetations in infective endocarditis and for confirming aortic dissection; intraoperative TEE is valuable in guiding surgical planning.

Other Imaging Modalities

Computed Tomography (CT)

• Preferred in acute AR when aortic dissection is suspected, given wide availability and rapid acquisition.
• Defines the site of intimal flap entry, extent of dissection, and involvement of branch vessels.
• Used more often than TEE in unstable patients.

Magnetic Resonance Imaging (MRI)

• Highly accurate for quantifying regurgitant volume and effective orifice area.
• Provides detailed measurement of LV dimensions, systolic/diastolic volumes, and function.
• Most useful for serial assessment in chronic AR when echocardiography is suboptimal; limited in acute settings due to availability and monitoring challenges.

Chest Radiography

• In chronic AR may reveal cardiomegaly from LV dilatation, and a prominent aortic knob in hypertensive or aortic root disease.
• Calcification of the aortic valve is uncommon in isolated AR but may be seen with mixed valve disease.

Electrocardiography (ECG)

• Provides supportive but non-specific information.
• Chronic AR: may show LV hypertrophy with left axis deviation, non-specific ST-T changes, or later conduction delays.
• Acute AR: sinus tachycardia, arrhythmias, or ST-T changes consistent with ischaemia.
• Infective endocarditis may cause conduction abnormalities from paravalvular abscess.

Cardiac Catheterisation

• Rarely used to establish diagnosis in acute AR due to urgency of surgical management.
• Coronary angiography is indicated in patients at risk for coronary artery disease before valve surgery.
• Aortography can confirm AR and assess dissection or root dilatation when non-invasive imaging is inconclusive.

Radionuclide Angiography

• Alternative non-invasive method when echocardiography is inadequate.
• Useful for quantifying ejection fraction, regurgitant fraction, and monitoring early systolic dysfunction.

Exercise Stress Testing

• Not diagnostic but employed in chronic AR to unmask symptoms and assess functional capacity when clinical history is equivocal.

Acute Coronary Syndrome / Myocardial Infarction

• May present with chest pain, dyspnoea, and features of left ventricular dysfunction similar to AR.
• ECG abnormalities and troponin elevation are typical distinguishing findings.
• AR itself can exacerbate ischaemia by reducing diastolic coronary perfusion.

Heart Failure

• Produces symptoms of dyspnoea, orthopnoea, fatigue, and pulmonary oedema, overlapping with AR.
• Echocardiography is required to identify AR as the underlying cause by demonstrating regurgitant flow and LV dilatation.

Infective Endocarditis

• May mimic or precipitate AR through cusp perforation, leaflet destruction, or paravalvular abscess.
• Clinical hallmarks include fever, systemic embolic phenomena, and a new diastolic murmur.
• Echocardiography is crucial for detecting vegetations and valvular pathology.

Mitral Regurgitation (MR)

• Murmur is pansystolic, best at the apex, radiating to the axilla.
• Associated signs include right ventricular heave, soft S1, and loud P2.
• Imaging may reveal left atrial and ventricular enlargement, pulmonary oedema, and mitral valve calcification.
• Differentiated from AR by systolic murmur timing.

Mitral Stenosis (MS)

• Features include malar flush, low-volume pulse, tapping apex beat, loud S1 with opening snap, and mid-diastolic rumbling murmur.
• The murmur is best heard at the apex and differs from the Austin Flint murmur of severe AR by its opening snap and accentuated S1.
• Echocardiography confirms diagnosis.

Aortic Stenosis (AS)

• Presents with exertional dyspnoea, syncope, and angina.
• Signs include slow-rising pulse, heaving apex, and harsh ejection systolic murmur radiating to the carotids with an ejection click.
• ECG and imaging may demonstrate LV hypertrophy and calcified aortic valve.
• Distinguished from AR by radiation pattern and presence of ejection click.

Pulmonary Regurgitation (PR)

• Produces a diastolic murmur at the second and third left intercostal spaces, accentuated with inspiration.
• A loud P2 is common in pulmonary hypertension.
• CXR may show pulmonary artery dilatation and RV enlargement; ECG often demonstrates RV hypertrophy.
• Echocardiography is diagnostic.
• Differentiation from AR is aided by inspiratory augmentation in PR vs expiratory augmentation in AR.

Tricuspid Stenosis (TS)

• Presents with diastolic murmur at the lower left sternal border, associated with jugular venous distension and hepatomegaly.
• Differentiated from AR by right-sided signs of venous congestion and absence of wide pulse pressure.

Blunt Abdominal Trauma

• Rarely, traumatic AR occurs following severe chest or abdominal trauma.
• Sudden haemodynamic deterioration with a new diastolic murmur in trauma patients should raise suspicion.

General Approach

• Acute aortic regurgitation (AR) represents a surgical emergency, whereas chronic AR typically follows a protracted, often asymptomatic course.
• The therapeutic strategy is dictated by the acuity of presentation, severity of regurgitation, left ventricular (LV) function, symptom burden, and surgical candidacy.
• Definitive therapy in acute severe AR is urgent surgery, while chronic AR management balances surveillance, medical therapy, and elective surgery.

Acute Aortic Regurgitation

• Requires immediate stabilisation with airway management and intubation if necessary.
• Intravenous inotropes (e.g., dobutamine, dopamine) are used to augment cardiac output, alongside vasodilators such as sodium nitroprusside to reduce afterload and improve forward flow.
• Digoxin may be occasionally employed for rate control; however, beta blockers should generally be avoided due to their suppression of compensatory tachycardia.
• Intra-aortic balloon counterpulsation is contraindicated as it worsens regurgitation during diastole.
• Extracorporeal membrane oxygenation (ECMO) has been described as a temporising measure prior to surgery in unstable patients.
• Definitive treatment is urgent aortic valve replacement (AVR) or repair, especially in cases due to infective endocarditis or aortic dissection. In dissection, ascending aortic replacement may suffice if valve function is preserved.

Chronic Aortic Regurgitation

• Patients with mild to moderate, asymptomatic AR and preserved LV function generally require no intervention other than surveillance. Symptoms in these individuals are often attributable to other causes such as hypertension or coronary disease.
• In moderate AR, AVR may be considered when patients undergo cardiac surgery for other indications.
• Severe AR management is guided by LV function and dimensions:
  • Asymptomatic with preserved LV function (LVEF >55%, LVESD <50 mm): conservative management with regular follow-up; surgery only if undergoing another cardiac operation.
  • Asymptomatic with reduced LVEF (≤55%) or significant LV dilatation (LVESD >50 mm or indexed LVESD >25 mm/m²): AVR is indicated.
  • Symptomatic severe AR: surgery is recommended regardless of LV function.
  • ESC guidelines apply a lower intervention threshold, recommending surgery in asymptomatic patients with LVEF <50%.
• In those unsuitable for surgery due to prohibitive risk, guideline-directed medical therapy (GDMT) for reduced LVEF and hypertension is used. Vasodilators may offer symptomatic relief in selected patients, but there is no strong evidence for long-term medical therapy in non-severe AR.
• Longitudinal surveillance with echocardiography is vital, as LV dysfunction can occur before symptoms. The frequency of follow-up depends on LV dimensions, with intervals ranging from 3 months to 12 months depending on progression.

Surgical Options

• AVR is the most common procedure, while valve-sparing repair may be appropriate in specialised centres, especially when valve morphology is favourable.
• Postoperative prognosis correlates strongly with preoperative LV function; earlier intervention before irreversible dysfunction confers the best outcomes.
• Both mechanical and bioprosthetic valves are used:
  • Mechanical valves are durable but require lifelong anticoagulation.
  • Bioprosthetic valves avoid anticoagulation but are less durable and more likely to require reoperation.
  • Selection is individualised, taking into account patient comorbidity, lifestyle, and age.
• Patients with prosthetic valves require antithrombotic therapy and may also require antibiotic prophylaxis before high-risk procedures if they have prosthetic material, previous endocarditis, certain congenital lesions, or post-transplant valvulopathy.

Transcatheter Aortic Valve Replacement (TAVR)

• TAVR has a limited role in isolated AR because anchoring of the prosthesis is technically challenging in non-calcified annuli.
• It may be considered for high-risk or inoperable patients with severe AR and heart failure.
• In patients with AR after TAVR for aortic stenosis, interventions may include balloon post-dilation, valve repositioning, vascular plugs, or valve-in-valve implantation.

Lifestyle and Long-Term Care

• No AR-specific dietary restrictions exist, though salt restriction is useful in hypertensive or volume-overloaded patients.
• Patients with preserved LV function and no symptoms may continue normal activities, although isometric exercise is discouraged. Stress testing can help guide exercise tolerance in equivocal cases.
• Lifelong cardiology follow-up is required, as progressive LV enlargement and dysfunction may necessitate surgery even in the absence of symptoms.

Acute Aortic Regurgitation

• Severe acute AR, if untreated, carries a high risk of death due to haemodynamic collapse. The sudden imposition of regurgitant volume on a non-compliant LV leads to abrupt rises in LV end-diastolic and left atrial pressures, resulting in pulmonary oedema and reduced coronary perfusion gradients.
• This setting predisposes to myocardial ischaemia, arrhythmias, and sudden cardiac death.
• Early surgical intervention is essential; without it, mortality approaches 100%.

Chronic Aortic Regurgitation

• The natural course is more gradual, typically beginning with a long asymptomatic period. During this time, compensatory LV dilation maintains forward stroke volume.
• Event rates in conservatively managed severe chronic AR are: all-cause mortality around 4–5% per year, heart failure 6% per year, and aortic valve surgery 14–15% per year.
• The yearly risk of death stratified by functional class shows a steep gradient:
  • Asymptomatic: ~3%
  • NYHA class I: ~3%
  • NYHA class II: ~6%
  • NYHA class III–IV: >20%
• Once symptoms emerge, deterioration is usually rapid, with mortality exceeding 10% per year if surgery is not performed.

Prognostic Predictors

• The most powerful determinants of outcome are echocardiographic parameters: LV ejection fraction (EF) and LV end-systolic dimension (LVESD).
• Asymptomatic patients with preserved EF have a favourable outlook, with less than 6% annual risk of progression to symptoms or dysfunction, and less than 0.2% annual risk of sudden death.
• In asymptomatic patients with reduced EF, more than 25% develop symptoms within a year.
• LVESD indexed to body surface area and exercise-derived LV end-systolic volume index (LVESVi) provide additional prognostic information, even in patients with moderate AR.

Post-Surgical Outcomes

• Long-term outcomes after timely valve surgery are generally excellent when LV function is preserved.
• Five-year survival rates are reported at 90–96% for patients with normal preoperative LV function, compared with around 60% for those with reduced function.
• Improvement in LV size and EF is most likely if reductions in LV dilatation are seen early after surgery. Failure to improve EF in the first 6 months predicts poor late recovery.

Complications

• Progressive LV dysfunction and dilatation remain the main long-term risks in chronic AR.
• Other complications include heart failure, arrhythmias, myocardial ischaemia, and sudden death.
• Underlying causes may contribute further risks, such as dissection in patients with bicuspid aortic valve and dilated root, or systemic complications of infective endocarditis.

After Transcatheter Aortic Valve Replacement (TAVR)

• Moderate or severe residual AR after TAVR is associated with significantly increased morbidity and mortality compared with none or mild AR.
• Registry data indicate more than a doubling in mortality risk among patients with greater than mild AR post-procedure.

Coronary Artery Disease Interaction

• An inverse relationship has been observed between AR and coronary artery disease (CAD) in patients with rheumatic valve disease. AR appears to be less commonly associated with significant CAD compared with aortic stenosis, though the clinical relevance of this finding is debated.

Heart failure

• The most frequent long-term complication of chronic severe AR.
• Patients may initially remain asymptomatic, but progressive LV dilatation eventually results in decompensated heart failure.
• Symptom onset, impaired exercise tolerance, or reduced ejection fraction should prompt consideration for valve surgery.

Operative mortality

• Surgical valve replacement or repair carries a risk of early mortality, approximately 4% with isolated AVR and up to 7% when combined with coronary bypass surgery.
• Outcomes are significantly influenced by preoperative ventricular function and associated comorbidities.

Arrhythmias

• Structural remodelling of the left atrium predisposes to atrial fibrillation, presenting with palpitations, breathlessness, and sometimes syncope.
• The anatomical proximity of the aortic valve to the conduction system may also cause bradyarrhythmias or varying degrees of heart block, occasionally requiring pacemaker implantation.

Myocardial ischaemia

• Chest pain resembling angina may occur despite normal coronary arteries.
• This results from increased oxygen demand in the hypertrophied and dilated ventricle, coupled with reduced coronary flow reserve.

Sudden death

• Although uncommon in patients with preserved LV systolic function (annual risk around 0.4%), sudden cardiac death has been reported in those with severe ventricular dilatation even when ejection fraction is maintained.
• This underscores the importance of close monitoring of ventricular size in addition to function.

Infective endocarditis

• Structural abnormalities of the valve increase susceptibility to bacterial colonisation, though overall incidence is relatively low.
• Prophylactic antibiotics are no longer universally recommended, but remain advised in high-risk groups (e.g., prosthetic valves, prior endocarditis, selected congenital lesions).

Transcatheter aortic valve replacement (TAVR)-related complications

• Pure native AR has historically been a challenge for TAVR because anchoring is difficult without annular calcification.
• Registry data suggest risks include residual regurgitation, need for re-intervention or valve-in-valve implantation, conversion to open surgery, aortic root injury, conduction disturbances requiring permanent pacing, stroke, bleeding, vascular injury, and acute kidney injury.
• Although outcomes have improved with newer generation devices, robust evidence is still lacking to support routine TAVR use for isolated native AR.

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