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Aortic Regurgitation

Clinical Subject Page

Aortic Regurgitation

Also called

leaky aortic valve

ICD-10

I35.1

Specialty

Cardiology

Onset

Acute & Chronic

Reviewed

June 2026

On This Page

Overview

Aortic regurgitation (AR), commonly known as a leaky aortic valve, is a condition in which the aortic valve does not close completely, allowing blood to flow backward from the aorta into the left ventricle during diastole

Etiology & Risk Factors

Acute Aortic Regurgitation

  • Infective endocarditis (most common valvular cause)
  • Ascending aortic dissection (most common aortic cause)
  • Chest trauma
  • Iatrogenic complications (e.g., after TAVR or balloon valvuloplasty)

Chronic Aortic Regurgitation

  • Congenital bicuspid aortic valve (most common cause in young adults in high-income countries)
  • Calcific aortic valve disease (most common cause in older adults in high-income countries)
  • Rheumatic heart disease (most common cause in lower-income countries)
  • Aortic root dilation due to:
    • Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
    • Chronic hypertension
    • Aortitis (e.g., tertiary syphilis)
    • Thoracic aortic aneurysm

Risk Factors

  • Congenital bicuspid aortic valve
  • Calcific aortic valve disease
  • Rheumatic heart disease
  • Chronic hypertension
  • Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
  • Thoracic aortic aneurysm
  • Infective endocarditis
  • Aortic dissection

Pathophysiology

    • Aortic valve fails to close completely → blood flows backward from the aorta into the left ventricle (LV) during diastole.
    • This causes volume overload of the LV, leading to:
      • Increased systolic blood pressure
      • Decreased diastolic blood pressure
      • Widened pulse pressure (water hammer pulse)

    Acute AR

    • The LV cannot dilate quickly enough to accommodate the regurgitant blood.
    • LV end-diastolic pressure rises rapidly → blood backs up into the lungs → pulmonary edema and dyspnea.
    • Severe cases can cause decreased cardiac output, cardiogenic shock, and myocardial ischemia.

    Chronic AR

    • Initially, the LV compensates by increasing stroke volume to maintain cardiac output.
    • Over time, persistent volume overload causes LV enlargement (dilation) and eccentric hypertrophy.
    • Eventually, LV systolic dysfunction develops, leading to left-sided heart failure.

    Flow summary:
    Incomplete aortic valve closure → Backflow into LV during diastole → LV volume overload → LV dilation & eccentric hypertrophy → LV dysfunction → Left heart failure (chronic)

Clinical Presentation

  1. Acute Aortic Regurgitation

    Symptoms

    • Sudden severe dyspnea
    • Pulmonary edema
    • Rapid heart failure/cardiac decompensation
    • Symptoms of the underlying cause:
      • Fever (infective endocarditis)
      • Chest pain (aortic dissection)

    Auscultation

    • Soft S1
    • Soft, short early diastolic murmur

    Chronic Aortic Regurgitation

    Symptoms

    • May be asymptomatic for years
    • Palpitations
    • Exertional dyspnea
    • Angina
    • Orthopnea
    • Easy fatigability
    • Syncope

    Signs

    • Widened pulse pressure
    • Water hammer pulse (bounding pulse)

    Auscultation

    • High-pitched, blowing, decrescendo early diastolic murmur (best heard along the left sternal border/Erb point in valvular AR)
    • S3 heart sound
    • Austin Flint murmur (in severe AR)

    Key features to remember

    • Wide pulse pressure + Water hammer pulse
    • High-pitched early diastolic murmur
    • Chronic AR can remain asymptomatic for many years before symptoms of left-sided heart failure develop.

History Taking

  • “Do you get short of breath, especially when walking or exercising?”
  • “Do you have chest pain or discomfort?”
  • “Do you notice your heart racing or pounding (palpitations)?”
  • “Do you feel unusually tired or fatigued?”
  • “Do you feel short of breath when lying flat or wake up at night short of breath?”
  • “Have you ever fainted or felt dizzy?”
  • “When did your symptoms start? Were they sudden or gradual?”
  • “Have you had a recent fever or heart infection?” (suggestive of infective endocarditis)
  • “Have you had sudden severe chest pain?” (suggestive of aortic dissection)
  • “Have you ever been told you have a heart murmur or valve disease?”
  • “Do you have a history of rheumatic fever, high blood pressure, or a connective tissue disorder (e.g., Marfan syndrome)?”
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Aortic Stenosis Vs Aortic Regurgitation

Valvular Heart Disease · Aortic Stenosis vs Aortic Regurgitation

Aortic Stenosis (AS)
Obstruction to LV outflow → pressure overload → concentric LVH. Most common cause: calcific degeneration in elderly (>65 yrs) or bicuspid aortic valve in younger patients.
Aortic Regurgitation (AR)
Backflow from aorta into LV → volume overload → eccentric LVH + LV dilatation. Causes: aortic root dilatation, bicuspid valve, rheumatic fever, endocarditis, Marfan syndrome.
Parameter Aortic Stenosis Aortic Regurgitation
Pathology Narrowed aortic valve orifice → LV must generate high pressure to eject blood (pressure overload) Incompetent aortic valve → blood regurgitates back into LV during diastole (volume overload)
LV Response Concentric hypertrophy — wall thickens, cavity size normal or reduced Eccentric hypertrophy — wall thickens AND cavity dilates (Laplace law)
Onset Usually chronic & insidious (years of compensated disease before symptoms) Can be chronic (insidious) or acute (endocarditis, aortic dissection — surgical emergency)
Classic Triad / Symptoms
Syncope Angina Dyspnea
SAD triad — appear in this order as severity progresses. Syncope on exertion is a red flag.
Exertional dyspnea Palpitations Angina
Long asymptomatic phase. Symptoms indicate LV decompensation. Acute AR: flash pulmonary edema.
Pulse Pulsus parvus et tardus — small volume, slow-rising, delayed peak Corrigan's (water-hammer) pulse — large volume, bounding, rapid rise and collapse
Blood Pressure Narrow pulse pressure (<40 mmHg); systolic BP may be low in severe AS Wide pulse pressure (>60–80 mmHg); high systolic, low diastolic
Apex Beat Sustained (heaving), non-displaced — pressure-loaded LV Displaced laterally & downward, hyperdynamic — volume-loaded dilated LV
Murmur Type Ejection systolic (crescendo-decrescendo) — heard best at aortic area; radiates to carotids Early diastolic decrescendo — heard best at left sternal border, leaning forward in expiration
Additional Murmurs S4 (stiff LV); paradoxically split S2 (severe); ejection click (bicuspid valve) Austin Flint murmur (low-pitched mid-diastolic rumble at apex); S3 (dilated LV)
ECG Findings LVH with strain pattern (ST depression & T-wave inversion in V5–V6, I, aVL); LV strain LVH (voltage criteria); broad notched P (if LA enlarges); LV volume overload pattern
CXR Findings Normal heart size (concentric LVH); calcified aortic valve; post-stenotic aortic dilatation Cardiomegaly (LV enlargement); prominent aorta; pulmonary edema if decompensated
Echo / Severity Valve area: mild >1.5 cm², moderate 1.0–1.5 cm², severe <1.0 cm²; mean gradient severe >40 mmHg Regurgitant fraction: mild <30%, moderate 30–49%, severe ≥50%; LV end-systolic diameter
Medical Management No effective medical therapy to slow progression. Manage comorbidities (HTN, AF). Avoid vasodilators in severe AS. Vasodilators (nifedipine, ACEi/ARB) to reduce afterload & preload in chronic AR. Bridge to surgery.
Surgical Indications Severe AS + symptoms; severe AS + EF <50%; severe AS undergoing other cardiac surgery Severe AR + symptoms; severe AR + EF <50%; severe AR + LV ESD >50 mm
Intervention Options SAVR TAVR Balloon valvuloplasty (palliation only) SAVR Valve repair (if feasible) — TAVR emerging but less established
Prognosis Untreated symptomatic severe AS: 50% mortality at 2–3 yrs. Rapid decline after symptom onset. Chronic: long compensated phase. Once symptomatic: 10–20% annual mortality without surgery.
Pathophysiology cascade
Aortic Stenosis
1Valve orifice narrows → increased resistance to LV outflow
2LV generates higher systolic pressure → pressure overload
3Concentric LVH (parallel sarcomere addition) — wall:cavity ratio increases
4Diastolic dysfunction → reduced coronary reserve → subendocardial ischaemia
5Decompensation: systolic dysfunction, reduced CO, symptoms (SAD triad)
Aortic Regurgitation
1Valve incompetent → blood regurgitates from aorta into LV during diastole
2LV must handle both forward stroke volume + regurgitant volume → volume overload
3Eccentric LVH (series sarcomere addition) — cavity dilates, wall thickens proportionally
4High diastolic aortic pressure maintained → wide pulse pressure; low LVEDP early
5LV decompensation: EF falls, LVEDP rises, pulmonary hypertension, heart failure
Auscultation findings
Aortic Stenosis
Harsh ejection systolic murmur (crescendo-decrescendo)
Best heard: Right 2nd intercostal space (aortic area)
Radiation: Both carotids — key distinguishing feature
Character: Harsh, rasping; peaks in mid-systole; later peak = more severe
Maneuvers: Louder on squatting (increased preload); softer on standing/Valsalva
S2: Soft or absent A2; paradoxical splitting in severe AS
Extras: Ejection click (bicuspid valve); S4 (non-compliant LV)
Aortic Regurgitation
High-pitched early diastolic decrescendo murmur
Best heard: Left sternal border, 3rd–4th ICS (Erb's point)
Position: Patient leaning forward, end-expiration — brings aorta closer to chest wall
Character: Blowing, high-pitched; begins immediately after S2
Maneuvers: Louder on squatting & handgrip (increased afterload)
Austin Flint murmur: Low-pitched mid-diastolic rumble at apex — regurgitant jet impinges on anterior mitral leaflet
Extras: S3 (dilated LV); wide pulse pressure
Peripheral signs of aortic regurgitation (absent in AS)
Named signs
Corrigan's pulseBounding carotid pulsation — rapid rise & collapse
de Musset's signHead nodding with each heartbeat
Quincke's signVisible nail bed capillary pulsations
Duroziez's signSystolic & diastolic femoral bruits on compression
Traube's sign'Pistol shot' sound over femoral artery
Müller's signVisible uvular pulsation
Key signs in Aortic Stenosis
Pulsus parvus et tardusSlow-rising, small-amplitude carotid pulse — most specific sign of severe AS
Sustained apex beatHeaving, non-displaced — reflects concentric LVH
Systolic thrillPalpable over aortic area in severe AS
Narrow pulse pressureReduced stroke volume → low systolic, near-normal diastolic BP
Absent / soft A2Calcified immobile valve fails to produce closing sound

Investigations

  • Transthoracic echocardiography (TTE) – Gold standard for diagnosing AR, identifying the cause, assessing severity, and evaluating left ventricular function.
  • Transesophageal echocardiography (TEE) – Used if TTE is inconclusive, for preoperative planning, or if aortic dissection or infective endocarditis is suspected.
  • ECG – May show left ventricular hypertrophy (LVH) in chronic AR; also helps assess for arrhythmias or ischemia.
  • Chest X-ray – May show left ventricular enlargement, pulmonary edema (acute AR), or a prominent aortic root.
  • Laboratory tests
    • Blood cultures if infective endocarditis is suspected.
    • BNP/NT-proBNP may help assess disease severity.
  • CT angiography (CTA) chest – Preferred if aortic dissection is suspected in acute AR.
  • Cardiac MRI – Used when echocardiography is inadequate or findings are inconclusive.
  • Cardiac catheterization/coronary angiography – Used in selected patients when noninvasive tests are inconclusive or before surgery.
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Diagnosis

Aortic Regurgitation · Diagnostic Criteria & Severity Classification

≥50%
Regurgitant Fraction
Severe AR threshold
≥60 mL
Regurgitant Volume
Severe AR threshold
≥0.30
EROA (cm²)
Effective Regurgitant Orifice Area — Severe
Leaflet disease
Bicuspid AV
Most common cause <60 yrs. Prolapse or calcification leads to coaptation failure.
Inflammatory
Rheumatic fever
Leaflet retraction & fusion. Usually mixed AS+AR. Common in developing countries.
Root dilatation
Marfan / Annuloaortic ectasia
Leaflets normal but root dilatation prevents coaptation. Aorta is primary target.
Acute cause
Infective Endocarditis
Leaflet destruction or perforation. Acute severe AR → surgical emergency.
Acute cause
Aortic Dissection (Type A)
Dissection flap undermines commissures. Acute severe AR — emergent surgery required.
Modality Finding Notes & Pitfalls
History Exertional dyspnea Palpitations Angina Orthopnea
Chronic AR: prolonged asymptomatic phase (LV compensates for years). Acute AR: flash pulmonary edema & cardiogenic shock with no prior symptoms.
 Palpitations reflect hyperdynamic circulation — LV senses its own forceful beat. Exertional symptoms signal LV decompensation. Nocturnal angina (diastolic BP drop → reduced coronary perfusion) is characteristic.
Pulse
Corrigan's (water-hammer) pulse — rapid rise, large volume, sudden collapse
Wide pulse pressure >60–80 mmHg (high systolic, low diastolic)
 Best felt by raising patient's arm above head and feeling radial pulse. Diastolic BP may fall to near zero in severe chronic AR. In acute AR, pulse pressure may be narrow — LV cannot dilate acutely so LVEDP rises rapidly.
Auscultation
Early diastolic decrescendo murmur — high-pitched, blowing; immediately after S2
Best heard: Left sternal border 3rd–4th ICS (Erb's point); patient sitting forward, end-expiration
Austin Flint murmur: Low-pitched mid-diastolic rumble at apex — regurgitant jet impinges on anterior mitral leaflet, causing functional MS
S3: Dilated, volume-overloaded LV
 Murmur duration correlates better with severity than intensity. Short murmur in acute AR (rapid equalization of aortic and LV pressures). Austin Flint must be distinguished from true MS (no opening snap, no loud S1 in AR).
Maneuvers Louder: squatting, handgrip (↑ afterload) Softer: standing, amyl nitrite (↓ afterload) Increased systemic vascular resistance (handgrip, squatting) augments regurgitant flow → louder murmur. Useful to distinguish from pulmonary regurgitation (Graham Steell murmur — not changed by handgrip).
Blood Pressure
Hill's sign: Popliteal systolic BP exceeds brachial systolic BP by >20 mmHg (mild) to >60 mmHg (severe)
Diastolic BP <60 mmHg common in severe chronic AR
 Hill's sign reflects peripheral amplification of pulse pressure. Sensitivity limited; useful when positive. Compare both arms if aortic dissection suspected.
Apex Beat Displaced laterally & downward (to 6th ICS, anterior axillary line); hyperdynamic, thrusting Reflects eccentric LVH and cavity dilatation. Sustained apex = pressure overload (AS); thrusting/diffuse apex = volume overload (AR). Heaving = hypertrophy; thrusting = dilatation.
ECG
LVH (voltage criteria: Sokolow-Lyon ≥35 mm)
Volume overload pattern: tall R in V5–V6, deep S in V1–V2, prominent Q in lateral leads
Sinus tachycardia in acute AR; AF or conduction defects (late/severe)
 ECG often lags behind echo in detecting LV changes. Sinus tachycardia in acute AR is a compensatory mechanism to maintain cardiac output (shorter diastole = less time for regurgitation).
Chest X-Ray
Cardiomegaly — boot-shaped heart, LV apex displaced down and left
Dilated ascending aorta — aortic root disease (Marfan, annuloaortic ectasia)
Acute AR: normal heart size + pulmonary edema (LV cannot dilate acutely)
 Normal heart size on CXR in an acutely unwell patient with pulmonary edema should raise suspicion of acute AR (endocarditis, dissection) — a diagnostic trap.
Echocardiography TTE — first-line TEE — if TTE suboptimal or endocarditis suspected 3D Echo — EROA planimetry, aortic root Gold standard for diagnosis, mechanism, severity, LV dimensions, and aortic root assessment. Color Doppler jet width, PHT, vena contracta, regurgitant volume/fraction, EROA by PISA method.
CT Aorta Aortic root diameter, annulus sizing, aortic morphology (bicuspid, root dilatation), calcium burden Essential pre-op for SAVR/TAVR planning. CT angiography for coronary assessment if ≥40 yrs or risk factors. Aorta ≥55 mm (or ≥50 mm in Marfan/bicuspid) = independent surgical indication.
CMR
Direct regurgitant volume & fraction measurement (phase-contrast flow)
LV volumes, mass, EF (most accurate)
Late gadolinium enhancement (LGE) — myocardial fibrosis
 CMR is the gold standard for regurgitant volume quantification — not angle-dependent unlike echo Doppler. LGE predicts adverse outcomes post-AVR. Use when echo is discordant or windows are poor.
Cardiac Catheterization
Aortography: contrast injection in aortic root — grades regurgitation 1+–4+
Coronary angiography prior to surgery
 Invasive; rarely needed purely for AR diagnosis if echo/CMR adequate. Aortography grade: 1+ (faint, clears quickly), 2+ (fills LV, clears), 3+ (LV opacifies fully = aorta), 4+ (LV denser than aorta). Reserved for discordant non-invasive findings.
Exercise Testing Exercise echo or stress CMR in asymptomatic severe AR — uncovers occult symptoms, LV dysfunction, EF drop EF drop ≥5% with exercise or failure of LV to augment EF = sign of subclinical dysfunction → may prompt earlier intervention even before threshold LV dimensions are reached.
Echo severity grading — AHA/ACC 2021 & ESC 2021 (integrated criteria)
Mild AR
Doppler
Jet width: <25% LVOT width
Vena contracta: <0.3 cm
PHT: >500 ms
Quantitative
RVol: <30 mL
RF: <30%
EROA: <0.10 cm²
Moderate AR
Doppler
Jet width: 25–64% LVOT
Vena contracta: 0.3–0.59 cm
PHT: 200–500 ms
Quantitative
RVol: 30–59 mL
RF: 30–49%
EROA: 0.10–0.29 cm²
Severe AR
Doppler
Jet width: ≥65% LVOT
Vena contracta: ≥0.6 cm
PHT: <200 ms
Quantitative
RVol: ≥60 mL
RF: ≥50%
EROA: ≥0.30 cm²
Supportive Signs
Additional Findings
Holodiastolic flow reversal in descending aorta (severe)
LV dilatation: LVEDD >70 mm, LVESD >50 mm
Premature MV closure on M-mode (acute severe AR)
Austin Flint murmur on echo color Doppler at mitral valve
EF <50% = decompensation; surgical urgency
Key echocardiographic parameters explained
Pressure Half-Time (PHT)
PHT = 0.29 × DT (deceleration time)
Time for peak diastolic gradient to halve. Reflects how fast aortic and LV pressures equalize. Short PHT (<200 ms) = rapid equalization = severe AR. Unreliable if aortic or LV compliance is abnormal (e.g., acute AR on stiff LV — PHT may be short even for moderate AR).
Vena Contracta
Narrowest jet width at valve level
The narrowest portion of the regurgitant jet just downstream from the valve orifice. ≥0.6 cm = severe AR. Relatively load-independent. Measured in parasternal long axis with color Doppler, Nyquist limit 50–60 cm/s. Eccentric jets can underestimate severity.
Jet Width / LVOT Ratio
AR jet width / LVOT width × 100%
Qualitative semi-quantitative method. ≥65% = severe. Simple but highly dependent on gain settings, Nyquist limit, and jet eccentricity. Central jets assessed in parasternal long axis. Eccentric (Coanda) jets often underestimated — always use quantitative methods.
EROA (by PISA method)
EROA = 2πr² × Va / Vmax
Effective regurgitant orifice area using proximal isovelocity surface area. ≥0.30 cm² = severe. Most accurate non-invasive measure of orifice size. Technically demanding; assumes hemispheric flow convergence — less accurate for non-circular or eccentric orifices.
Regurgitant Volume & Fraction
RVol = SVₗǕǕ − SVₐǕǕ  |  RF = RVol / SVₗǕǕ
Volumetric method: difference between LV stroke volume (by 2D biplane) and aortic forward stroke volume (by Doppler at LVOT). RF ≥50% = severe. Accurate but relies on precise LVOT diameter measurement — small errors are squared. CMR is more accurate for RVol.
Diastolic Flow Reversal
PW Doppler in descending / abdominal aorta
Holodiastolic flow reversal (extending through all of diastole) in descending or abdominal aorta = severe AR. Pan-diastolic reversal in abdominal aorta is highly specific for severe AR. Brief early-diastolic reversal alone is normal or seen with mild AR.
Peripheral signs of aortic regurgitation
Corrigan's pulse
Carotid / radial pulse
Bounding, rapid-rising, collapsing pulse — best felt by lifting arm above head. Reflects wide pulse pressure and rapid diastolic runoff.
de Musset's sign
Head nodding
Rhythmic head bobbing synchronous with heartbeat. Reflects transmitted carotid pulsation. Named after the French poet Alfred de Musset.
Quincke's sign
Nail bed capillaries
Visible systolic flushing and diastolic blanching of nail bed when gentle pressure applied to fingertip. Capillary pulsation from wide pulse pressure.
Duroziez's sign
Femoral artery
Systolic murmur on proximal compression + diastolic murmur on distal compression of femoral artery with stethoscope. Diastolic component indicates retrograde flow.
Traube's sign
Femoral artery
'Pistol shot' sound heard over femoral artery without compression. Caused by sudden distension and collapse of vessel wall with each pulse wave.
Hill's sign
Popliteal vs brachial BP
Popliteal systolic BP > brachial systolic BP by >20 mmHg (mild), >40 mmHg (moderate), >60 mmHg (severe). Due to peripheral pulse pressure amplification.
Müller's sign
Uvula / pharynx
Visible pulsation of the uvula synchronous with heartbeat. Transmitted carotid pulsation. Rare and mainly of historical interest.
Becker's sign
Retinal vessels
Visible pulsation of retinal arteries on fundoscopy. Reflects wide pulse pressure reaching end-organ vasculature.
Landolfi's sign
Pupils
Alternating constriction and dilatation of pupils synchronous with pulse. Extremely rare; found only in very severe AR with pronounced pulse pressure.
Acute vs Chronic AR — key diagnostic differences
Chronic AR
1Long compensated phase — LV dilates gradually (eccentric hypertrophy), maintaining normal EF for years
2Wide pulse pressure, displaced hyperdynamic apex, Corrigan's pulse — all present
3Cardiomegaly on CXR; early diastolic murmur audible, moderate-to-long duration
4Decompensation: EF falls, LVEDP rises, symptoms emerge — LV dimensions trigger surgery
5Annual mortality once symptomatic: 10–20% without intervention
Acute AR — Surgical Emergency
1Causes: infective endocarditis, Type A aortic dissection, trauma, iatrogenic
2LV cannot dilate acutely → LVEDP rises sharply → flash pulmonary edema & cardiogenic shock
3Heart size normal on CXR despite severe AR — a key diagnostic trap (no time for LV to dilate)
4Murmur short (rapid LV/aortic pressure equalization); pulse pressure may be narrow; peripheral signs absent
5Premature mitral valve closure on echo (M-mode) — hallmark of acute severe AR; indicates very high LVEDP
Indications for intervention (AVR) — AHA/ACC 2021 & ESC 2021
Class I — Recommended
Symptomatic severe AR (dyspnea, angina, HF) regardless of EF Class I
Asymptomatic severe AR + EF <50% Class I
Severe AR undergoing other cardiac surgery (CABG, other valve, aortic surgery) Class I
Acute severe AR (endocarditis, dissection) — emergent surgery Class I
Class IIa / IIb — Reasonable / May Consider
Asymptomatic severe AR + EF ≥50% + LVESD >50 mm (or >25 mm/m² indexed) Class IIa
Asymptomatic severe AR + EF ≥50% + LVEDD >70 mm + low surgical risk Class IIa
Asymptomatic severe AR + progressive LV dilatation on serial echo (rapid increase in LVEDD/LVESD) Class IIb
Aortic root ≥55 mm (≥50 mm in Marfan / bicuspid AV) — independent indication regardless of AR severity Class IIa
Vasodilator therapy (ACEi, ARB, nifedipine) — bridge to surgery or in non-surgical candidates; does not substitute for timely surgery Class IIb
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Management

1. Acute Aortic Regurgitation (Emergency)

  • Urgent cardiology and cardiothoracic surgery consultation
  • Urgent surgical aortic valve replacement (AVR) is the definitive treatment.
  • Stabilize the patient before surgery:
    • Treat cardiogenic shock (e.g., with dobutamine or dopamine)
    • Reduce afterload for acute heart failure (e.g., nitroprusside)
  • Treat the underlying cause (e.g., infective endocarditis or aortic dissection).
  • Avoid delaying surgery for medical treatment alone.
  • Avoid beta blockers unless the AR is caused by aortic dissection.
  • Intra-aortic balloon pump (IABP) is contraindicated because it increases the amount of regurgitation.

2. Chronic Aortic Regurgitation

Asymptomatic patients

  • Regular follow-up with serial echocardiography.
  • Screen for and treat cardiovascular risk factors.
  • Treat hypertension (vasodilators such as ACE inhibitors or ARBs may be preferred).
  • Treat heart failure if present.

Symptomatic or severe AR

  • Surgical aortic valve replacement (AVR) is the standard treatment.

3. Indications for Surgery

  • Acute severe AR
  • Symptomatic chronic severe AR
  • Asymptomatic severe AR with:
    • LVEF ≤ 55%
    • Consider if LV end-systolic diameter (LVESD) > 50 mm
    • Patient already undergoing cardiac surgery for another reason

4. Follow-up

  • Regular echocardiography to monitor progression:
    • Mild AR: every 3–5 years
    • Moderate AR: every 1–2 years
    • Severe asymptomatic AR: every 6–12 months

Complications

    • Left ventricular dilation
    • Left ventricular systolic dysfunction
    • Left-sided heart failure
    • Pulmonary edema (especially in acute AR)
    • Cardiogenic shock (severe acute AR)

Prognosis

  • Asymptomatic patients with normal LV function: Progression to symptoms or LV dysfunction is < 6% per year.
  • Asymptomatic patients with reduced ejection fraction: Progression to symptoms is > 25% per year.
  • Symptomatic patients: Mortality is > 10% per year and may reach 25% per year if left untreated
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Key Points / Clinical Pearls

  • Aortic Regurgitation= leaky aortic valve → blood flows back into the LV during diastole.
  • Can be acute or chronic.
  • Classic murmur: High-pitched, blowing early diastolic decrescendo murmur.
  • Classic sign: Wide pulse pressure with a water hammer pulse.
  • Gold standard diagnosis: Transthoracic echocardiography (TTE).
  • Definitive treatment: Aortic valve replacement.
  • Acute severe AR is a medical emergency requiring urgent surgery.
  •