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Aortic Regurgitation

General Principles

  • Aortic regurgitation (AR) may result from pathology of the aortic valve, the aortic root, or both; it is important that both the valve and the root are evaluated to determine the appropriate management and treatment.
  • AR usually progresses insidiously with a long asymptomatic period; when it occurs acutely, patients are often very sick and must be managed aggressively.


  • More common

    Bicuspid aortic valve, rheumatic disease, calcific degeneration, infective endocarditis, idiopathic dilatation of the aorta, myxomatous degeneration, systemic hypertension, dissection of the ascending aorta, Marfan syndrome

  • Less common

    Traumatic injury to the aortic valve, collagen vascular diseases (ankylosing spondylitis, rheumatoid arthritis, reactive arthritis, giant cell aortitis, and Whipple disease), syphilitic aortitis, discrete subaortic stenosis, ventricular septal defect with prolapse of an aortic cusp

  • Acute

    Infective endocarditis, dissection of the ascending aorta, trauma


Figure 6-4. Acute aortic regurgitation.

CO, cardiac output; HR, heart rate; LAP, left atrial pressure; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; SV, stroke volume.

Figure 6-5. Chronic aortic regurgitation.

CO, cardiac output; CHF, congestive heart failure; EF, ejection fraction; LV, left ventricle; LVED, left ventricular end-diastolic; LVEDP, left ventricular end-diastolic pressure; LVH, left ventricular hypertrophy; SV, stroke volume.


Clinical Presentation


  • Acute: Patients with acute AR may present with symptoms of cardiogenic shock and severe dyspnea. Other presenting symptoms may be related to the cause of acute AR.
  • Chronic: Symptoms depend on the presence of LV dysfunction and whether the patient is in the compensated versus decompensated stage. Compensated patients are typically asymptomatic, whereas those in the decompensated stage may note decreased exercise tolerance, dyspnea, fatigue, and/or angina.

Physical Examination

  • Acute
    • Tachycardia: Wide pulse pressure may be present, but is often not present because forward SV (and therefore systolic blood pressure) is reduced; brief soft diastolic murmur heard best at third left intercostal space (often not heard); systolic flow murmur (due to volume overload and hyperdynamic LV).
    • Look for evidence of aortic dissection, infective endocarditis, and Marfanoid characteristics.
  • Chronic
    • LV heave; point of maximal impulse is laterally displaced.
    • Diastolic decrescendo murmur heard best at left sternal border leaning forward at end-expiration (severity of AR correlates with duration, not intensity, of the murmur).
    • Systolic flow murmur (due mostly to volume overload; concomitant AS may also be present).
    • Widened pulse pressure (often >100 mm Hg) with a low diastolic pressure; there are numerous eponyms for the characteristic signs related to a wide pulse pressure.

Diagnostic Testing

  • ECG
    • Tachycardia, LVH, and LAE (more common in chronic AR).
    • New conduction block may suggest an aortic root abscess.
  • CXR

    Look for pulmonary edema, widened mediastinum, and cardiomegaly.

  • TTE

    LV systolic function, LV dimensions at end systole and diastole, leaflet number and morphology, assessment of the severity of AR; look for evidence of endocarditis or aortic dissection; dimension of aortic root.

  • TEE
    • Clarify whether there is a bicuspid valve if unclear on TTE.
    • Better sensitivity and specificity for aortic dissection than TTE.
    • Clarify whether there is endocarditis with or without root abscess if unclear on TTE.
    • Better visualization of aortic valve in patients with a prosthetic aortic valve.
  • Cardiac catheterization
    • In patients undergoing AVR who are at risk for CAD.
    • Assessment of LV pressure, LV function, and severity of AR (via aortic root angiography) is indicated in symptomatic patients in whom the severity of AR is unclear on noninvasive imaging or discordant with clinical findings.
  • MRI/CT
    • Depending on the institution, either of these may be the imaging modality of choice for evaluating aortic dimensions and/or for evaluation of aortic dissection.
    • If echocardiography assessment of the severity of AR is inadequate, MRI is useful for assessing the severity of AR.


  • The role of medical therapy in patients with AR is limited; there are currently no randomized, placebo-controlled data showing that vasodilator therapy delays the development of symptoms or LV dysfunction warranting surgery.
  • Vasodilator therapy (i.e., nifedipine, ACE inhibitor, hydralazine) is indicated to reduce systolic blood pressure in hypertensive patients with AR.
  • Retrospective data suggest that β-blocker use may be associated with a survival benefit in patients with severe AR, but prospective studies are needed.
  • When endocarditis is suspected or confirmed, appropriate antibiotic coverage is critical.

Surgical Management

  • AHA/ACC recommendations for intervention
    • Symptomatic patients with severe AR (stage D) regardless of LV systolic function (class I)
    • Asymptomatic patients with chronic severe AR and LV systolic dysfunction (EF ≤50%) (stage C2; class I)
    • Patients with severe AR (stage C or D) undergoing cardiac surgery for other indications (class I)
    • Asymptomatic patients with severe AR and normal LV systolic function (EF >50%) but with severe LV dilation (LV end-systolic dimension >50 mm) (stage C2; class IIa)
  • Acute, severe AR is almost universally symptomatic and is treated surgically.
  • If the aortic root is dilated, it may be repaired or replaced at the time of AVR. For patients with a bicuspid valve, Marfan syndrome, or a related genetically triggered aortopathy, surgery on the aorta should be considered at the time of AVR.


  • Asymptomatic patients with normal LV systolic function
    • Progression to symptoms and/or LV dysfunction <6% per year
    • Progression to asymptomatic LV dysfunction <3.5% per year
    • Sudden death <0.2% per year
  • Asymptomatic patients with LV dysfunction

    Progression to cardiac symptoms >25% per year

  • Symptomatic patients

    Mortality rate >10% per year


© Wolters Kluwer Health Lippincott Williams & Wilkins

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Williams, Dominique, et al., editors. "Aortic Regurgitation." Washington Manual of Medical Therapeutics, 35th ed., Wolters Kluwer Health, 2016. Washington Manual, www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602529/all/Aortic_Regurgitation.
Aortic Regurgitation. In: Williams D, Ramgopal R, Gdowski M, et al, eds. Washington Manual of Medical Therapeutics. 35th ed. Wolters Kluwer Health; 2016. https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602529/all/Aortic_Regurgitation. Accessed April 20, 2019.
Aortic Regurgitation. (2016). In Williams, D., Ramgopal, R., Gdowski, M., Dretler, A., & Bhat, P. (Eds.), Washington Manual of Medical Therapeutics. Available from https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602529/all/Aortic_Regurgitation
Aortic Regurgitation [Internet]. In: Williams D, Ramgopal R, Gdowski M, Dretler A, Bhat P, editors. Washington Manual of Medical Therapeutics. Wolters Kluwer Health; 2016. [cited 2019 April 20]. Available from: https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602529/all/Aortic_Regurgitation.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Aortic Regurgitation ID - 602529 ED - Williams,Dominique, ED - Ramgopal,Rajeev, ED - Gdowski,Mark, ED - Dretler,Alexandra, ED - Bhat,Pavat, BT - Washington Manual of Medical Therapeutics UR - https://www.unboundmedicine.com/washingtonmanual/view/Washington-Manual-of-Medical-Therapeutics/602529/all/Aortic_Regurgitation PB - Wolters Kluwer Health ET - 35 DB - Washington Manual DP - Unbound Medicine ER -