Aortic Regurgitation


  • Aortic valve regurgitation can be thought of as two entities based on chronicity: acute and chronic.
  • Both acute and chronic AR result in a volume overloaded state, with resulting hemodynamic disturbances.
    • In chronic AR, the left ventricle can gradually adapt to an increased volume state.
    • In acute AR, the left ventricle can’t quickly adapt to the regurgitant volume, leading to dramatic hemodynamic consequences.

Acute AR

  • Etiologies:
    • Endocarditis
    • Aortic dissection
    • Blunt chest trauma
    • Prosthetic valve failure
    • Complication of transcatheter procedure
  • Pathophysiology
    • In acute AR, there is a sudden increase in regurgitant volume placed upon an LV that has not had time to adapt.
    • There is a rapid and progressive increase in LV diastolic pressure → pulmonary edema and decreased cardiac output.

Rapid diagnosis is vital: 

  • CT chest if suspected aortic dissection
  • Echo (TTE or TEE)
    • Consider point-of-care cardiac ultrasound


  • Urgent surgery to correct the underlying cause
  • IABP is contraindicated in acute severe AR

Chronic AR - Introduction


Consider the origin of aortic regurgitation as arising from either the aortic valve or the level of the aorta.

  • Aortic valve:
    • Bicuspid aortic valve (most common)
    • Rheumatic disease
    • Degenerative
    • Endocarditis
  • Aorta:
    • Aortic dilation (numerous underlying causes; see separate post on aortopathy)
    • Aortic dissection
    • Trauma


  • Chronic AR is a volume overload state on the left ventricle.
  • With continued regurgitation, there is progressive dilation of the LV, leading to an eventual drop in LV ejection fraction and heart failure symptoms.

Chronic AR - History & Physical


  • Symptoms are those of chronic heart failure: exertional dyspnea and exercise intolerance, leg swelling, and orthopnea/PND.


  • Vitals: wide pulse pressure (with low diastolic BP)
  • Peripheral signs (in severe chronic AR):
    • Corrigan’s (water hammer) pulse:  visibly pulsating carotid artery with collapse
    • de Musset’s sign: head bob with each beat
    • Muller’s sign: pulsation of the uvula with each beat
    • Quincke’s pulse: pulsating capillaries upon gentle pressure at the distal nail-bed
    • Traube’s sign: loud “pistol shot” sound heart in diastole with gentle auscultation over the femoral artery
    • Duroziez’s sign: “to-and-fro” bruit over femoral artery with pressure applied
  • Auscultation:
    •  Diastolic decrescendo murmur, best assessed with patient seated, leaning forward, and at end expiration
  • Excellent review of physical exam (important for OSCEs)

Chronic AR - Investigations

Echo (TTE) is vital to diagnosis and monitoring.

Echo allows for assessment of valve morphology, severity and mechanism of AR, presence of aortic dilation, and LV size and function.

Monitoring in asymptomatic patients

  • The goal of monitoring asymptomatic patients with chronic AR is to identify them at the optimal moment for surgery: before there is a decompensation in LV function.
  • After first diagnosis, clinical follow-up +/- echo at  3-6 months is recommended to ensure interval stability.
  • With mild-to-moderate AR, echo every 2 years is recommended.
  • If echo shows a dilated ascending aorta (> 40mm), CT or cardiac MRI should also be performed.

Chronic AR - Management

  • Management of chronic aortic regurgitation centres on intervening on the aortic valve before there is potentially irreversible LV dysfunction.
  • Medical therapy can be used in patients who aren’t candidates for surgery: beta blockers, ACE inhibitors or ARBs.
    • Medical Therapy Class 1 indications: treat SBP <140 and for those not undergoing surgery, treating low EF with ACE/ARB/ARNI
  • Equally important is consideration of surgical intervention when there is an increased risk of aortic dissection or rupture (again, see separate post on aortopathy)
  • Class 1 Indications for surgery noted in the AHA figure on the right/below.
AHA 2020 - Timing of intervention for AR


  • Primary Author: Dr. Matthew Church (MD, FRCPC, Cardiology Fellow)
  • Reviewer: Dr. Atul Jaidka (MD, FRCPC, Cardiology Fellow)
  • Last Updated: May 7, 2021
  • Comments or questions please email