7th March 2024

Aortic Regurgitation

Aortic regurgitation (AR) is characterised by an early decrescendo diastolic murmur. There is no correlation between the presence of murmur and severity of AR or aetiology. A wide pulse pressure may be found and is caused by blood returning to the left ventricle from the aorta during diastole, causing a drop in diastolic pressure. To compensate, there is peripheral vasoconstriction. A water hammer pulse, also called a collapsing pulse, is characteristic of AR. Other signs in AR include:

• Austin Flint murmur. In severe aortic regurgitation, the regurgitant jet of blood can exert pressure on the anterior mitral valve cusps during diastole, resulting in a mid/late diastolic murmur like that of and virtually indistinguishable from mitral stenosis.  
• The first heart sound may be absent in severe AR 

AR can be caused by primary disease of the aortic valve cusps and/or abnormalities of the aortic root and ascending aortic geometry. 

Degenerative tricuspid and bicuspid aortic regurgitation are the most common aetiologies in high-income countries.

Valvular causes include:

• Rheumatic fever
• Bicuspid aortic valve
• Infective endocarditis
• Connective tissue diseases e.g., RA/SLE

AR due to aortic root disease can occur in:

• Hypertension
• Syphilis
• Marfan’s, Ehler-Danlos syndrome
• Aortic dissection
• Spondyloarthropathies (e.g., ankylosing spondylitis)

Diagnosis

Echocardiography is key to confirm valve anatomy, quantify aortic regurgitation, define the morphology of the aorta and determine the feasibility of valve-sparing aortic surgery or valve repair. 

CMR should be used to quantify AR when echocardiographic measurements are equivocal or discordant with clinical findings. In patients with aortic dilatation, a cardiac CCT is recommended. CMR can be used for follow-up, but indication for surgery should preferably be based on CCT measurements.

Management

Acute aortic regurgitation may require urgent surgery. It is mainly caused by infective endocarditis and aortic dissection but may also occur after blunt chest trauma and iatrogenic complications during catheter-based cardiac interventions.

In symptomatic patients who are fit for surgery with severe AR, replacement is recommended irrespective of the LVEF. Replacement is also recommended in symptomatic and asymptomatic patients with severe aortic regurgitation undergoing coronary artery bypass grafting (CABG) or surgery of the ascending aorta or another valve. 

In asymptomatic patients with severe aortic regurgitation, impairment of LV function [LVEF ≤50% or left ventricular end-systolic diameter (LVESD) >50 mm] is associated with worse outcomes and surgery should therefore be pursued when these cut-offs are reached. 

TAVI may be considered in experienced centres for selected patients with aortic regurgitation and ineligible for SAVR. Medical therapy, especially ACEI or dihydropyridines, may provide symptomatic improvement in individuals with chronic severe aortic regurgitation in whom surgery is not feasible. In patients who undergo surgery but continue to suffer from heart failure or hypertension, ACEI, angiotensin receptor blockers (ARBs), and beta-blockers are useful. 

All asymptomatic patients with severe aortic regurgitation and normal LV function should be followed up at least every year.