6th May 2025

Aortic Regurgitation

Pathology and Epidemiology

Aortic regurgitation is incompetence of the trileaflet aortic valve, leading to backwards flow from the aorta to the left ventricle during diastole. When significant this can lead to elevated filling pressures and wall stress, leading to elevated pulmonary pressures both of which ultimately lead to typical signs and symptoms.

In large case series it is the third most common valve disease after MR and AS with a prevalence of between 5-10%, though rarely are these cases severe.

Common primary causes of AR include bicuspid aortic valve, degenerative valve disease and infective endocarditis.

Relevant secondary causes of AR include aortic root dilation (typically caused by hypertension, with collagen and fibrillin disorders less common) and type A aortic dissection.

Presentation – Symptoms

Symptoms of AR depend on the acuity of the presentation. As discussed earlier, acute onset regurgitation does not allow time for the left ventricle to adapt to an increased stroke volume by dilating, and thus can lead to elevated wall stress, elevated diastolic pressures and pulmonary oedema alongside failure of forward flow leading to circulatory collapse. In contrast, compensatory adaptations can occur in the setting of chronic regurgitation so that when these compensatory mechanisms fail, the presenting symptoms are more typical of heart failure, i.e. shortness of breath on exertion, orthopnoea, fatigue and peripheral oedema. Some patients may complain of anginal type symptoms due to impaired diastolic perfusion in the coronary arteries due to retrograde flow.

Diagnosis / Investigations

AR should be considered as a differential diagnosis with the above history and clinical signs. As per AS, confirmatory testing is typically with transthoracic echocardiography. In acute regurgitation, bedside echocardiography may be necessary in an acutely unwell patient, but they will also need formal departmental testing. 

TTE will show reversal of flow during diastole, evidenced by colour flow, pulse wave or continuous wave doppler. In addition, it may demonstrate the underlying causative pathology, be that significant root dilation or perforation of the valve leaflet.

Alongside TTE, early investigations should include a 12-lead ECG, chest Xray, blood tests including full blood count, urea and electrolytes and NT pro-BNP, as well as any further investigations to elucidate the cause, for example three sets of blood cultures when considering infective endocarditis, or CT angiography of the aortic root if considering aortic dissection as an underlying cause.

There are no specific ECG signs, though sequelae of underlying issues may be noted – ie PR prolongation in infective endocarditis with aortic root abscess, or ST depression in proximal aortic root dissection with coronary involvement.

Chest Xray will likely only show signs of decompensation such as pulmonary congestion and pleural effusion, though in chronic AR the cardiac shadow can be enlarged and laterally displaced.

Blood tests will likely be non-specific, though can indicate evidence of organ failure secondary to AR, while NT pro BNP values can help prognosticate.

Transoesophageal echocardiography is often performed to assess for mechanism of regurgitation, and can help plan surgical interventions. Cardiac MRI can also be used to quantify regurgitant volumes but is less commonly used in the acute phase. CT may be used to accurately map out aortic root dimensions, and is also a good modality for assessment of aortic root abscess formation if not clearly seen on transthoracic or transoesophageal echocardiogram.

Grading Severity 

As with AS, severity of AR is typically assessed with echocardiography. A number of parameters are used which are beyond the scope of this document, but severe AR is typically diagnosed in the context of a combination of the following:

• Flail leaflets
• Dense continuous wave doppler signal
• Holodiastolic flow reversal in the descending aorta
• Vena contracta >6mm
• Pressure half time <200ms
• Regurgitant volume >60ml
• Effective regurgitant orifice area >30mm²

Of these, holodiastolic flow reversal in the descending aorta is most specific for severe AR, but in general a combination of the above is considered.

Criteria for treatment 

If non-severe then AR is typically followed up with routine outpatient echocardiography, typically every year if moderate, and every 3-5 years if less severe.

As with AS, patients with symptomatic severe AR require consideration for intervention. In asymptomatic patients, intervention is typically recommended if resting LVEF is <50% or the left ventricular end systolic diameter is >50mm, or >25mm/m2 BSA.

As with AS, valve intervention can also be considered if a patient is undergoing CABG, aortic intervention or alternative valve surgery and has asymptomatic severe AR.

Treatment options

There are no particular medical treatments for AR, though diuretics can be given for symptom management, and typical heart failure therapies can be given in the context of a reduced LVEF.

Almost universally, surgical intervention is recommended for severe disease meeting the above criteria. If ineligible for surgical intervention, then some centres may consider TAVR as an alternative, though this is not common and SAVR may need to be considered as a bail-out therapy where TAVR is unsuccessful. SAVR options are the same as those for AS, discussed above.

When aortic root dilation is the underlying pathology, concomitant aortic root surgery is typically performed, and patients will again be screened for significant coronary artery disease as per AS in case simultaneous coronary artery bypass grafting needs to be performed.