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Aortic regurgitation
  1. Gerald Maurer
  1. Correspondence to:
    Professor Gerald Maurer
    Division of Cardiology, Medical University of Vienna, AKH, Waehringer Guertel 18-20, 1090 Vienna, Austria; gerald.maurer{at}

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The incidence of clinically significant aortic regurgitation (AR) increases with age, typically peaking in the fourth to sixth decade of life. It is more common in men than women. The prevalence of AR in the Framingham study was reported to be 4.9%, with regurgitation of moderate or greater severity occurring in 0.5%.


AR may be caused by malfunction of the valve leaflets themselves, by dilatation of the aortic root and annulus, or may be due to a combination of these factors (table 1). Rheumatic disease is still the most common aetiology of AR in developing countries; however, in Western Europe and North America the leading cause of AR is either congenital (particularly due to bicuspid leaflets) or degenerative disease, including annuloaortic ectasia. Understanding the mechanism leading to AR is essential for proper patient management, including the surgical approach. Thus, knowledge of the morphology of the valve leaflets, the annulus and the ascending aorta are essential.

Table 1

 Aetiology of aortic regurgitation (AR)


AR causes volume overload of the left ventricle (LV). The total stroke volume ejected by the LV (sum of effective stroke volume plus regurgitant volume) is increased; in severe AR regurgitant volume may equal or even exceed effective stroke volume. An increase in LV end-diastolic volume is the main compensatory mechanism needed to maintain a normal effective stroke volume. Left ventricular ejection fraction is initially normal, however, LV end-diastolic pressure rises. In time LV end-diastolic volume continues to increase further and ejection fraction drops; these changes may actually precede the development of clinical symptoms. Considerable eccentric myocardial hypertrophy can occur with chronic AR and at autopsy heart weights of up to 1000 g have been reported.

Acute AR can be life threatening, as LV dilatation and other compensatory mechanisms cannot develop rapidly enough to avoid haemodynamic deterioration. The same regurgitant volume that would be well tolerated in chronic AR can lead to notable increases in LV end-diastolic pressure and a drop in effective stroke volume, leading to pulmonary oedema, hypotension and even cardiogenic shock.

In AR there is not only volume overload but also an increase in afterload and therefore of systolic wall stress. This distinguishes AR from mitral regurgitation (MR),1 where LV volume overload is also present, but where systolic wall stress is normal or even low, since the regurgitant blood is ejected into the low pressure left atrium. Thus valve surgery in MR usually results in an increase in afterload and commonly in worsening of the LV ejection fraction, while surgical correction of AR results in a decrease in afterload and frequently an improvement of the ejection fraction. The differences in afterload between the two disorders could also explain why vasodilator treatment may be beneficial in AR, but not in MR.


Patients with chronic AR typically remain asymptomatic for many years, with symptoms developing only in the late stages of the disease. The most common clinical complaint is shortness of breath, initially occurring during exercise, but later also at rest. Patients may be aware of a prominent, bounding heart beat and may experience sinus tachycardia at minimal exertion as well as palpitations, which can be caused by ventricular or supraventricular arrhythmias. In some instances angina can be present even in the absence of coronary artery disease.

Physical examination reveals a characteristic high-pitched, blowing decrescendo diastolic murmur and—as soon as AR becomes moderate to severe—low diastolic arterial blood pressure, widened pulse pressure, and bounding pulses. Often an increase in systolic pressure also takes place. Widened pulse pressure is a useful indicator of haemodynamically significant AR; however, its absence does not reliably exclude severe regurgitation.

Diagnostic tools

The ECG may be normal in mild AR. With greater degrees of regurgitation LV hypertrophy with or without strain pattern can be seen.

Chest x ray shows evidence of LV enlargement. Dilatation of the ascending aorta and aortic knob may be seen. Aneurysmal dilatation of the aorta can be present, particularly in patients in whom the AR is related to primary disease of the aortic wall.

Echocardiography (fig 1) presently is the principal tool for diagnosis and grading of AR severity as well as for serial follow-up. Colour Doppler is a highly sensitive and specific technique for detecting AR and provides visualisation of the regurgitant jet. Continuous and pulsed wave Doppler offer additional haemodynamic information and aid quantitation. Importantly, two dimensional echocardiography permits evaluation of LV size and function as well as visualisation of valve structures and of the aorta. Three dimensional echocardiography may play an increasing role in obtaining more precise measurements of ventricular volumes and may offer enhanced images of valve morphology.

Figure 1

 Echo-Doppler evaluation of aortic regurgitation (AR): panels A, B, C—mild AR; panels D, E, F—severe AR. (A) Narrow colour Doppler jet in mild AR (parasternal long axis view). (B) CW-Doppler tracing in mild AR (slow velocity decay). (C) PW-Doppler tracing from the descending aorta (suprasternal approach) in mild AR (minimal diastolic flow reversal). (D) Broad colour Doppler jet and large convergence zone in severe AR (parasternal long axis view). (E) CW-Doppler tracing in severe AR (steep diastolic velocity decay). (F) PW-Doppler tracing from the descending aorta (suprasternal approach) in severe AR (holodiastolic flow reversal). Ao, aorta; LA, left atrium; LV, left ventricle.

Aortic root angiography and cardiac magnetic resonance imaging (MRI) are alternative imaging techniques, particularly in rare instances when echocardiography is technically impossible or technically limited. Radionuclide ventriculography can be used to serially assess LV ejection fraction at rest and during exercise.

Grading AR severity

Table 2 summarises the most important parameters to be considered and has been adapted from a consensus paper recently published in the US2 and European literature.

Table 2

 Grading of aortic regurgitation (AR)

A valuable and simple parameter for grading AR is measurement of the narrowest width of the proximal regurgitant jet (vena contracta) by Colour Doppler3 (fig 1). A jet width < 0.3 cm is highly specific for mild AR whereas a width > 0.6 cm is highly specific for severe AR.2 In very eccentric jets this measurement becomes unreliable.

Evaluation of the flow pattern in the proximal descending aorta using PW-Doppler yields additional important information.2 Holodiastolic flow reversal is specific for severe AR (fig 1), while no or only brief diastolic flow reversal indicates mild AR.

CW-Doppler can be used to measure regurgitant flow velocity of the AR jet, which reflects the diastolic pressure gradient between the aorta and the LV. The rate of deceleration and the derived pressure half-time correspond to the rate of equalisation of these pressures. With increasing AR severity, aortic diastolic pressure decreases more rapidly, the late diastolic jet velocity becomes lower, and pressure half-time becomes shorter. A pressure half-time > 500 ms is usually consistent with mild AR, whereas values < 200 ms (according to some authors < 300 ms) is considered compatible with severe AR2 (fig 1). These measurements are not always reliable, as they are affected by other causes of elevated LV diastolic pressure or low aortic diastolic pressure.

A more quantitative approach using PW Doppler is based on comparison of measurements of aortic stroke volume at the level of the LVOT with mitral or pulmonic stroke volume.2 Effective regurgitant orifice area (EROA) can be calculated from the regurgitant stroke volume and the regurgitant jet velocity time integral by CW Doppler: a regurgitant volume ⩾ 60 ml and EROA ⩾ 0.30 cm2 are consistent with severe AR. Assessment of PISA (proximal isovelocity surface area) constitutes an alternative quantitative approach, although considerably less experience exists for assessment of AR than with MR. The PISA approach is limited by the interposition of valve tissue when imaging from the apex. Nevertheless, minimal or no flow convergence suggests mild regurgitation, whereas a larger flow convergence is consistent with severe AR. Quantitation using the PISA method has also been applied for AR4 and has been reported to yield regurgitant volume and, when combined with CW-Doppler measurements of jet velocity, effective regurgitant orifice area (EROA). Both quantitative methods, however, suffer from intrinsic limitations and considerable sources of error exist. Many investigators therefore recommend an integrative approach utilising all the parameters described above to provide an accurate judgement as a basis for clinical decision making.

Alternative imaging tools

Although grading is possible by Doppler echocardiography in the vast majority of patients, uncertainty may remain in some, particularly when ultrasound image quality is poor. In this case, cardiac catheterisation is still commonly used. Invasive evaluation, however, also does not provide true quantitation, since it mostly relies on aortic root angiography which is graded semiquantitatively, as well on haemodynamic measurements. In case of uncertainty with echocardiographic grading, cardiac MRI may be a useful next step. Although regurgitant volume and regurgitant fraction can be calculated from stroke volume measurements derived from LV and RV volume estimates, the currently preferred approach involves quantification of forward and backward flow in the ascending aorta.

Mechanism of AR

Understanding the aetiology and mechanisms leading to regurgitation may be essential for proper management. Aortic valve repair, while performed infrequently at this point, may be considered in suitable cases, such as bicuspid aortic valves with leaflet prolapse.

Conversely there may be severe AR with intact aortic leaflets and a normal annulus in some cases of aortic dissection, where prolapse of the dissection membrane prevents valve closure. In such circumstances the valve may not require replacement at the time of aortic root surgery. Obtaining information about the aetiology and mechanism of AR is currently the domain of echocardiography, particularly using the transoesophageal approach. Newer imaging tools, such as three dimensional echocardiography and magnetic resonance imaging, may contribute to the assessment of the complex spatial relationships of the aortic valve structures and may ultimately improve the facility of aortic valve repair.

Ascending aorta

In all instances information about morphology and size of the ascending aorta are needed. Aortic root and annular dilatation may cause AR even when leaflets are normal. In the presence of a bicuspid aortic valve, the aortic root is frequently dilated, probably due to an abnormality of the wall,5 which may also explain the increased incidence of aortic dissection in patients with bicuspid aortic valves. Aortic root dilatation may be independent of haemodynamics and can progress further even after valve surgery. As in other types of aortic dilatation, elective surgical correction is recommended when the diameter exceeds 55 mm.6

Additional pathology

Information about additional findings is also needed, including presence of abnormalities of other valves and of endocarditis. Knowledge about possible coexistent congenital abnormalities is also essential, especially in view of the fact that some are associated with AR, such as subaortic stenosis and some forms of ventricular septal defects (VSDs).


Patients with severe AR have been shown to have a significant increase in mortality and morbidity compared to the general population.7 With conservative management approximately half the surviving patients developed heart failure after 10 years and almost all others required valve surgery. Patients who became symptomatic are at increased risk; in particular, the highly symptomatic ones (New York Heart Association functional class III–IV) have been noted to have an annual mortality rate of approximately 25%.7

A diminished LV ejection fraction (below 50–55%) is associated with reduced prognosis even in asymptomatic patients7,8 (fig 2A). LV dysfunction of short duration is, however, usually reversible9; thus serial evaluation of LV function is recommended on a routine basis in these patients and surgery should be considered as soon as a drop in ejection fraction occurs. LV enlargement in and of itself also constitutes an indication for surgery10,11 (fig 2B). The most commonly used parameters are echocardiographic end-systolic and end-diastolic diameters.10 At present ejection fraction is most commonly measured using two dimensional echocardiography or radionuclide ventriculography. For assessment of LV size actual volume measurements may increasingly replace single dimensional measurements in the future, particularly using accurate and reproducible techniques, such as MRI and three dimensional echocardiography.

Figure 2

 Postoperative survival of patients with preoperative reduced versus normal left ventricular function (panel A) and of patients with preoperative left ventricular end-systolic diameter (LVESD) ⩽ 55 mm versus > 55 mm (panel B). LVEF, left ventricular ejection fraction. Reproduced from Bonow et al,8,10 with permission.


The goal of managing AR is no longer just relief of symptoms but also to provide optimal long term outcome with regard to mortality and morbidity. Achieving this goal is critically dependent on preservation of LV function and some patients may require surgical repair before onset of symptoms. In AR, criteria for early detection of myocardial damage focus on ventricular size and function. Current practice guidelines for the timing of surgery in asymptomatic patients use cut-offs derived from the published literature (table 311,12).

Table 3

 Indication for surgery in patients with severe aortic regurgitation

AR patients have an increased risk for developing endocarditis and should therefore receive antibiotic prophylaxis.

Surgical options

Valve replacement, using either a mechanical or a biological prosthesis, continues to be the mainstay of surgical treatment. The use of homografts or pulmonary autografts is limited by concerns about their durability.13 Valve repair is being performed in selected patients, particularly in those with prolapsing bicuspid aortic valves and eccentric jets,14 but outcomes have generally been less favourable than for mitral valve repair.

Conservative management

Patients with mild or moderate AR can usually be managed conservatively unless surgery is indicated for correction of concomitant lesions, such as a markedly dilated aortic root. Even severe AR can be managed conservatively as long as the patient remains asymptomatic and no LV dysfunction or pronounced LV enlargement are present. Patients with moderate to severe AR often receive vasodilator treatment, particularly when the ventricle is already dilated. One study comparing nifedipine with digoxin15 found the patients on nifedipine developed fewer symptoms and less LV dysfunction; however, no placebo group was included and the number of included patients was small. Similar benefits have been reported with angiotensin converting enzyme inhibitors and other vasodilators, although these trials also included only small numbers of patients. In a recent randomised trial16 in 95 patients with asymptomatic severe AR comparing nifedipine or enalapril to placebo, vasodilators did not reduce or delay the need for aortic valve replacement and did not reduce regurgitant volume, did not decrease LV size, and did not improve LV function. Thus, in spite of the fact that some trials suggest a benefit from using vasodilators in AR, evidence supporting their use must be considered limited.17

A step by step approach to managing the patient with aortic regurgitation

After aortic regurgitation has been detected by physical examination or by echocardiography the next step is to assess its severity (fig 3). This is most commonly done by echo-Doppler; in case of uncertainty, cardiac MRI (CMRI) should preferably be used. Aortography can be an alternative. Even in the absence of severe AR, prophylactic surgery may be needed for aortic root aneurysm, and this requires further evaluation of the ascending aorta. Surgery is recommended when the maximum diameter reaches 55–60 mm. If echocardiography cannot provide reliable measurements, CMRI or computed tomography (CT) should be performed.

Figure 3

 Management strategy for aortic regurgitation —a stepwise approach using imaging (see text). AR, aortic regurgitation; AV, aortic valve; CMRI, cardiac magnetic resonance imaging; CT, computed tomography; LV, left ventricle; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; LVESD, left ventricular end-systolic diameter; LVESI, left ventricular end-systolic index. *Consider body size. †These methods use volumes rather than diameters for evaluation of left ventricle size.

In the case of severe AR, the next question is about symptoms. In their presence, surgery is indicated.18 Exercise testing may be helpful to clarify symptom status.

In a definitely asymptomatic patient, the next step is to assess LV function. In the case of reduced LV function as defined by ejection fraction < 50% (some even recommend < 55%), surgery should be performed.19

Asymptomatic patients with normal LV function should be considered for valve surgery for preservation of myocardial function in presence of pronounced LV enlargement,20 particularly when the end-systolic diameter exceeds 55 mm11 (50 mm by European guidelines12) or when the end-diastolic diameter of the LV exceeds 75 mm. These cut-off values must take body size into account. They are valid for average-sized men but may be too large for women, especially if the patient is small. For this reason, some prefer a cut-off LV end-systolic index > 25 mm/m2. However, indexing has its own limitations and both the absolute value and index must always be viewed on the background of individual patient size. Uncertain echo measurements may require clarification by CMRI or LV angiography.

If surgery is indicated for any of the above mentioned reasons, echocardiography should evaluate whether a valve repair is feasible or whether valve replacement must be performed.

In addition, aortic size and morphology must be assessed in order to evaluate the need for concomitant aortic surgery.

If surgery is not indicated, serial clinical and echocardiographic evaluation is required in patients who remain asymptomatic. In stable patients, one year follow-up intervals may be appropriate as studies have shown that LV dysfunction developing over 12–14 months is usually reversible9 (fig 4).

Figure 4

 Change in left ventricular (LV) ejection fraction at rest pre- and postoperatively in patients with severe aortic regurgitation and prolonged LV dysfunction (>14 months), LV dysfunction of unknown duration, and brief LV dysfunction (⩽14 months). Reproduced from Bonow et al,9 with permission.


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