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CURRENT Diagnosis & Treatment in Cardiology > Chapter 8. Aortic Regurgitation >

Essentials of Diagnosis

  • Following a long asymptomatic period, presentation with heart failure or angina.
  • Wide pulse pressure with associated peripheral signs.
  • Diastolic decrescendo murmur at the left sternal border.
  • Left ventricular dilation and hypertrophy with preserved function.
  • Presentation and findings dependent on the rapidity of onset of regurgitation.
  • Diagnosis confirmed and severity estimated by Doppler echocardiography, aortography, magnetic resonance imaging, or computed tomography angiography.


Normally, the integrity of the aortic orifice during diastole is maintained by an intact aortic root and firm apposition of the free margins of the three aortic valve cusps. Aortic regurgitation (AR) may therefore be caused by a variety of disorders affecting the valve cusps or the aortic root (or both) (Table 8–1). With rheumatic heart disease becoming less common, nonrheumatic causes currently account for most of the underlying causes of aortic insufficiency, including congenitally malformed aortic valves, infective endocarditis, and connective tissue diseases. Disorders affecting the aortic root also account for a large number of patients with AR. These conditions include cystic medial necrosis, Marfan syndrome, aortic dissection, and inflammatory diseases. Even in the absence of any obvious abnormality of the aortic valve or root, severe systemic hypertension has been reported to cause significant AR.

Table 8–1. Causes of Aortic Regurgitation.

Aortic cusp abnormalities


Infectious: Bacterial endocarditis, rheumatic fever


Congenital: Bicuspid aortic valve, Marfan syndrome


Inflammatory: Systemic lupus erythematosus, rheumatoid arthritis, Beçhet syndrome


Degenerative: Myxomatous (floppy) valve, calcific aortic valve




Postaortic valvuloplasty


Diet drug valvulopathy

Aortic root abnormalities


Aortic root dilatation: Marfan syndrome, syphilis, ankylosing spondylitis, relapsing polychondritis, idiopathic aortitis, annuloaortic ectasia, cystic medial necrosis, Ehlers-Danlos syndrome


Loss of commissural support: Aortic dissection, trauma, ventricular septal defect

Increased afterload


Systemic hypertension


Supravalvular aortic stenosis

Roberts WC et al. Causes of pure aortic regurgitation in patients having isolated aortic valve replacement at a single US tertiary hospital (1993 to 2005). Circulation. 2006 Aug 1;114(5):422–9. [PMID: 16864725]


The presentation and findings in patients with AR depend on its severity and rapidity of onset. The hemodynamic effects of acute severe AR are entirely different from the chronic type and the two will be discussed separately.

Chronic Aortic Regurgitation

In response to the left ventricular volume overload associated with AR, progressive left ventricular dilation occurs. This results in a higher wall stress, which stimulates ventricular hypertrophy and which, in turn, tends to normalize wall stress. Patients with severe AR may have the largest end-diastolic volumes produced by any other heart disease and yet, their end-diastolic pressures are not uniformly elevated. In keeping with the Frank-Starling mechanism, the stroke volume is also increased. Thus, despite the presence of regurgitation, a normal effective forward cardiac output can be maintained. This state persists for several years. Gradually, left ventricular diastolic properties and contractile function start to decline. The adaptive dilation and hypertrophy can no longer match the loading conditions. The left ventricular end-diastolic pressure begins to rise and the ejection fraction drops with a decline in effective forward output and development of heart failure.

Acute Aortic Regurgitation

In contrast to chronic AR, when sudden severe regurgitation occurs, the left ventricle has no time to adapt. The acute ventricular volume overload therefore results in a small increase in end-diastolic volume and severe elevation of end-diastolic pressure, which is transmitted to the left atrium and pulmonary veins, culminating in acute pulmonary edema. Because the ventricular end-diastolic volume is normal, the total stroke volume is not increased and the effective forward cardiac output drops. To compensate for the low output state, sympathetic stimulation occurs, which produces tachycardia and peripheral vasoconstriction, the latter further worsening AR.

Clinical Findings

Symptoms and Signs

Chronic Aortic Regurgitation

Patients with chronic AR remain asymptomatic for a long time. Palpitations are common and may be due to either awareness of forceful left ventricular contractions or occurrence of premature atrial or ventricular beats. Angina may occur either from concomitant coronary disease or from a combination of low diastolic pressure and increased oxygen demand from ventricular hypertrophy. When left ventricular dysfunction supervenes, patients initially experience exertional dyspnea and fatigue. At a later stage, resting heart failure symptoms occur with orthopnea and paroxysmal nocturnal dyspnea.

On physical examination, visible cardiac pulsations are common. The area of the apical impulse is increased on palpation and is displaced caudally and laterally. The first heart sound is usually normal. The aortic component of the second heart sound may be decreased in conditions where cusp excursion is reduced, such as with valve calcification. An S4 is often present due to underlying hypertrophy, and an S3 is audible when ventricular failure occurs. On auscultation, the characteristic sound of AR is a soft, high-pitched diastolic decrescendo murmur best heard in the third intercostal space along the left sternal border at end expiration, with the patient sitting and leaning forward. In the presence of aortic root disease, the murmur may be best heard to the right of the sternum. A systolic ejection murmur may be present at the aortic area due to the high flow state. Occasionally, a diastolic rumble may be heard at the apex, referred to as the Austin Flint murmur. The mechanism underlying this murmur remains unclear. A number of different causes have been proposed, the most recent being the aortic jet encountering the mitral inflow resulting in turbulence.

The systolic arterial pressure is increased due to a large stroke volume, whereas the diastolic pressure is decreased due to runoff from the aorta into both the ventricle and peripheral arteries. This is the underlying reason for a wide pulse pressure and for a variety of associated peripheral signs in chronic significant AR (Table 8–2). However, it must be remembered that these signs are not specific for AR and may occur in any high flow state such as occurs in anemia, thyrotoxicosis, and arteriovenous malformations. With the development of heart failure, the pulse pressure narrows and the peripheral signs of AR are attenuated.

Table 8–2. Peripheral Signs of Aortic Regurgitation.

Name of Sign Description
Corrigan pulse Rapid and forceful distention of arterial pulse with quick collapse
De-Musset sign To and fro head bobbing
Müller sign Visible pulsation of uvula
Quincke sign Capillary pulsations seen on light compression of nail bed
Traube sign Systolic and diastolic sounds (pistol shots) over the femoral artery
Duroziez sign Bruits heard over femoral artery on light compression by stethoscope
Hill sign Popliteal cuff pressure exceeding brachial pressure by 60 mm Hg or greater

Acute Aortic Regurgitation

In contrast to chronic AR, most patients with acute severe AR are symptomatic. Initial presentation may vary depending on the underlying cause, which most commonly is aortic dissection, infective endocarditis, or trauma. In the presence of associated acute AR, clinical manifestations of severe dyspnea, orthopnea, and weakness often develop. The onset of symptoms is sudden, with rapid progression to hemodynamic collapse if left untreated.

In acute AR, the left ventricle has had no time to adapt to the volume overload state. The peripheral signs associated with chronic AR are therefore absent. Pulse pressure is usually normal, and hypotension may be present in severe cases. Bilateral rales are usually present on examination of the lungs and reflect underlying pulmonary edema. On precordial palpation, the apical impulse is not shifted. The first heart sound may be soft or absent due to the premature closure of the mitral valve. An S3 is often present, but an S4 is usually absent because there is little or no atrial contribution to ventricular filling due to high left ventricular end-diastolic pressure. The typical diastolic murmur of AR is shortened in duration, often difficult to hear, and easily missed.

Laboratory Findings

Laboratory findings depend on the underlying cause of AR. Elevated white blood cell count and erythrocyte sedimentation rate are seen in inflammatory conditions, such as infection and aortitis. Abnormal antinuclear antigen and rheumatoid factor titers may be seen in patients with rheumatologic disorders. When syphilis is suspected, serologic tests may be indicated.

Diagnostic Studies


No specific electrocardiographic abnormalities are characteristic of AR. Signs of left atrial enlargement, left ventricular hypertrophy, and a “strain pattern” (ST depression with T-wave inversion in lateral leads) are often seen in chronic significant AR. Arrhythmias, including ventricular ectopy and ventricular tachycardia, may occur in advanced cases with left ventricular dysfunction. In acute AR, sinus tachycardia may be the only abnormality. In cases of infective endocarditis, inflammation or abscess formation may spread to the atrioventricular node, resulting in prolongation of the PR interval or development of atrioventricular block.

Chest Radiography

Chest radiographic findings are not specific for AR and reflect an estimate of cardiac size and pulmonary vascular changes. In chronic significant AR, an increase in the size of the cardiac silhouette is seen. In acute AR, the cardiac size is normal; the lung fields show increased markings due to pulmonary edema. When AR is due to aortic dissection, the chest film may show an enlarged ascending aorta. If calcification of the aortic knob is present, a helpful sign of dissection is increased separation between the outer margin of the aorta and the calcific density.

Echocardiography and Doppler Techniques

With recent technologic advances, particularly the introduction of color-flow Doppler, echocardiography has become the method of choice for evaluating patients with AR. Two-dimensional echocardiography in combination with various Doppler modalities and, in selected cases, transesophageal imaging has provided a noninvasive means for not only diagnosing AR with a high sensitivity and specificity but also for assessing its etiology and severity. Furthermore, important information can be obtained on the hemodynamic impact of the regurgitant lesion, prognosis, and effectiveness of therapy.

Detection of Aortic Regurgitation

Currently, the best noninvasive method for detecting AR is Doppler echocardiography. Doppler techniques are extremely sensitive and specific in the detection of AR, manifested as a diastolic flow abnormality arising from the aortic valve, directed toward the left ventricle. Even trivial regurgitation can be detected, which commonly is not audible on physical examination. Although most cases of moderate-to-severe chronic AR have typical findings on physical examination, moderate lesions may occasionally be missed on examination because of the subtlety of auscultatory findings. Doppler echocardiography is also extremely valuable in patients with acute AR when the typical clinical findings of chronic AR are absent and the murmur can often be missed. Among the available Doppler techniques (including color Doppler, pulsed and continuous wave Doppler), color Doppler echocardiography has proven to be extremely helpful in the evaluation of AR (Figure 8–1). Its major advantage over conventional Doppler is that it provides a spatial orientation of the regurgitant jet arising from the aortic root. A completely negative color Doppler examination in multiple planes virtually excludes the presence of AR. Although pulsed and continuous wave Doppler are almost equally sensitive in the detection of AR, eccentric aortic insufficiency jets can be missed with these techniques and are better delineated with color-flow imaging.

Figure 8–1.

Color Doppler echocardiographic frames in diastole from the parasternal long axis view in (A) a patient with mild aortic regurgitation and another with (B) severe regurgitation. The patient with severe aortic regurgitation (B) has a large ascending aortic aneurysm (Ao Ann). The width of the aortic regurgitation jet in the left ventricular outflow (between arrows) provides a good estimate of the severity of aortic regurgitation by color Doppler echocardiography. Ao, aorta; Ao Ann, aortic aneurysm; LA, left atrium; LV, left ventricle.

Echocardiographic imaging with M-mode and two-dimensional examinations cannot detect the presence of AR but can provide indirect clues to its presence. These include diastolic fluttering of the anterior mitral leaflet or septum depending on the impingement of the regurgitant flow on these structures. These signs, although specific, are not sensitive for the detection of AR and do not relate to the severity of regurgitation.

Assessment of Cause

Because two-dimensional echocardiography can image cardiac structures, it provides valuable information on the cause of the AR. Structural abnormalities of the aortic valve, including calcifications or thickening, congenital deformities, vegetations, rupture, or prolapse, can be identified. Dilatation of the aortic root, calcifications, or dissection can also be evaluated. Although most of these conditions can be assessed with transthoracic echocardiography, transesophageal echocardiography has provided high-resolution images that allow for improved detection of such abnormalities, especially in technically difficult cases or in conditions such as infective endocarditis. Transesophageal echocardiography is also routinely performed when an aortic abnormality, such as aneurysm or dissection, is suspected (Figure 8–2). In patients with AR due to aortic disease, precisely defining the morphology of the valve and involvement of the aortic root is important in determining the surgical approach and deciding whether the valve can be preserved or requires replacement.

Figure 8–2.

Transesophageal echocardiographic frames in systole (SYS) and diastole (DIAST), showing a vegetation attached to the aortic valve that prolapses into the left ventricular outflow tract during diastole. In this patient, transthoracic echocardiographic imaging was difficult and failed to demonstrate the large vegetation.

Assessment of Severity

In addition to the detection of AR, Doppler echocardiography combined with two-dimensional echocardiographic imaging has recently allowed an assessment of the severity of the lesion. Several methods have been proposed, including color Doppler assessment of regurgitant jet size, continuous wave Doppler using the pressure half-time method, measurements of regurgitant volume and effective regurgitant orifice area derived from two-dimensional echocardiography and pulsed Doppler techniques.

With color-flow Doppler, the AR jet can be spatially oriented in the two-dimensional plane arising from the aortic valve and directed toward the left ventricle. The ratio of the AR jet diameter just below the leaflets to that of the left ventricular outflow diameter has been shown to correlate well with the severity of regurgitation when compared with the angiographic standard (Table 8–3, see Figure 8–1). Similarly, a good estimation of AR severity has been found by relating the cross-sectional area of the jet at its origin to the left ventricular outflow area. Recently, measurement of the width of the AR jet at the level of the leaflets (vena contracta) has been used to quantitatively approximate AR severity. A vena contracta of > 0.6 cm is considered a sign of severe AR. On the other hand, it is important to note that the length of the AR jet does not correlate well with AR severity. This is in part because color Doppler flow mapping is also highly dependent on the velocity of regurgitation, or the driving pressure, in addition to the regurgitant volume.

Table 8–3. Grading the Severity of Aortic Regurgitation Using Doppler Techniques Combined with Echocardiography.

Severity of AR Color-Flow Doppler JH/LVOH (%) Continuous Wave Doppler PHT (ms) Pulsed Doppler Regurgitant Fraction (%)
Mild < 24 > 500 < 20
Moderate 25–45 500–349 20–35
Moderately severe 46–64 349–200 36–50
Severe > 65 < 200 > 50

AR, aortic regurgitation; JH/LVOH, Ratio of aortic regurgitant jet height to left ventricular outflow height in the parasternal long axis view, PHT, pressure half-time.

Another index of AR severity that has been useful clinically is the pressure half-time derived from continuous wave Doppler recordings of the AR jet velocity. The velocity of the regurgitant jet is related to the instantaneous pressure difference between the aorta and left ventricle in diastole by the modified Bernoulli equation: = 4V  2, where P is the pressure gradient in millimeters of mercury and V is the blood velocity in meters per second. The pressure half-time index is the time it takes for the initial maximal pressure gradient in diastole to fall by 50%. In patients with mild regurgitation, there is a gradual small drop in the pressure difference in diastole, whereas with severe AR, a more precipitous drop occurs (Figure 8–3). A pressure half-time greater than 500 ms is seen in mild AR, but more significant regurgitation is usually associated with a shorter pressure half-time (see Table 8–3, Figure 8–3). The severity of AR using this index may be overestimated in patients who have elevated left ventricular end-diastolic pressure.

Figure 8–3.

Schematic of aortic and left ventricular pressure tracings in (left) a patient with mild and (right) another with severe aortic regurgitation and corresponding examples of continuous wave Doppler recording of aortic jet velocity in such patients. In mild aortic regurgitation, a gradual, small drop in the difference between aortic and ventricular pressures occurs in diastole, reflected by the small decrease in the velocity of the aortic regurgitation jet. In contrast, in severe aortic regurgitation, a more precipitous drop occurs in the pressure gradient and in the corresponding jet velocity. AR, aortic regurgitation; Ao, aorta; LV, left ventricle.

The severity of AR can also be assessed using regurgitant volume and regurgitant fraction derived from two-dimensional and pulsed Doppler echocardiography. This method is based on the continuity equation, which states that, in the absence of regurgitation, blood flow is equal across all valves. Stroke volume at the level of a valve annulus is calculated as the product of the cross-sectional area obtained by two-dimensional echocardiography and the time velocity integral of flow recorded by pulsed Doppler. In the presence of AR, stroke volume at the left ventricular outflow tract is higher than that across another valve without regurgitation. Therefore, AR volume can be calculated as the difference between stroke volume at the left ventricular outflow and that derived at another valve site. Dividing the regurgitant volume by stroke volume across the aortic valve gives an estimate of regurgitant fraction. A regurgitant fraction of less than 30% is usually mild, whereas regurgitant fraction greater than 50% denotes severe AR (see Table 8–3). A similar approach to estimating severity of AR can be achieved using pulsed Doppler echocardiography in the proximal descending aorta. In patients with significant AR, a large reversal of flow is observed in diastole toward the aortic arch and ascending aorta. This simple method should be used routinely to qualitatively grade the severity of regurgitation and can also be used quantitatively to derive a regurgitant fraction.

Proximal flow convergence is more difficult to identify in AR, but when it is present, the proximal isovelocity surface area method can be used to determine the effective regurgitant orifice area. This method is less accurate in eccentric jets and aortic root dilatation.

Although color-flow Doppler allows a good estimation of the severity of AR in most patients, its accuracy depends on optimization of the color Doppler examination, including gainsettings, frame rate, and interrogation of multiple tomographic planes. The availability of other independent Doppler indices of AR severity further allows the corroboration of color Doppler findings. This is particularly helpful in patients with eccentric AR jets, for which severity may be difficult to assess by color-flow Doppler alone. A detailed transthoracic examination usually provides all the necessary information. When the transthoracic approach is inadequate or inconclusive, transesophageal echocardiography can be performed in this setting for the diagnosis and assessment of severity of the lesion.

Another important caveat in classifying the severity of AR is that it is in part dependent on hemodynamic status, including preload and, more importantly, afterload. Raising blood pressure may significantly increase AR severity.

Assessment of Hemodynamic Effects

The hemodynamic effects of AR are assessed with both echocardiographic imaging and Doppler echocardiography. Two-dimensional echocardiography provides quantitation of ventricular size and function, in addition to the degree of left ventricular hypertrophy and ventricular mass. End-diastolic and end-systolic left ventricular dimensions and volumes as well as left ventricular ejection fraction provide important measures of the hemodynamic effects of AR and help identify patients at higher risk. In patients with acute AR, premature closure of the mitral valve can be demonstrated by both two-dimensional and M-mode imaging. In these situations, diastolic mitral regurgitation can also be detected by Doppler echocardiography, reflecting the rapid rise of left ventricular pressure in diastole, exceeding that of left atrial pressure. These findings indicate severe AR. In patients with chronic AR, assessment of the ventricular and atrial filling dynamics at the mitral and pulmonary venous inflow, respectively, allows for noninvasive estimation of ventricular diastolic pressure, further adding to the overall evaluation of the hemodynamic effect of AR on ventricular function. Newer modalities such as Doppler tissue imaging further enhance the accuracy of noninvasive assessment of ventricular diastolic function. Thus, in patients with chronic AR, two-dimensional echocardiography with Doppler provides serial assessment of left ventricular volumes, hypertrophy, and function and helps assess the progression of the disease and optimum timing of surgical intervention.

Cardiac Catheterization and Angiography

Prior to the introduction of Doppler echocardiography, the evaluation of the severity of AR invariably required invasive testing by cardiac catheterization. With the improvement in the accuracy of noninvasive tests, routine cardiac catheterization is no longer necessary in most patients. At catheterization, the detection of AR is achieved with the injection of radiopaque contrast into the aortic root and the appearance of dye in the left ventricle (Figure 8–4). In addition, aortography allows evaluation of the ascending aorta for dilatation or dissection. Some of the structural abnormalities of the aortic valve may also be identified. The severity of AR is quantitatively approximated using a grading system that takes into account the intensity of contrast dye in the left ventricle and its clearance (Table 8–4). This grading system has been helpful clinically in the assessment of AR severity. However, it is important to emphasize that, similar to other diagnostic techniques, a number of technical factors may also affect interpretation. Positioning the catheter too close to the valve may itself cause regurgitation. The volume and rapidity of contrast injection, ventricular function, and type of catheter used are important factors that may affect the interpretation of AR severity.

Figure 8–4.

Aortic root contrast injection in the left anterior oblique projection in a patient with severe aortic regurgitation, showing significant opacification of the left ventricle. The aortography also shows an ascending aortic aneurysm. AoA, aortic aneurysm; Lv, left ventricle.

Table 8–4. Angiographic Grading of the Severity of Aortic Regurgitation.

Grade Degree of LV Opacification Intensity of Dye Clearance of Dye from LV
I (mild) Incomplete Ao > LV Completely cleared on each beat
II (moderate) Complete but faint Ao > LV Incomplete clearance
III (moderately severe) Complete opacification in several beats Ao = LV Slow
IV (severe) Complete on first beat Ao < LV Slow

Ao, aorta; LV, left ventricle.

At catheterization, the severity of AR can also be assessed by the determination of regurgitant volume and regurgitant fraction. In the absence of regurgitation or shunts, the left ventricular stroke volume derived from contrast ventriculography is equal to right ventricular stroke volume obtained by the Fick method or thermodilution. When isolated AR is present, subtracting left ventricular from right ventricular stroke volume gives the regurgitation volume. Regurgitant fraction is derived as the regurgitant volume divided by left ventricular stroke volume. In the presence of concomitant mitral regurgitation, a total regurgitant volume or fraction can only be assessed using this method. Because of inherent variability in the determination of stroke volume, a 10–15% error in these measurements is not infrequent and is similar to those obtained with Doppler echocardiography.

Cardiac catheterization provides an accurate assessment of the hemodynamic effect of AR. Using contrast ventriculography, preferably in biplanar projections, accurate determination of left ventricular volumes and ejection fraction can be performed. Furthermore, direct measurements of pressures in the various cardiac chambers can be recorded. In compensated chronic AR, the only abnormality that may be observed is a widened pulse pressure on the aortic pressure tracing. As decompensation occurs, left ventricular end-diastolic pressure rises. In severe, particularly acute AR, aortic and left ventricular pressures may equalize at end-diastole.

With the improvement in noninvasive testing, routine cardiac catheterization is no longer necessary in most patients for the sole assessment of the lesion. Currently, cardiac catheterization is indicated in the assessment of AR severity when noninvasive testing is equivocal or discordant with the clinical presentation and, more commonly, in the assessment of coronary artery disease prior to aortic valve surgery. Preoperative coronary angiography should be performed prior to elective surgery for AR in men older than 35 years of age, premenopausal women over 35 who have risk factors for coronary artery disease, postmenopausal women, and any patients with clinical suspicion of coronary artery disease.

Electrocardiographically Gated 64-Slice Computed Tomography Angiography (CTA)

This test allows rapid diastolic frame rates from which the regurgitant orifice can be planimetered. Studies have shown excellent agreement with echo Doppler measures in the same patients. In addition, the size of the aorta and left ventricle can be determined as well as ejection fraction. CTA can also be used to detect significant coronary artery disease in patients with chest pain or who are being considered for surgery.

Magnetic Resonance Imaging

Advances in magnetic resonance imaging (MRI) have recently allowed for evaluation of patients with AR. At present, three basic approaches are available: spin echo imaging, gradient echo imaging (cine-MRI), and phase velocity mapping. Spin echo imaging provides an excellent approach for depicting cardiac morphology and detecting aortic root disease. However, aortic valve visualization is poor. Using cine-MRI, AR is detected as a decrease in the signal intensity in the left ventricular outflow during diastole. In preliminary studies, the ratio of area of low-intensity signal to the area of the left ventricular outflow has provided an accurate estimate of AR severity. Regurgitant fractions have been determined by comparing right and left ventricular volumes and stroke volumes. Furthermore, using phase velocity mapping, flow in a region of interest can be assessed. Regurgitant fraction with this method can be derived by comparing flows in the ascending aorta and pulmonary artery.

The use of MRI is promising in the assessment of AR. It is particularly helpful in defining the severity and extent of AR. Imaging can be performed in any plane, without attenuation from lung or bone. However, this modality cannot be used in patients carrying metallic objects such as defibrillators or pacemakers. Its current drawbacks are lack of availability of cardiac MRI and high cost. It is an alternative to echocardiography and for centers with expertise in cardiac MRI.

Exercise Stress Testing

Exercise stress testing can be used to evaluate patients with equivocal symptoms or to guide patients who wish to participate in athletic activities. Early studies using exercise radionuclide angiography to assess ejection fraction suggested that a failure to rise or a fall in ejection fraction correlated with poor outcomes and was a criteria for considering surgery. However, when resting ejection fraction and end-diastolic left ventricular volume were considered, this exercise response in asymptomatic patients had no independent predictive value. Thus, radionuclide imaging with exercise in patients has been largely abandoned. In patients with inadequate echocardiograms, radionuclide imaging can be used to assess left ventricular size and function, but MRI or CT are probably superior.

Alkadhi H et al. Aortic regurgitation: assessment with 64-section CT. Radiology. 2007 Oct;245(1):111–21. [PMID: 17717329]

Bekeredjian R et al. Valvular heart disease: aortic regurgitation. Circulation. 2005 Jul 5;112(1):125–134. [PMID: 15998697]

Debl K et al. Assessment of the anatomic regurgitant orifice in aortic regurgitation: a clinical magnetic resonance imaging study. Heart. 2008 Mar;94(3):e8. [PMID: 17686805]

Scheffel H et al. Accuracy of 64-slice computed tomography for the preoperative detection of coronary artery disease in patients with chronic aortic regurgitation. Am J Cardiol. 2007 Aug 15;100(4):701–6. [PMID: 17697832]

Willett DL et al. Assessment of aortic regurgitation by transesophageal color Doppler imaging of the vena contracta: validation against an intraoperative aortic flow probe. J Am Coll Cardiol. 2001 Apr;37(5):1450–5. [PMID: 11300460]


The treatment of AR depends on its underlying cause, severity, cardiac function, and the presence or absence of symptoms. Mild-to-moderate AR may not require any specific treatment, whereas severe acute AR due to aortic dissection is a medical and surgical emergency.

Acute Aortic Regurgitation

Severe acute AR carries a high mortality rate if left untreated. It requires aggressive supportive measures, a rapid assessment of cause, and institution of definitive therapy. Because early death due to left ventricular failure and hemodynamic collapse is frequent in these patients despite intensive medical therapy, prompt surgical intervention is indicated. While the patient is being prepared for surgery, pharmacologic therapy can be initiated. Vasodilator therapy with sodium nitroprusside is the treatment of choice in acute AR because of its afterload and preload reduction. The dose is titrated to optimize forward cardiac output and pulmonary capillary wedge pressure. Positive inotropic agents such as dobutamine can be used if the patient remains hypotensive with a low systemic cardiac output.

When acute AR is associated with hemodynamic instability, the only definitive therapy is surgical correction. The timing of surgery depends on the cause and degree of hemodynamic derangement. In infective endocarditis with severe AR, it is preferable to give several days of appropriate antibiotics prior to aortic valve replacement (AVR), provided the patient is hemodynamically stable. Indications for urgent surgery are New York Heart Association (NYHA) class III–IV congestive heart failure, systemic embolization, persistent bacteremia, fungal endocarditis, or abscess formation. When AR results from aortic dissection with disruption of commissural support, urgent surgical repair is indicated.

Chronic Aortic Regurgitation

Mild-to-Moderate Aortic Regurgitation

Patients who have mild or moderate AR and are asymptomatic and who have normal or minimally increased cardiac size, require no therapy for the AR. They should be followed with clinical evaluation yearly and echocardiography at 2–3 year intervals. In patients with a history of rheumatic fever, prophylaxis using either penicillin or erythromycin is indicated until the age of 25 years and 5 years after the last episode. If rheumatic carditis has already occurred, lifelong prophylaxis is recommended, even following valve replacement. Any occurrence of systemic hypertension should be treated because it aggravates the degree of regurgitation. Patients with AR secondary to syphilis should receive a full course of penicillin therapy. Patients with moderate AR should avoid isometric exercise, competitive sports, and heavy physical exertion. If symptoms present in such patients, an alternative cause for the symptoms should be considered.

Moderate-to-Severe Aortic Regurgitation with Symptoms and Normal Left Ventricular Function

Patients with chronic significant AR and normal left ventricular ejection fraction (LVEF) (> 50%) who have NYHA class III or IV symptoms or Canadian Cardiovascular Society class II–IV angina should undergo AVR. Patients with NYHA class II symptoms should be evaluated on a case-by-case basis. If the cause or severity of symptoms is unclear, an exercise test should be done. If exercise capacity is normal, treatment should be given as for asymptomatic patients as outlined in the following section. If new, even mild symptoms appear in a patient with chronic significant AR—particularly if left ventricular size is increased or the ejection fraction is on the low side of normal—then AVR should be considered.

Medical therapy is attempted in symptomatic patients who are awaiting surgery or are not surgical candidates due to refusal, terminal medical illness, or advanced age. The aim of therapy in these patients is primarily relief of symptoms and improvement of exercise capacity. Medical therapy includes digitalis, diuretics, and vasodilator drugs. Oral vasodilators, such as hydralazine, and angiotensin-converting enzyme (ACE) inhibitors reduce afterload, allowing for greater forward cardiac output which may improve exercise tolerance. Preload reduction with diuretics and nitrates is also helpful in reducing pulmonary congestion.

Moderate-to-Severe Aortic Regurgitation with Symptoms and Abnormal Left Ventricular Function

Symptomatic patients with mild-to-moderate left ventricular dysfunction (LVEF = 25–50%) should undergo AVR. Treatment decisions for patients with more advanced left ventricular dysfunction (LVEF < 25% or left ventricular end-systolic dimension > 60 mm) is difficult. The operative risk is high, and not all patients benefit from AVR. On the other hand, outcome with medical therapy is poor as well. Patients with class II–III symptoms and recent onset of left ventricular dysfunction should be considered for surgical treatment. In patients not considered surgical candidates, aggressive medical therapy is useful in controlling symptoms. Diuretics and vasodilators are the mainstay of medical treatment. If symptoms persist, short-term inotropic support using dobutamine along with intravenous nitroprusside and diuretics may provide relief.

Moderate-to-Severe Aortic Regurgitation Without Symptoms

The optimal timing of AVR in asymptomatic patients remains a challenging clinical decision. Clearly, patients with normal left ventricular function and good exercise capacity can live for several years without symptoms or left ventricular dysfunction, and surgery is clearly not indicated for such patients. These patients are candidates for long-term oral vasodilator therapy. It has been shown that the use of oral hydralazine in patients with AR produces a number of beneficial hemodynamic effects, including a reduction in regurgitant volume, end-diastolic and end-systolic volumes, and improvement in ejection fraction and effective cardiac output. Similar results have been shown with nifedipine and ACE inhibitors. Vasodilator therapy has also been shown to delay onset of symptoms, occurrence of left ventricular dysfunction, and the need for AVR. However, not all studies have demonstrated a benefit from vasodilator drugs.

When the evidence of left ventricular dysfunction (ejection fraction < 50%) is clear, despite the absence of symptoms, AVR is recommended to prevent further left ventricular dysfunction and improve prognosis. However, once the ejection fraction is decreased, surgical risk is higher and left ventricular dysfunction may become irreversible. The ideal time to intervene is late enough in the course of the disease to justify the surgical risk and postoperative sequelae such as anticoagulation, but early enough to prevent irreversible left ventricular contractile dysfunction. To determine the optimal time for surgery in chronic asymptomatic AR, it is important to identify preoperative variables that predict postoperative left ventricular function. A number of parameters have been investigated in the hope of identifying the ideal predictor. Regurgitant volume or fraction are not predictors of postoperative outcome because they are significantly influenced by loading conditions. End-diastolic volume has modest correlation with surgical outcome. The cutoff used varies from 150 to 250 mL/m2. An end-diastolic minor dimension of greater than 70 mm has also been associated with a poor postoperative outcome. A major limitation of end-diastolic indices is their dependence on preload and thus may not reflect intrinsic myocardial contractile function. Left ventricular ejection fraction has been shown to be an important predictor of postoperative survival. An LVEF of less than 0.50 is associated with significantly reduced 3-year survival rate (64 ± 10%) compared with an LVEF greater than 0.50 (91 ± 28%). Although LVEF has high sensitivity for identifying patients with worse postoperative outcome, it is less specific. This is understandable because LVEF reflects loading conditions in addition to the inotropic state of the myocardium. Similarly, LVEF response to exercise may be modulated by multiple factors, including peripheral resistance, preload heart rate, sympathetic tone, and type of exercise. Therefore, although a decrease in ejection fraction during exercise was previously considered to predict a poor outcome in chronic AR, recent data suggest that this is a nonspecific response. However, exercise capacity by itself is an important predictor of survival in AR.

End-systolic indices are less load-dependent and have been used to predict left ventricular function following surgery for AR. An end-systolic minor dimension greater than 55 mm or end-systolic volume greater than 60 mL/m2 identifies patients with persistent left ventricular dysfunction and a poor survival rate following AVR. Recently, the ratio of left ventricular end-systolic dimension in millimeters and body surface area in square meters that exceeds 25 has been advocated as a marker of occult left ventricular dysfunction. If, in addition to an increased end-systolic ventricular size, the ejection fraction is also reduced, the survival rate drops further. Even though they are preload-independent, end-systolic indices are still affected by afterload. The ratio of end-systolic pressure or wall stress to end-systolic volume has been advocated as an index of contractility, which is less dependent on loading conditions. In patients with chronic severe AR, abnormalities of the end-systolic pressure-volume relationship have been shown, despite a normal LVEF, reflecting depressed myocardial contractility. Such patients are more likely to have symptoms and a need for earlier valve replacement.

For asymptomatic patients with moderate-to-severe AR, a noninvasive evaluation of left ventricular size and function is recommended as well as an exercise test if functional capacity is unclear (Figure 8–5). If exercise capacity is poor or LVEF is less than 50%, surgical treatment is recommended. Those with good exercise tolerance and normal left ventricular function should be followed at 6- to 12-month intervals. Oral vasodilators may be considered in these patients. In patients who remain asymptomatic, AVR should be considered when serial testing shows decreased exercise tolerance, progressive left ventricular enlargement, or worsening left ventricular function.

Figure 8–5.

Schematic of proposed treatment of patients with chronic significant aortic regurgitation. AR, aortic regurgitation; AVR, aortic valve replacement; LV, left ventricle.


Asymptomatic patients with chronic AR have a stable course for many years. The mean rate of progression to surgery is approximately 4% per year. Symptoms are the major determinant of outcome in AR. The mortality rate for patients with NYHA class II–IV symptoms is over 20% per year. Even for patients with class II symptoms, the mortality rate is 6% per year compared with 3% for patients with class I symptoms. In general, good results have been observed with AVR for AR, with an average operative mortality rate of 3–4% and a 5-year survival rate of 85%. These results depend on several factors, including preoperative ventricular function, concomitant coronary artery disease, and the underlying cause of AR. Aortic valve replacement is necessary in most patients. In some cases of AR secondary to loss of commissural support, aortic valve repair can be performed. The feasibility of aortic valve repair can be determined by a transesophageal echocardiogram. In patients with excessive aortic root dilatation or aneurysm, a composite aortic graft with reimplantation of the coronary arteries is performed more frequently. Most patients show resolution of symptoms following surgery to correct AR. The end-diastolic volume is reduced immediately, with some further reduction occurring over several days after surgery. The LVEF continues to improve up to 1–2 years after surgery. There is also a gradual decline in left ventricular mass. About 20–30% of patients will have incomplete symptomatic relief and persistent left ventricular dysfunction. These findings are associated with the presence of preoperative left ventricular dysfunction, particularly if the duration of dysfunction is prolonged (> 18 months). Even though the outcome is less than optimal in patients with moderate left ventricular dysfunction, with recent surgical advances, many of them still do better with surgery than with medical management. Surgery should be considered in all symptomatic patients unless left ventricular dysfunction is very severe.

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