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Acute aortic regurgitation in adults

Acute aortic regurgitation in adults
Literature review current through: Jan 2024.
This topic last updated: Mar 04, 2022.

INTRODUCTION — The acute onset of severe aortic regurgitation (AR, also called aortic insufficiency) is usually a medical emergency due to the inability of the left ventricle to quickly adapt to the abrupt increase in end-diastolic volume caused by the regurgitant flow. If not surgically corrected, acute severe AR commonly results in cardiogenic shock. By contrast, clinical symptoms are a relatively late feature of chronic AR, since the gradually dilating left ventricle and the chronically increased diastolic volume dampens many of the hemodynamic effects of acute AR [1-3]. (Related Pathway(s): Acute decompensated heart failure: Management of patients with cardiogenic shock.)

Issues related to acute AR will be reviewed here. Chronic AR is discussed separately. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults" and "Natural history and management of chronic aortic regurgitation in adults".)

ETIOLOGY — The causes of acute AR with a native aortic valve are limited and include:

Endocarditis – Endocarditis results in valve destruction and leaflet perforation. In addition, aortic perivalvular abscess may rupture into the left ventricle, resulting in AR, or into the left atrium or right ventricular outflow tract, with a clinical presentation that mimics acute AR. (See "Complications and outcome of infective endocarditis", section on 'Perivalvular abscess'.)

Aortic dissection – Aortic dissection can result in AR by four mechanisms: dilation of the sinuses with incomplete coaptation of the leaflets at the center of the valve; involvement of a valve commissure resulting in inadequate leaflet support; direct extension of the dissection into the base of a leaflet, resulting in a flail valve leaflet; and prolapse of the dissection flap across the aortic valve into the left ventricular outflow tract in diastole impeding leaflet closure. Patients with a bicuspid aortic valve are at higher risk of aortic dissection [4,5]. (See "Clinical features and diagnosis of acute aortic dissection" and "Clinical manifestations and diagnosis of bicuspid aortic valve in adults", section on 'Aortic regurgitation'.)

Rupture of a congenitally fenestrated cusp – A congenital valve fenestration in the overlap segment of valve closure may rupture, resulting in acute severe regurgitation [6-8].

Traumatic rupture of the valve leaflets – Traumatic rupture of the aortic valve can occur after deceleration injury or blunt trauma to the chest [9,10].

Iatrogenic – Complication of procedures such as aortic balloon valvotomy or transcatheter aortic valve implantation (TAVI) [11,12]. (See "Percutaneous balloon aortic valvotomy for native aortic stenosis in adults".)

The two most common causes of acute AR of a native aortic valve are endocarditis and aortic dissection. This was illustrated in a single center review of 268 adults referred for aortic valve replacement for isolated AR, 18 percent of whom had acute AR [13]. All of the cases were due to active endocarditis (56 percent) or acute aortic dissection (44 percent).

In addition, acute AR may develop in patients with prosthetic aortic valves. With bioprosthetic valves, AR may occur with structural valve deterioration (eg, valve rupture adjacent to areas of leaflet calcification) or leaflet destruction due to endocarditis. Acute mechanical valve regurgitation can be caused by valve thrombosis or pannus formation with incomplete leaflet closure or disk escape with older valve models. Paravalvular AR is caused by prosthetic valve dehiscence which can occur as a complication of endocarditis or other cause of inadequate valve attachment such as the aortopathy associated with Marfan syndrome. (See "Mechanical prosthetic valve thrombosis or obstruction: Clinical manifestations and diagnosis" and "Prosthetic valve endocarditis: Epidemiology, clinical manifestations, and diagnosis", section on 'Echocardiography'.)

PATHOPHYSIOLOGY — In chronic AR, the volume overload of the left ventricle (LV) results in a gradual increase in LV size that provides a normal forward cardiac output despite the regurgitant valve flow; LV diastolic pressures remain normal. By contrast, with acute AR, the regurgitant volume fills a small ventricle that has not had time to dilate, resulting in an acute increase in LV diastolic pressure and a fall in forward cardiac output [14,15]. (See "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults".)

Acute AR results in the following pathophysiologic events:

The LV cannot acutely increase total stroke volume, resulting in a decline in forward stroke volume and cardiac output. The decline in forward stroke volume may be exacerbated by a shortening of diastolic filling time due to the combination of early closure of the mitral valve (due to high diastolic pressures) and tachycardia (related to a decrease in forward flow and cardiac output). The net effect is often profound hypotension and cardiogenic shock.

With severe AR, LV diastolic pressure rises sharply, with equalization of end-diastolic aortic and LV pressures. The elevated LV diastolic pressure leads to elevated left atrial and pulmonary venous pressures, which can lead to pulmonary edema. (See "Hemodynamics of valvular disorders as measured by cardiac catheterization".)

These effects may be more pronounced in patients who develop acute AR and have a small, noncompliant LV cavity due to preexisting LV hypertrophy. Examples include acute AR caused by aortic dissection in patients with systemic arterial hypertension and acute AR after balloon valvotomy (or transcatheter aortic valve implantation [TAVI]) in patients with aortic stenosis.

CLINICAL PRESENTATION — Severe acute AR commonly presents with sudden cardiovascular collapse and pulmonary edema. Other presenting symptoms are related to the cause of acute AR (eg, signs and symptoms of endocarditis or aortic dissection). However, in some cases, acute AR is the first clue suggesting one of these diagnoses. Aortic dissection should always be suspected in patients with AR and chest or back pain. (See "Clinical features and diagnosis of acute aortic dissection".)

Physical examination — Manifestations of cardiogenic shock usually dominate in patients with severe acute AR. These include profound hypotension, pallor, diaphoresis, occasional cyanosis and other signs of peripheral vasoconstriction, as well as signs of pulmonary edema. The pulse pressure is normal or may be reduced, but the arterial pulsation is usually low amplitude and rapid. The cardiac apex is generally not displaced and is not hyperdynamic.

If aortic dissection is the cause, an inequality of pulses and blood pressure between the left and right arms may be observed. However, this finding may not be appreciated in the setting of profound hypotension.

The peripheral manifestations of chronic AR, associated with an increased pulse pressure, such as Traube's sign, Duroziez's murmur, and water hammer (Corrigan) pulses, are less apparent or may be entirely absent with acute AR. This difference from chronic AR is due to the fact that left ventricular (LV) stroke volume is not increased, and as a result the wide pulse pressure of chronic AR is not seen. (See 'Pathophysiology' above and "Clinical manifestations and diagnosis of chronic aortic regurgitation in adults", section on 'Physical examination'.)

Cardiac auscultation — Acute AR alters the quality of most of the heart sounds:

The early closure of the mitral valve generally produces a soft or absent S1, which can occasionally be heard in mid-diastole.

The aortic component of S2 is often soft, while P2 is usually increased, reflecting pulmonary hypertension.

An S3 is often heard, but an S4 is absent.

By contrast to the high pitched holodiastolic decrescendo murmur of chronic AR, the murmur with acute AR is a low pitched early diastolic murmur beginning after S2 (movie 1 and movie 2). The murmur, however, may not be audible or recognized as regurgitation, especially if there is only a small diastolic gradient between the aorta and LV and the location of the murmur is variable, so it may be helpful to check multiple locations (eg, left sternal border, right sternal border, and back). (See "Auscultation of cardiac murmurs in adults", section on 'Aortic regurgitation'.)

A systolic murmur resulting from the increased volume of blood crossing the aortic valve may be heard, but is usually not loud. The combination of a soft systolic and a low-pitched diastolic murmur often produces a "to-and-fro" murmur at the cardiac base in acute AR. (See "Auscultation of cardiac murmurs in adults" and "Auscultation of heart sounds".)

Electrocardiogram — There are no specific electrocardiographic (ECG) changes with acute AR. Nonspecific ST and T wave abnormalities are common. If acute AR is due to aortic dissection, involvement of the right coronary artery can result in ECG findings of acute myocardial infarction. (See "Right ventricular myocardial infarction".)

Chest radiograph — The size of the cardiac silhouette on the chest radiograph is generally normal in acute AR, although there may appear to be a slight increase in the LV size. Radiographic evidence of heart failure and pulmonary edema include the redistribution of blood flow to the upper lobes and an increase in size and amount of the pulmonary vasculature.

In acute AR caused by aortic dissection, the cardiac silhouette may be markedly enlarged due to pericardial effusion, and aortic root dilation (normal diameter ≤35 mm) may give the appearance of a wide mediastinum.

DIAGNOSIS

Echocardiography — Echocardiography is diagnostic in acute AR. Echocardiography confirms the presence of AR and aids in the assessment of its severity. The cause of AR can be determined by identification of characteristic findings such as those of aortic valve endocarditis (see "Role of echocardiography in infective endocarditis") or aortic dissection. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Cardiovascular imaging'.)

Color Doppler echocardiography demonstrates the backflow of blood across the aortic valve in diastole. Recognizing that echocardiography provides only semiquantitative information, the identification of severe acute AR is based upon the following findings [16,17]:

Doppler study is used to identify and quantify AR. However, the following criteria for severe chronic AR may underestimate the severity of acute AR [1]:

The vena contracta width (narrowest segment of the color flow jet) is >6 mm.

The color Doppler jet width in the left ventricular (LV) outflow tract is large (≥65 percent of the outflow tract width) for central severe jets. For severe eccentric jets, the visualized jet width is variable.

The presence of holodiastolic flow reversal in the descending thoracic and proximal abdominal aorta.

In very severe cases of acute AR, the late diastolic velocity approaches zero, indicating that aortic diastolic pressure and LV diastolic pressure are nearly equal [18,19]. Signs of rapid pressure equalization of diastolic aortic and LV pressures include the following:

A dense continuous wave Doppler signal with a steep diastolic slope (pressure half-time <200 msec).

A short mitral deceleration time (<150 msec) and premature closure of the mitral valve. Diastolic mitral regurgitation may be detected.

Echocardiographic imaging also permits evaluation of LV size and systolic function, which are usually normal with acute regurgitation and may provide information on the possible cause of valve dysfunction (eg, evidence for aortic dilatation and/or dissection or the presence of valvular vegetations). Transesophageal imaging is more accurate than transthoracic imaging for both of these diagnoses. (See "Clinical features and diagnosis of acute aortic dissection" and "Clinical manifestations and evaluation of adults with suspected left-sided native valve endocarditis" and "Role of echocardiography in infective endocarditis".)

Intraoperative transesophageal echocardiography (TEE) imaging is useful for identifying the mechanism of acute AR in the setting of aortic dissection, which may affect decision-making about the surgical procedure [5].

Other imaging modalities

CT or TEE — In the patient with acute AR who has a suspected aortic dissection, both computed tomography (CT) imaging and TEE have high sensitivity and specificity for diagnosis. However, CT imaging is performed most often in these unstable patients because CT imaging is available quickly 24 hours a day, seven days a week at most emergency medical centers, whereas TEE often requires additional time for personnel to be available to do the procedure. CT imaging has additional advantages in delineating the anatomy by identifying the entry site of the intimal flap, as well as the site and extent of dissection and the possible involvement of major branch arteries. Transthoracic echocardiography (TTE) is not indicated to diagnose aortic dissection since its sensitivity and specificity are only 60 to 80 percent for this condition. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Diagnosis'.)

MRI — Magnetic resonance imaging (MRI) is generally of less utility than CT or TEE in the acute setting due to less availability and concerns about limitations of clinical monitoring and patient accessibility while the patient is in the MR scanner.

Cardiac catheterization — Given the gravity of the patient's condition with severe acute AR and the severity of the hemodynamic alterations, there is usually no time to perform cardiac catheterization or contrast angiography. Emergency valve surgery should not be delayed for coronary angiography if there is severe acute AR with hemodynamic instability. If the patient is reasonably stable, coronary angiography is generally performed in patients with known coronary artery disease, particularly in those with coronary artery bypass grafts [17]. Aortography is indicated only when the diagnosis cannot be established by noninvasive imaging. Aortography can confirm the presence of severe AR as well as identify aortic dissection and associated aortic root widening. However, an aortogram (or color Doppler) may underestimate the severity of AR in the setting of acute severe AR with late diastolic LV pressure equal to aortic diastolic pressure.

TREATMENT — The treatment for acute severe AR is emergency aortic valve replacement or repair. If there is any delay in surgery, temporary stabilization may be attempted in the intensive care unit using intravenous vasodilators, such as nitroprusside, and possibly inotropic agents such as dobutamine in an attempt to enhance forward flow and lower the left ventricular (LV) diastolic pressure (and pulmonary venous pressure).

An intra-aortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR. Similarly, LV assist devices are not helpful with acute severe AR because the ventricle continues to fill retrograde across the incompetent aortic valve with no improvement in forward cardiac output or LV diastolic pressure.

Patients with aortic dissection are treated with beta blockers but beta blockers should be used with caution in patients with concomitant acute AR since they will block compensatory tachycardia and may cause marked hypotension [17]. Beta blockers should generally be avoided in patients with acute AR without aortic dissection. (See "Management of acute type B aortic dissection", section on 'Anti-impulse therapy' and "Overview of acute aortic dissection and other acute aortic syndromes", section on 'Acute medical management' and "Management of acute type A aortic dissection", section on 'Acute management'.)

The only effective treatment of patients with concomitant acute severe AR and aortic dissection is emergency surgery. Interim pharmacologic therapy is guided by the clinical presentation, particularly the systemic blood pressure. If the patient is hypertensive, we suggest vasodilator therapy with cautious use of beta blockers. Although standard recommendations for beta-blocker therapy patients with aortic dissection suggest a target heart rate <60 BPM prior to initiation of vasodilator therapy, in patients with concomitant acute severe AR, such heart rate lowering may not be tolerated; a higher target may be more appropriate.

In hemodynamically stable patients with acute AR that is only mild to moderate in severity, the timing and type of intervention depends upon the cause of AR. When due to endocarditis, antibiotic therapy alone may be sufficient unless the patient has another indication for urgent valve replacement [17]. When due to aortic dissection, graft replacement of the ascending aorta may restore normal aortic valve function without the need for an aortic valve procedure. (See "Surgery for left-sided native valve infective endocarditis".)

In patients with severe acute AR, the surgical approach depends upon the cause of AR. For example, a composite valve and root replacement often are needed for endocarditis with a paravalvular abscess. When due to aortic dissection, aortic valve resuspension along with graft replacement of the ascending aorta often allows preservation of the native valve with resolution of valve incompetence. Valve repair might be possible for rupture of a fenestrated cusp [8,20]. (See "Management of acute type B aortic dissection" and "Surgery for left-sided native valve infective endocarditis" and "Surgery for left-sided native valve infective endocarditis", section on 'Choice of procedure'.)

A variety of factors affect the risk for in-hospital mortality after aortic valve replacement, but standard operative models are not applicable to most patients with acute severe AR because the predominant factor affecting outcome is the cause of acute AR: ascending aortic dissection or endocarditis. Mortality for acute severe AR is nearly 100 percent, so surgical intervention is appropriate unless considered futile or declined.

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Cardiac valve disease".)

SUMMARY AND RECOMMENDATIONS

Causes of acute native valve aortic regurgitation (AR) include endocarditis, aortic dissection, rupture of a congenitally fenestrated cusp, traumatic leaflet rupture, and iatrogenic valve injury during aortic balloon valvotomy or a failed surgical valve repair. (See 'Etiology' above.)

Causes of acute prosthetic AR include mechanical valve thrombosis or disk escape. With bioprosthetic valves, AR may occur with valve rupture adjacent to areas of leaflet calcification or leaflet destruction due to endocarditis. (See 'Etiology' above.)

Severe acute AR commonly presents with sudden cardiovascular collapse and pulmonary edema. Other presenting symptoms and signs are related to the cause of acute AR (eg, signs and symptoms of endocarditis or aortic dissection). Aortic dissection should always be suspected in patients with AR and chest or back pain. (See 'Clinical presentation' above.)

Acute AR is associated with a low pitched early diastolic murmur, although this murmur may not be heard because of the low diastolic gradient between the aorta and the left ventricle. The arterial pulse is generally weak and rapid. (See 'Physical examination' above.)

Echocardiography is diagnostic in acute AR and enables identification of its cause. However, the reduced diastolic gradient between the aorta and the left ventricle limits the value of quantitative measures. Computed tomography imaging is recommended when aortic dissection is a diagnostic concern. (See 'Echocardiography' above.)

The treatment for acute severe AR is emergency aortic root replacement or aortic valve replacement or repair, depending upon the cause of AR. (See 'Treatment' above.)

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