Aortic Regurgitation
David S. Bach
Michael J. Shea
G. Michael Deeb
USUAL CAUSES
The aortic valve comprises three semilunar aortic cusps, the sinuses of Valsalva, and the sinotubular junction. Aortic regurgitation is caused by acquired or congenital abnormalities of the aortic valve cusps or by acquired abnormalities of the aortic root that affect the competence of what may be anatomically normal cusps. In general, aortic regurgitation caused by aortic root disease necessitates dilation at the level of the sinotubular junction; isolated aortic annular dilation is relatively unlikely to occur, owing to the dense surrounding fibrous tissue.
Chronic Aortic Regurgitation
Chronic aortic regurgitation can be caused by congenital or acquired abnormalities (Table 22.1). The most common congenital abnormality of the aortic valve associated with aortic regurgitation is bicuspid aortic valve; fenestrations of the aortic valve cusps are a less frequent cause. Acquired causes of chronic aortic regurgitation resulting from predominant disease of the valve cusps include calcific degeneration, rheumatic disease, infective endocarditis, myxomatous degeneration, and long-term anorectic drug use. Less common etiologies of aortic regurgitation caused by abnormalities of the cusps include discrete subaortic stenosis and aortic cusp prolapse caused by perimembranous ventricular septal defect.
Aortic root disease resulting in chronic aortic regurgitation can be idiopathic, associated with bicuspid aortic valve, or caused by systemic hypertension, cystic medial necrosis with or without other features of Marfan syndrome, or aortic dissection. Other, less commonly encountered causes of aortic root disease include connective tissue diseases such as Reiter syndrome, ankylosing spondylitis, and rheumatoid arthritis. Luetic (syphilitic) aortitis is still described as a potential cause of aortic root disease but, in effect, is no longer encountered clinically in the United States.
Finally, dysfunction of a mechanical or bioprosthetic aortic valve prosthesis can result in aortic regurgitation. Mild transvalvular regurgitation is an anticipated finding with most mechanical prostheses, and small amounts of paraprosthetic regurgitation are common with any prosthesis. Larger paravalvular leaks can be of clinical importance either because of their hemodynamic significance or because of associated hemolysis. Significant valvular regurgitation with a mechanical prosthesis suggests entrapment or dysfunction of the occluder; significant regurgitation in association with a bioprosthesis suggests leaflet fracture or tear.
Acute Aortic Regurgitation
Acute severe aortic regurgitation is caused by infective endocarditis, aortic dissection, nonpenetrating (or, in rare cases, penetrating) chest trauma, or prosthetic valve dysfunction.
PRESENTING SYMPTOMS AND SIGNS
Symptoms
Patients with chronic aortic regurgitation usually remain asymptomatic for years or
decades. During this compensated phase, the left ventricular volume overload of aortic regurgitation is accommodated through increases in left ventricular volume and chamber compliance and through both eccentric and concentric hypertrophy. Increased stroke volume maintains normal forward cardiac output, and increased left ventricular compliance maintains normal filling pressures with maintained preload reserve. The increase in chamber size results in increased wall stress, with compensatory hypertrophy in response to increased afterload. During this period, myocardial contractility and left ventricular ejection fraction remain normal. Symptoms during this phase of compensated chronic aortic regurgitation may include a sensation of pounding in the chest, palpitations, or head pounding, caused by increased stroke volume and a wide pulse pressure.
decades. During this compensated phase, the left ventricular volume overload of aortic regurgitation is accommodated through increases in left ventricular volume and chamber compliance and through both eccentric and concentric hypertrophy. Increased stroke volume maintains normal forward cardiac output, and increased left ventricular compliance maintains normal filling pressures with maintained preload reserve. The increase in chamber size results in increased wall stress, with compensatory hypertrophy in response to increased afterload. During this period, myocardial contractility and left ventricular ejection fraction remain normal. Symptoms during this phase of compensated chronic aortic regurgitation may include a sensation of pounding in the chest, palpitations, or head pounding, caused by increased stroke volume and a wide pulse pressure.
TABLE 22.1. Causes of aortic regurgitation | ||||||||||||||||||||||||||||||||||||||
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Eventually, persistent volume and pressure overload exhaust left ventricular preload reserve; in addition, hypertrophy may become inadequate for increased afterload. At this point, further increases in afterload result in decreased left ventricular ejection fraction. Exertional dyspnea is typically the first manifestation of left ventricular decompensation, with later development of orthopnea and paroxysmal nocturnal dyspnea.
Initially, left ventricular systolic dysfunction is caused by pure afterload excess and is reversible after aortic valve replacement. Later, depressed myocardial contractility causes progressive and irreversible systolic dysfunction. In addition, inadequate coronary flow reserve in the setting of left ventricular hypertrophy, along with decreased perfusion pressure associated with low diastolic pressures, can result in coronary insufficiency. Symptoms of more advanced disease eventually include angina pectoris (which may be nocturnal) and symptoms of right-sided congestive heart failure with ascites and peripheral edema.
Acute severe aortic regurgitation usually occurs in the setting of infective endocarditis, acute aortic dissection or, more rarely, after blunt chest trauma. Patients typically exhibit symptoms referable to the underlying disease, including fever with infective endocarditis or chest or back pain with aortic dissection. In the absence of the compensatory mechanisms present in chronic aortic regurgitation, acute severe aortic regurgitation is poorly tolerated hemodynamically, and patients frequently have pulmonary edema or cardiogenic shock.
Signs
Physical findings in patients with chronic severe aortic regurgitation reflect the combination of increased stroke volume and widened pulse pressure. Findings can be extensive, and no other single lesion may be so rich with associated eponyms (Table 22.2). In general appearance, patients can exhibit a bobbing motion of the torso or the head (de Musset sign) synchronous with the heartbeat. Systolic pulsation of the uvula may be visible (Müller sign). Arterial pulses are unusually prominent, with exaggerated systolic distention and exaggerated diastolic collapse on palpation (water-hammer or Corrigan pulse). Palpation of the carotid arteries reveals a bisferiens, or double-peaking, pulse. Capillary pulsation may be visible in the nail beds when
the distal nail is softly compressed (Quincke pulse). Auscultation of large arteries may reveal a brief, loud systolic (pistol shot) sound. Auscultation of the femoral artery reveals booming systolic and diastolic sounds (Traube sign); light pressure of the stethoscope proximally reveals a systolic murmur, with a diastolic murmur when pressure is applied distally (Duroziez sign). The systolic blood pressure is typically elevated, and the diastolic blood pressure is often very low, revealing a wide pulse pressure.
the distal nail is softly compressed (Quincke pulse). Auscultation of large arteries may reveal a brief, loud systolic (pistol shot) sound. Auscultation of the femoral artery reveals booming systolic and diastolic sounds (Traube sign); light pressure of the stethoscope proximally reveals a systolic murmur, with a diastolic murmur when pressure is applied distally (Duroziez sign). The systolic blood pressure is typically elevated, and the diastolic blood pressure is often very low, revealing a wide pulse pressure.
TABLE 22.2. Selected physical findings and eponyms associated with severe chronic aortic regurgitation | ||||||||||||||||||
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The left ventricular apical impulse is enlarged and displaced as a result of left ventricular enlargement, and it may be visible. A systolic thrill may be evident along the base of the heart or in the carotid arteries, caused by the large left ventricular stroke volume. On auscultation, the aortic component of S2 may be diminished or absent. An S3 is common and is not indicative of congestive heart failure. The murmur of aortic regurgitation is a high-pitched, blowing decrescendo diastolic murmur, loudest at the left or right upper sternal border. Held end-expiration with the patient upright and leaning forward and the stethoscope diaphragm held firmly against the chest aids in the auscultation of soft murmurs of aortic regurgitation. The aortic regurgitant jet may result in vibration of the anterior mitral valve leaflet, resulting in a low-pitched diastolic rumble at the cardiac apex (Austin Flint murmur) that can mimic mitral stenosis, albeit without presystolic accentuation. A systolic ejection murmur, often louder and more easily heard than the diastolic murmur, is caused by the large stroke volume and is not indicative of aortic stenosis.
Many of the typical physical findings associated with chronic aortic regurgitation are absent in patients with acute severe aortic regurgitation. Because the left ventricle is not dilated in acute aortic regurgitation, stroke volume is not increased, pulse pressure is not widened, and the associated peripheral arterial manifestations are absent. Tachycardia is typical, in a compensatory attempt to maintain forward cardiac output without the benefit of increased stroke volume. Premature closure of the mitral valve may be associated with decreased intensity of S1. The diastolic murmur in acute, severe aortic regurgitation is often shorter and softer than that associated with chronic aortic regurgitation, because diastolic pressure equilibration between the ascending aorta and left ventricle occurs earlier in diastole. Although chronic severe aortic regurgitation usually can be diagnosed on physical examination, the detection of acute severe regurgitation is less certain.
HELPFUL TESTS
Echocardiography with Doppler imaging is an ideal modality for the assessment of the presence, etiology, severity, and impact of aortic regurgitation (Table 22.3). Echocardiography is indicated for patients with
suspected aortic regurgitation to confirm the presence of and to establish the severity and cause of regurgitation. The dimensions, mass, and systolic function of the left ventricle should be determined, as well as the size and anatomy of the aortic root. Because absolute and subsequent change in left ventricular dimensions directly affect management, accurate quantification is important, both on baseline measurement and on subsequent examinations.
suspected aortic regurgitation to confirm the presence of and to establish the severity and cause of regurgitation. The dimensions, mass, and systolic function of the left ventricle should be determined, as well as the size and anatomy of the aortic root. Because absolute and subsequent change in left ventricular dimensions directly affect management, accurate quantification is important, both on baseline measurement and on subsequent examinations.
TABLE 22.3. Echocardiographic imaging in aortic regurgitation (AR) | ||||||||||||||||||||||||
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Transthoracic echocardiography allows assessment of aortic valve structure and may establish the cause of aortic regurgitation with evidence of congenital abnormalities, calcific or rheumatic disease, or findings suggestive of infective endocarditis. In addition, the proximal 2 to 3 cm of ascending aorta can usually be visualized on transthoracic imaging, allowing assessment for gross dilation of the aortic root. In the absence of Doppler imaging, aortic regurgitation is suggested by diastolic fluttering of the anterior mitral valve leaflet, and acute severe regurgitation is associated with premature closure of the mitral valve. Doppler imaging allows reliable detection and semiquantification of aortic regurgitation (1,2). Aortic regurgitation severity is estimated by the size of the regurgitant jet in relation to the left ventricular outflow tract (3), as well as deceleration characteristics of regurgitant flow (4,5). Diastolic flow reversal in the descending thoracic aorta is a marker of severe aortic regurgitation. Transesophageal echocardiographic imaging allows optimal assessment of aortic valve structure, as well as definitive assessment of anatomy of the thoracic aorta. Transesophageal imaging is indicated if aortic dissection (6,7) or prosthetic valve dysfunction (8) is suspected.
Neither electrocardiography nor chest radiography is accurate in the detection or estimation of severity of aortic regurgitation. However, the electrocardiogram may reveal evidence of left ventricular hypertrophy or interventricular conduction delay, and the chest radiograph may reveal cardiomegaly, dilation of the aortic root, or evidence of pulmonary venous congestion.
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