Summary
Aortic regurgitation (AR) is a valvular heart disease characterized by incomplete closure of the aortic valve that leads to reflux of blood from the aorta into the left ventricle (LV) during diastole. Aortic regurgitation may be acute (occurring primarily after bacterial endocarditis or aortic dissection) or chronic (due to congenital bicuspid valve or rheumatic fever) and may be caused by valvular disease or an abnormality of the aorta. In most cases, acute AR leads to rapid deterioration of LV function with subsequent pulmonary edema and cardiac decompensation. Frequently, chronic AR may remain compensated for a long period of time, becoming symptomatic only when left heart failure develops. Auscultation reveals an S3 and a high-pitched, decrescendo early diastolic murmur. Another characteristic diagnostic finding is widened pulse pressure. Echocardiography is the most important diagnostic tool, both for confirming the diagnosis and determining the severity of disease. In asymptomatic patients, conservative treatment consists of symptom management and physical activity as tolerated. However, symptomatic patients or those with severely reduced LV function should undergo surgical aortic valve replacement.
Etiology
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Acute AR
- Infective endocarditis
- Aortic dissection (ascending aorta)
- Chest trauma
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Chronic AR
- Congenital bicuspid valve: most common cause of AR in young adults and in developed countries
- Rheumatic heart disease: most common cause of AR in developing countries
- Distortion or dilation of the ascending aorta and aortic root
- Connective tissue disorders (e.g., Marfan syndrome, Ehlers-Danlos syndrome)
- Tertiary syphilis
- Also see heart valve disease
References:[1][2][3][4]
Pathophysiology
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General
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Regurgitation of blood from the aorta into the left ventricle (LV)
- → Increased systolic blood pressure and decreased diastolic pressure
- → Widened pulse pressure → water hammer pulse (see “Diagnostics” below)
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Regurgitation of blood from the aorta into the left ventricle (LV)
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Acute AR
- Because LV cannot sufficiently dilate in response to regurgitant blood, LV end-diastolic pressure increases rapidly → pressure transmits backwards into pulmonary circulation → pulmonary edema and dyspnea
- Decreased cardiac output if severe → cardiogenic shock and myocardial ischemia
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Chronic AR
- Initially, a compensatory increase in stroke volume can maintain adequate cardiac output despite regurgitation (compensated heart failure)
- Over time, increased left ventricular end-diastolic volume → LV enlargement and eccentric hypertrophy of myocardium → left ventricular systolic dysfunction → decompensated heart failure
References:[1][2][3]
Clinical features
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Acute AR
- Sudden, severe dyspnea
- Rapid cardiac decompensation secondary to heart failure
- Pulmonary edema
- Symptoms related to underlying disease (e.g., fever due to endocarditis, chest pain due to aortic dissection)
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Chronic AR
- May be asymptomatic for up to decades despite progressive LV dilation
- Palpitations
- Symptoms of left heart failure
- Symptoms of high pulse pressure (e.g., head pounding, rhythmic nodding, or bobbing of the head in synchrony with heartbeats- de Musset sign)
References:[1][2]
Diagnostics
Physical examination
- For detailed information about the individual tests, see cardiovascular examination.
- High pulse pressure
- Point of maximal impulse (PMI): displaced inferolaterally, diffuse, and hyperdynamic
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Auscultation
- S3
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High-pitched, blowing, decrescendo early diastolic murmur
- AR due to valvular disease: best heard in the left third and fourth intercostal spaces and along the left sternal border (Erb point)
- AR due to aortic root disease (e.g., aortic dissection): best heard along the right sternal border
- Worsens with squatting and handgrip
- Austin Flint murmur
- In more severe stages, possibly a harsh, crescendo-decrescendo mid-systolic murmur that resembles the ejection murmur heard in aortic stenosis
Confirmatory tests
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Transthoracic echocardiogram (TTE)
- Indicated for suspected AR as well as to monitor confirmed AR to determine the staging and optimal timing of surgery
- Findings
- Abnormal aortic valve leaflets
- Regurgitant AR jet on Doppler flow tracing
- Increased LV size and volume
- Dilated aorta
- Fluttering of anterior mitral valve leaflet
- Transesophageal echocardiogram (TEE): indicated if suboptimal or nondiagnostic TTE
Screening tests (optional)
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ECG
- Signs of left ventricular hypertrophy
- Chest x-ray
- Prominent aortic root/arch
- Enlarged cardiac silhouette
References:[1][2][3][5][6]
Treatment
Conservative
- Indication: asymptomatic patients and symptomatic patients who are not candidates for surgical treatment
- Treatment of heart failure
- Physical activity , but without excessive straining
Surgical
- Indications [7]
- Symptomatic patients with acute severe AR
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Asymptomatic patients with:
- Chronic severe AR and EF < 50%
- Left ventricular systolic diameter > 50 mm
- Surgical procedure: aortic valve replacement (occasionally valve reconstruction is possible) and long-term anticoagulation therapy for mechanical valve
References:[1][3]
Prognosis
- Asymptomatic patients with normal EF: progression to symptoms or LV dysfunction at a rate of < 6% per year
- Asymptomatic patients with decreased EF: progression to symptoms at a rate of > 25% per year
- Symptomatic patients: mortality rate is > 10% per year
References:[1]