Aortic Regurgitation

  • AR may result from pathology of the aortic valve, the aortic root, or both; it is important that both the aortic valve and the aortic root are evaluated to determine the appropriate management and treatment.
  • AR usually progresses insidiously with a long asymptomatic period; when it occurs acutely, patients are often very sick and must be managed aggressively.

Etiology

  • More common

Bicuspid aortic valve, rheumatic disease, calcific degeneration, infective endocarditis, idiopathic dilatation of the aorta, myxomatous degeneration, systemic hypertension, dissection of the ascending aorta, Marfan syndrome.

  • Less common

Traumatic injury to the aortic valve, collagen vascular diseases (ankylosing spondylitis, rheumatoid arthritis, reactive arthritis, giant cell aortitis, and Whipple disease), syphilitic aortitis, discrete subaortic stenosis, ventricular septal defect with prolapse of an aortic cusp.

  • Acute AR

Infective endocarditis, dissection of the ascending aorta, trauma.

Pathophysiology

  • Acute AR (Figure 6-4)
    Figure 6-4 Acute aortic regurgitation.
    Descriptive text is not available for this image

    CO, cardiac output; HR, heart rate; LAP, left atrial pressure; LV, left ventricle; LVEDP, left ventricular end-diastolic pressure; SV, stroke volume.

  • Chronic AR (Figure 6-5)
    Figure 6-5 Chronic aortic regurgitation.
    Descriptive text is not available for this image

    CO, cardiac output; CHF, congestive heart failure; EF, ejection fraction; LV, left ventricle; LVED, left ventricular end-diastolic; LVEDP, left ventricular end-diastolic pressure; LVH, left ventricular hypertrophy; SV, stroke volume.

Diagnosis

History

  • Acute AR: patients with acute AR may present with symptoms of cardiogenic shock and severe dyspnea. Other presenting symptoms may be related to the cause of acute AR.
  • Chronic AR: symptoms depend on the presence of LV dysfunction and whether the patient is in the compensated versus decompensated stage. Compensated patients are typically asymptomatic, whereas those in the decompensated stage may note decreased exercise tolerance, dyspnea, fatigue, and/or angina.

Physical Examination

  • Acute AR
    • Widened pulse pressure may be present, but it is often not present because forward SV (and therefore systolic blood pressure) is reduced.
    • May hear brief soft diastolic murmur or systolic flow murmur.
    • Look for evidence of aortic dissection, infective endocarditis, and characteristics associated with Marfan’s disease.
  • Chronic AR
    • LV heave; point of maximal impulse is laterally displaced.
    • Diastolic decrescendo murmur heard best at left sternal border leaning forward at end-
expiration (severity of AR correlates with duration, not intensity, of the 
murmur).
    • Systolic flow murmur (mostly because of volume overload; concomitant AS may also be present).
    • Widened pulse pressure (often >100 mm Hg) with a low diastolic pressure; 
there are numerous eponyms for the characteristic signs related to a wide pulse pressure.

Diagnostic Testing

  • ECG: tachycardia, LVH, and LAE (more common in chronic AR).
  • CXR: pulmonary edema, widened mediastinum, and cardiomegaly.
  • TTE:
    • Assess LV systolic function, LV dimensions at end systole and diastole, leaflet number and morphology, assessment of the severity of AR.
    • Look for evidence of endocarditis or aortic dissection; dimension of aortic root.
  • TEE:
    • Clarify whether there is a bicuspid valve if unclear on TTE.
    • Better sensitivity and specificity for aortic dissection than TTE.
    • Clarify whether there is endocarditis with or without root abscess if unclear on TTE.
    • Better visualization of aortic valve in patients with a prosthetic aortic valve.
  • Cardiac catheterization: assessment of LV pressure, LV function, and severity of AR (via aortic root angiography) is indicated in symptomatic patients in whom the severity of AR is unclear on noninvasive imaging or discordant with clinical findings.
  • MRI/CT
    • Either of these may be the imaging modality of choice for evaluating aortic dimensions and/or for evaluation of aortic dissection.
    • If echocardiography assessment of the severity of AR is inadequate, MRI is useful for assessing the severity of AR.

Treatment

  • The role of medical therapy in patients with AR is limited.
  • Vasodilator therapy (i.e., nifedipine, ACE inhibitor, hydralazine) is indicated to reduce systolic blood pressure in hypertensive patients with AR.
  • Retrospective data suggest that β-blocker use may be associated with a survival benefit in patients with severe AR, but prospective studies are needed.
  • When endocarditis is suspected or confirmed, appropriate antibiotic coverage is critical.

Surgical Management

  • AHA/ACC recommendations for intervention1,2:
    • Symptomatic patients with severe AR (stage D) regardless of LV systolic function (Class I).
    • Asymptomatic patients with chronic severe AR and LV systolic dysfunction (EF ≤50%) (stage C2; Class I).
    • Patients with severe AR (stage C or D) undergoing cardiac surgery for other indications (Class I).
    • Asymptomatic patients with severe AR and normal LV systolic function (EF >50%) but with severe LV dilation (LV end-systolic dimension >50 mm) (stage C2; Class IIa).
  • Acute, severe AR is almost universally symptomatic and is treated surgically.
  • If the aortic root is dilated, it may be repaired or replaced at the time of aortic valve replacement (AVR). For patients with a bicuspid valve, Marfan syndrome, or a related genetically triggered aortopathy, surgery on the aorta should be considered at the time of AVR.

Outcome/Prognosis

  • Asymptomatic patients with normal LV systolic function (LVEF ≥50%): progression to symptoms and/or LV dysfunction approximately 6% per year.3
  • Asymptomatic patients with LV dysfunction (LVEF <50%): progression to cardiac symptoms >25% per year.3,4
  • Symptomatic patients: mortality rate approximately 9.4% per year.3

References

  1. Nishimura RA, Otto CM, Bonow RO, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association task force on practice guidelines. J Am Coll Cardiol. 2014;63:2438-2488.  [PMID:24603192]
  2. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC focused update of the 2014 AHA/ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association task Force on clinical practice guidelines. Circulation. 2017;135:e1159-e1195.  [PMID:28298458]
  3. Dujardin KS, Enriquez-Sarano M, Schaff HV, et al. Mortality and morbidity of aortic regurgitation in clinical practice. A long-term follow-up study. Circulation. 1999;99:1851-1857.  [PMID:10199882]
  4. Maurer G. Aortic regurgitation. Heart. 2006;92:994-1000.  [PMID:16775114]

Outline


© Wolters Kluwer Health Lippincott Williams & Wilkins

Aortic Regurgitation is a sample topic from the Washington Manual of Medical Therapeutics.

To view other topics, please or purchase a subscription.

The Washington Manual of Medical Therapeutics helps you diagnose and treat hundreds of medical conditions. Consult clinical recommendations from a resource that has been trusted on the wards for 50+ years. Complete Product Information.