AUTHOR AND EDITOR INFORMATION

Section 1 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

INTRODUCTION

Section 2 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Background

Aortic regurgitation is the diastolic flow of blood from the aorta into the left ventricle. Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular apparatus (eg, leaflets, annulus of the aorta) resulting in diastolic flow of blood into the left ventricular chamber.

Pathophysiology

Incompetent closure of the aortic valve can result from intrinsic disease of the cusp, diseases of the aorta, or trauma. Aortic regurgitation may be a chronic disease process or it may occur acutely, presenting as heart failure. The most common cause of chronic aortic regurgitation used to be rheumatic heart disease, but presently it is most commonly bacterial endocarditis. In developed countries, it is caused by dilatation of the ascending aorta (eg, aortic root disease, aortoannular ectasia).

Diastolic reflux through the aortic valve can lead to left ventricular volume overload. The severity of the aortic regurgitation is dependent on the diastolic valve area, the diastolic pressure gradient between the aorta and left ventricle, and the duration of diastole. An increase in systolic stroke volume and low diastolic aortic pressure produces an increased pulse pressure.

Frequency

United States

Rheumatic fever and syphilis used to be major causes of aortic regurgitation, but these diseases have diminished in recent years because of the introduction of new antibiotics.

Mortality/Morbidity

• Three fourths of patients with significant aortic regurgitation survive 5 years after diagnosis; half survive for 10 years. Patients with mild-to-moderate regurgitation survive 10 years in 80-95% of the cases.
• Average survival after onset of congestive heart failure (CHF) is less than 2 years.
• Acute aortic regurgitation is associated with significant morbidity, which can progress from pulmonary edema to refractory heart failure and cardiogenic shock.

Age

Chronic aortic regurgitation often begins in the late 50s and is documented most frequently in patients older than 80 years.

CLINICAL

Section 3 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

History

• General
• • The clinical signs of aortic regurgitation are caused by forward and backward flow of blood across the aortic valve, leading to increased stroke volume.
  • The degree of regurgitation is determined by the degree of valvular incompetence; left ventricular compliance; and end-ventricular, end-diastolic volume.
• Acute aortic regurgitation: Symptoms are manifestations of cardiovascular collapse.
• • Weakness
  • Severe dyspnea
  • Hypotension
  • Angina
• Chronic aortic regurgitation
• • Exertional dyspnea
  • Nocturnal dyspnea
  • Orthopnea
  • Diaphoresis
  • Abdominal discomfort
  • Uncomfortable awareness of heartbeat
  • Palpitations

Physical

• The hallmark of aortic regurgitation/insufficiency is a high-pitched decrescendo diastolic murmur at the left sternal border after the second heart sound.
• Acute aortic regurgitation
• • Patients who have CHF or shock associated with severe aortic regurgitation often appear gravely ill.
  • Tachycardia
  • Peripheral vasoconstriction
  • Cyanosis
  • Pulmonary edema
  • Arterial pulsus alternans; normal left ventricular impulse
  • Early diastolic murmur (lower pitched and shorter than in chronic aortic regurgitation) may be present. An Austin-Flint murmur, which is caused by the regurgitant flow causing vibration of the mitral apparatus, is lower pitched and short in duration. The decrescendo diastolic murmur is heard best with the patient leaning forward in full expiration in a quiet room. It is the cardiac murmur most commonly missed.
  • A murmur at the right sternal border is associated more often with dissection than any other cause of aortic regurgitation.
• Chronic aortic regurgitation
• • All auscultatory phenomena indicate vasodilatation of peripheral circulation.
  • Hyperdynamic apical impulse displaced laterally and inferiorly may be associated with an ejection click.
  • Decrescendo diastolic murmur is heard best while the patient is leaning forward on deep expiration.
  • Apical middiastolic rumble
  • Austin-Flint murmur
  • Pulsus bisferiens; increased pulse pressure; visible, forceful, and bounding peripheral pulses (water hammer)
  • Corrigan pulse - Quickly collapsing pulses
  • Musset sign - Bobbing of the head
  • Quincke sign - Capillary pulsations of the nail bed
  • Muller sign - Pulsations of the uvula
  • Hill sign - Systolic pressure in lower extremity greater than systolic pressure in upper extremity by at least 100 mm Hg
  • Traube sign - Loud systolic sound over femoral arteries
  • Duroziez sign - Systolic-diastolic murmur produced by compression of femoral artery with a stethoscope

Causes

• Multiple causes of this valvular abnormality are known, including connective tissue disease and anatomic abnormalities. Acute aortic regurgitation is usually due to aortic dissection, bacterial endocarditis, or trauma, which may be either penetrating or blunt.
• Acute aortic regurgitation
• • Rheumatic
  • Infective endocarditis
  • Ruptured sinus of Valsalva
  • Trauma, prosthetic valve surgery
  • Aortic dissection, laceration of the aorta
• Chronic aortic regurgitation
• • Rheumatic
  • Syphilis
  • Aortitis (ie, Takayasu disease)
  • Marfan syndrome
  • Osteogenesis imperfecta
  • Bicuspid aortic valve, defect of the interventricular septum or sinus of Valsalva
  • Ankylosing spondylitis
  • Reiter syndrome
  • Rheumatoid arthritis
  • Systemic lupus erythematosus
  • Hypertension
  • Infective endocarditis

DIFFERENTIALS

Section 4 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

WORKUP

Section 5 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Lab Studies

• CBC
• Prothrombin time (PT)/activated partial thromboplastin time (aPPT)
• Type and screen
• Electrolytes
• Myocardial muscle creatine kinase isoenzyme (CK-MB)
• Lactate dehydrogenase panel
• Isoenzymes

Imaging Studies

• Chest x-ray
• • Acute aortic regurgitation
    • Minimal cardiac enlargement
    • Normal aortic root/arch
    • Pulmonary venous pattern increased
  • Chronic aortic regurgitation
    • Marked cardiac enlargement
    • Prominent aortic root/arch
    • Normal pulmonary venous pattern
• 2-Dimensional echocardiogram, transesophageal
• • Acute aortic regurgitation
    • Valve anatomy disrupted
    • Intimal flap
    • Vegetations on valve
    • Pericardial effusion
  • Chronic aortic regurgitation
    • Valve anatomy disrupted
    • Estimation of degree of regurgitation
    • Aortic root size and anatomy
    • Left ventricular function
• Radionuclide techniques
• • These allow for determination of regurgitant fraction and left ventricular/right ventricular stroke-volume ratio. In the absence of mitral regurgitation and tricuspid regurgitation, a left ventricular/right ventricular stroke-volume ratio of 2.5 or more denotes severe aortic regurgitation.
  • Demonstration of a fall in ejection fraction with exercise is one of the best indicators for surgery in patients who are asymptomatic.
• Cardiac catheterization/angiography
• • Consider for patients with coronary artery disease who are possible candidates for aortic valve replacement, those with a complex lesion associated with a diastolic murmur of unknown cause, and those with left ventricular dysfunction out of proportion to the degree of aortic regurgitation.
  • Assess the anatomy of the aorta and coronary ostia. Findings are usually normal except for visible reflux of dye from the aortic root into the ventricle.

Other Tests

• ECG
• • Normal (early in disease)
  • Left axis deviation (chronic aortic regurgitation)
    Specific waves
  • Specific waves
    • Prominent Q wave in I, AVF, V3 to V6
    • Small R wave in V1
    • T wave inverted with ST-segment depression
    • P-R prolongation (possible)
  • Of patients in a study done at the Mayo Clinic, 22% had atrial fibrillation. This is uncommon before disease has become advanced and has an ominous prognosis unless caused by another disease.

TREATMENT

Section 6 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Emergency Department Care

• General
• • Provide adequate airway management.
  • Intubate when necessary.
  • Consider prompt surgical intervention in acute aortic regurgitation.
• Acute aortic regurgitation
• • Administer a positive inotrope (eg, dopamine, dobutamine) and a vasodilator (eg, nitroprusside). Rarely, administration of cardiac glycosides (eg, digoxin) for rate control may be necessary.
  • Avoid beta-blockers in the acute setting.
  • Administration of vasodilators may be appropriate to improve systolic function and to decrease afterload.
• Chronic aortic regurgitation
• • Consider antibiotic prophylaxis for patients with endocarditis when performing procedures likely to result in bacteremia.
  • Administration of pressors and/or vasodilators may be appropriate.
• Hemodynamically significant aortic regurgitation may require surgical intervention according to the following criteria:
• • Cardiac-thoracic ratio >0.64
  • Fractional shortening <25-29%
  • End-systolic diameter >55 mm
  • End-diastolic radius to myocardial wall thickness ratio >4.0
  • Ejection fraction <0.45
  • Cardiac index <2.2-2.5 L/min/m²

Consultations

• Cardiology
• Cardiothoracic surgery

FOLLOW-UP

Section 7 of 8  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

Further Inpatient Care

• Admit to a monitored bed.
• Transport the patient directly to the OR if indicated.

REFERENCES

Section 8 of 8

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Follow-up
• References

• Babu AN, Kymes SM, Carpenter Fryer SM. Eponyms and the diagnosis of aortic regurgitation: what says the evidence?. Ann Intern Med. May 6 2003;138(9):736-42. [Medline].
• Braunwald E. Heart Disease: A Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia: Saunders;1988.
• Giuliani E. Cardiology: Fundamentals and Practice. 2nd ed. Philadelphia: Mosby Year Book. [Medline].
• Hagan PG, Nienaber CA, Isselbacher EM, et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA. Feb 16 2000;283(7):897-903. [Medline].
• Hwang MS, Chu JJ, Su WJ. Natural history and risk stratification of discrete subaortic stenosis in children: an echocardiographic study. J Formos Med Assoc. Jan 2004;103(1):17-22. [Medline].
• Kloner R. The Guide to Cardiology. 2nd ed. New York: Le Jacq Communications;1990.

Article Last Updated: Aug 29, 2006