Aortic insufficiency

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Phone:617-525-6884

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Synonyms and related words: Aortic regurgitation, AI, AR

Aortic Insufficiency refers to retrograde or backwards flow of blood from the aorta into the left ventricle during diastole.

Epidemiology and Demographics

There are two broad underlying causes of aortic regurgitation:

  1. Disease of the aortic valve itself and
  2. Disease of the aortic root leading to dilation and regurgitation of the aortic valve

Aortic regurgitation secondary to dilation of the ascending aorta has overtaken valvular aortic disease as the most common cause of aortic regurgitation.

Pathophysiology

Aortic Valve Disease

A full list of causes of aortic regurgitation can be found in the differential diagnosis section below.

One of the most common causes of aortic valvular disease in the past has been rheumatic fever in which case the aortic cusps are infiltrated with fibrous tissue. This then leads to retraction of the cusps and prevents their apposition during diastole. The cusps may also fuse and this may cause a component of aortic stenosis. It is therefore not uncommon for these patients to have mixed aortic regurgitation and aortic stenosis. Often these patients will have involvement of the mitral valve as well.

In the modern era, a more common cause of acquired aortic valve regurgitation is degenerative disease of the aorta and aortic valve in which case there is calcification and fibrosis of the cusps. As is the case with rheumatic fever, there is similar retraction of the cusps that results in aortic insufficiency.

A third not uncommon cause of acquired aortic regurgitation is infective endocarditis. In this disease state, regurgitation develops as a result of a hole or perforation that develops in the leaflet, or alternatively the cusps may not oppose each other due to a vegetation lying between the cusps which prevents their apposition.

A final not uncommon cause of acquired aortic insufficiency is trauma in which case there is distortion of the valve architecture leading to failure of the cusps to oppose.

Congenital conditions such as congenital bicuspid aortic stenosis or a ventricular septal defect can also result in aortic insufficiency.

Aortic Root Disease

Aortic root disease as a cause of aortic insufficiency has overtaken acquired forms of valvular disease and congenital forms of valvular disease as the leading cause of aortic regurgitation. The following is a list of those conditions that lead to dilation of the aortic root and thereby cause aortic insufficiency:

Hemodynamic Consequences of Aortic Insufficiency

Chronic Aortic Regurgitation

The hemodynamic impact of aortic regurgitation is to cause progressive dilation and hypertrophy of the left ventricle. The mitral valve ring may also dilate which may lead in turn to mitral regurgitation. The left atrium may dilate as a result of the mitral regurgitation.

It has been said that 'aortic regurgitation begets aortic regurgitation'. The high oscillatory shear associated with aortic regurgitation may lead to further dilation of the aorta, which in turn may lead to further aortic regurgitation.

Volume overload associated with aortic regurgitation leads to left ventricular hypertrophy. The sarcomeres replicate in series and there is elongation of the myocytes and myocardial fibrils. As a result of this hypertrophy the ratio of the ventricular wall thickness to cavity radius remains normal and therefore wall stress is normal. In aortic regurgitation there is eccentric hypertrophy where as in aortic stenosis there is concentric hypertrophy where there is replication of the sarcomeres in parallel. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the left ventricle fails. The dramatic enlargement of the heart that is seen with aortic regurgitation is called cor bovinum. Over time the left ventricle will decompensate and there will be increasing interstitial fibrosis and a stiffening or a reduction in the compliance of the left ventricular wall. At this point the patient will experience a rise in the end diastolic pressure and volume. The first decline is seen with exercise and then the patient begins to have a reduction in forward output at rest. Patients with chronic aortic insufficiency may also develop myocardial ischemia. This is due to the fact that they have an increase in demand due to an increased thickness of the LV and also a reduction in the supply due to a lower perfusion pressure during diastole.

Acute aortic insufficiency

Acute aortic insufficiency is often secondary to either trauma or infective endocarditis. While the heart can accommodate the changes of chronic aortic insufficiency over time, the acute changes of acute aortic insufficiency are not well accommodated by the left ventricle. The rapid rise in left ventricular pressure causes the mitral valve to close earlier during diastole. This early closure fortunately prevents backwards flow of blood into the pulmonary vascular bed. The very high left ventricular end diastolic pressure often keeps the aortic diastolic pressure from falling too low and thus there is often not a wide pulse pressure. Indeed absence of a wide pulse pressure in the patient with acute aortic insufficiency should alert the clinician to potential failure of the left ventricle.

Diagnosis

Differential Diagnosis of the Etiologies of Aortic Insufficiency

Acute Aortic Insufficiency

Chronic Aortic Insufficiency

History

Physical Examination

Ear Nose and Throat

The uvula may bob

Heart

Extremities

The pulses are bounding with a "water hammer pulse"

Laboratory Findings

Electrocardiogram

Chest X Ray

Echocardiography

  • Increased duration between E and A peaks
  • Fluttering of the anterior mitral valve leaflet due to AI jet turbulence
  • Clinical setting to decide mechanism
Aortic Regurgitation M Mode
Aortic Regurgitation M Mode

Severe aortic insufficiency 1

Severe aortic insufficiency 2

Severe aortic insufficiency 3

Severe aortic insufficiency in patient after aortic valve replacement 1

Severe aortic insufficiency in patient after aortic valve replacement 2

Severe aortic insufficiency in patient after aortic valve replacement 3

Severe aortic insufficiency in patient after aortic valve replacement 4

Severe aortic insufficiency in patient after aortic valve replacement 5

Severe aortic insufficiency in patient after aortic valve replacement 6

Severe aortic insufficiency in patient after aortic valve replacement 7

Severe aortic insufficiency in patient after aortic valve replacement 8

MRI and CT

Quantification of Aortic Insufficiency by Aortography

The pigtail catheter is placed a few centimeters above the aortic root. Grading the amount of regurgitation is based on the amount of opacification of the ventricle 2 complete cardiac cycles after injection compared to that of the aortic root.

Grade 1

Brief and incomplete ventricular opacification. Clears rapidly.

Grade 2

Moderate opacification of the ventricle that clears in less that 2 cycles. Never greater than aortic root opacification.

2+ AI Marfan Syndrome

Grade 3

Opacification of the ventricle equal to aortic root opacification within 2 cycles. Delayed clearing of ventricle over several cycles.

3+ AI

Grade 4

Opacification of the ventricle almost immediately that is greater than that of the aortic root with delayed clearing of the ventricle.

4+ AI

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Acknowledgments

Person who first created this page was Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3] Phone:617-525-6884

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Acknowledgement and Attribution Regarding Sources of Content

Some of the initial content on this page may be incorporated in part from copyleft sources in the public domain including wikis such as Wikipedia and AskDrWiki. Drug information for patients came from the The National Library of Medicine. Infectious disease information may have come from the Centers for Disease Control (CDC). Differential Diagnoses are drawn from clinicians as well as an amalgamation of 3 sources: 1.The Disease Database; 2. Kahan, Scott, Smith, Ellen G. In A Page: Signs and Symptoms. Malden, Massachusetts: Blackwell Publishing, 2004:3; 3. Sailer, Christian, Wasner, Susanne. Differential Diagnosis Pocket. Hermosa Beach, CA: Borm Bruckmeir Publishing LLC, 2002:7 .

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