Aortic Regurgitation

BASIC
Definition

Retrograde flow from the aorta into the left ventricle trough an
incompetent aortic valve
Primary valve disease
o An abnormality in the aortic valve leads to regurgitant flow
Primary aortic root disease
o Widening of the aortic annulus and seperation of the aortic
leaflets cause regurgitation

Epidemiology

Age
o Prevalence increases with age.
o Mild to moderate regurgitation is found in 10-15% adults 60
years of age.
Sex
o ~75% of patients with pure or predominant valvular aortic
regurgitation (AR) are male
o Women predominate among patients with primary valvular AR
who have associated mitral valve disease

Risk factor

Bicuspid aortic valve

Aortic stenosis
Increasing age
Use of anorectic drugs, such as fenfluramine and dexfenfluramine
(removed from the U.S. market in 1997)

Etiology

Primary valve disease

o Rheumatic in origin in about two-thirds of patients
Caused by thickening, deformity, and shorteningof
individual aortic valve cusps
o Congenital valve defects
Bicuspid aortic valves
Venticular septal defect: 15% develop AR from prolapse
of an aortic cusp
Membranous subaortic stenosis: associated with
thickening of the aortic valve leaflets
Fenestrations of the aortic valve
o Secondary to acute infective endocarditis
o Traumatic rupture of aortic valve
Uncommon cause of acute AR
Most frequent serious lession in patients who survive
nonpenetrating cardiac injuries
Primary aortic root disease
o Causes aortic dilatation, widening of aortic annulus, and
seperation of aortic leaflets
Marfan syndrome
Idiopathic dilatation of aorta
Cyctic medionecrosis of aorta
Severe hypertension
Syphilis
Rheumatoid ankylosing spondylitis
Osteogenesis imperfecta (rare)
o Occasionally caused by retrograde dissection of the aorta
involving the aortic annulus
Mechanism of disease
o Total stroke volume ejected by the left ventricle (i.e., sum of
effective forward stroke volume and volume of blood that
regurgitates back into the left ventricle) is increased
o An increased in left ventricular (LV) end-diastolic volume
(increased
preload)
constitutes
major
hemodynamic
compensation for AR
o Reduction in arterial diastolic pressure reduces afterload and
serves as compensation
o Dilatation and eccentric hypertrophy of the left ventricle allow
it to eject a larger stroke volume without an increase in
relative shortening of each myofibril
o Myocardial ischemia may occur in patients with AR because
myocardial oxygen requirements are increased by LV
dilatation and elevated LV systolic tension

o Ultimately, LV function deteriorates

Forward stroke volume and ejection fraction decrease
Deterioration of LV function often precedes symptom
development

Associated conditions

Coronary artery disease

Mitral valve disease
Aortic stenosis

DIAGNOSIS
Symptoms & signs

Symptoms
o Exertional dyspnea; usually the first symptom of diminished
cardiac reserve
o Orthopnea
o Paroxysmal nocturnal dyspnea
o Excessive diaphoresis
o Anginal chest pain; can be prolonged and often does not
respond to nitroglycerin
o Uncomfortable awareness of the heartbeat, especially on lying
down
o Sinus tachycardia during exertion or with emotion
o Palpitations, head pounding from premature ventricular
contractions
o In severe acute AR, pulmonary edema and/or cardiogenic
shock may develop rapidly
o In severe chronic AR, patients may remain relatively
asymptomatic for 10-15 years
Signs
o Corrigans pulse-a rapidly increasing water hammer pulse
Collapses suddenly as arterial pressure rapidly
decreases during late systole and throughout diastole
o Capillary pulsations-alternate flushing and paling of skin at the
root of the nail while pressure is applied to the tip of the nail
(Quinckes pulse)
o Traubes sign-a booming, pistol-shot sound heard over
femoral arteries
o Duroziezs sign-a to-and-fro murmur if the femoral artery is
lightly compressed with a stethoscope

o Widened arterial pulse pressure

Elevation of systolic pressure, sometimes as high as 300
mmHg
Depression of diastolic pressure
Systolic sounds are frequently heard with the cuff
completely deflated
Severity of AR does not always correlate directly with
arterial pulse pressure
o Palpation
LV impulse is heaving and displaced laterally and
inferiorly
Diastolic thrill is often palpable along the left sternal
border
Systolic thrill may be palpable in the jugular notch and
transmitted upward along the carotid arteries
o Aortic valve closure sound (A2) is ussually absent
o An S3 and systolic ejection sound are frequently audible
o Occasionally, an S4 also may be heard
o Typical murmur of chronic AR
High-pitched, blowing, decrescendo diastolic murmur
Heard best in the third intercostal space along the left
sternal border
In patient with mild AR, murmur is brief
As the severity of murmur increases, it generally
becomes louder and longer, then holodiastolic
o Other murmurs heard with AR
Mild-systolic ejection murmur; can be quite loud without
signifying aortic obstruction
Austin Flint murmur-a soft, low-pitched, rumbling middiastolic bruit
o Auscultatory features of AR are intensified by isometric
exercise, such as strenuous handgrip
o In severe AR, jarring of the entire body and a bobbing motion
of the head with each systole can occur

Differential Diagnosis

Pulmonic regurgitation with high pulmonary pressures

Mitral stenosis mimicking an Austin Flint murmur
Patent ductus arteriousus
Arteriovenous malformation with wide pulse pressure
Arteriovenous fistula near heart, with continuous murmur

Diagnostic Approach

History
o Family history of marfan syndrome
o Closed chest trauma
o History compatible with infective endocarditis
Physical exemination
Electrocardiography
Echocardiography
Cardiac catheterization and angiography

Laboratory tests

General tests to assess associated physiologic derangements

o Complete blood count
o Electrolytes
o Renal panel
o Prothrombin time

Imaging

Electrocardiography
o Sensitive in detection of AR
o Helpful in assessing severity
o Useful in determining cause
Dilatation of aortic annulus
Thickening and failure of coaptation of leaflets
o Characteristic findings
Extent and velocity of wall motion are normal or
supernormal, until myocardial contractility declines
Rapid, high-frequency fluttering of anterior mitral leaflet
is produced by impact of regurgitant jet
Chest radiography in severe AR
o Apex is displaced downward and leftward in the frontal
projection
o Cardiac shadow extends below the left diaphragm
o LV enlargement may be apparent in the left anterior oblique
and lateral projections
o Ascending aorta and aortic knob may be moderately dilated in
primary valvular disease

o Aneurysmal dilatation of the aorta is seen in the frontal view,

and the aorta fills the retrostrenal space in the lateral view
when AR is causedby primary disease of the aortic wall
Cardiac catheterization and angiography
o Accurate confirmation of magnitude of regurgitation and
status of LV function
o Condition of the coronary arterial bed should ordinarily be
evaluated preoperatively

Diagnostic Procedures

Electrocardiography
o In patients with severe chronic AR
Signs of LV hypertrophy
ST-segment depression and T-wave inversion in leads I,
aVL, V5 and V6 (LV strain)
o QRS prolongation
Indicates diffuse myocardial disease
Generally associated with patchy fibrosis
Signifies poor prognosis

TREATMENT
Treatment Approach

Medical therapy
o Symptom control
Diuretics and angiotensin-converting enzyme (ACE)
inhibitors for heart failure
o Prevention
Vasodilators (nifedipine or ACE inhibitors)
To protect LV myocardium
To delay need surgery
Surgery
o Definitive treatment
o Indicated in symptomatic patients or asymptomatic patients
with LV dysfunction

Specific Treatment
MEDICAL TREATMENT

Salt restriction
Diuretics
Digitalis
Long-acting nifedipine
o Has been found to delay need for surgery
Nitrates
o Not as helpful in relieving anginal pain as in patients with
ischemic heart diseasee, but worth a trial
ACE inhibitors
Cardiac arrhythmias and infections are poorly tolerated in patients
with severe AR and must be trated promptly and vigorously
Patients with syphilitic aortitis should receive a full course of
penicillin therapy

SURGERY

Timing
o Surgery can be deferred as long as patient both remains
asymptomatic and normal LV function
Chronic AR is usually not symptomatic until after
myocardial dysfunction develops
When delayed too long, surgical treatment often does
not restore normal LV function
Surgery should be carried out in asymptomatic patients
with progressive LV dysfunction and an LV ejection
fraction <55% or an LV end-systolic volume >55 mL/m 2
(the 55/55 rule)
o Patients with acute, severe AR require prompt surgical
treatment, which may be life saving
Aortic valve replacement (AVR)
o Generally necessary in patients with rheumatic AR and in
many patients with other forms of regurgitation
Surgical repair
o Sometimes possible in congenital AR
o Occasionally possible when a leaflet has been perforated
during infective endocarditis or torn from its attachments to
the aortic annulus by thoracic trauma
o When AR is due to aneurysmal dilatation of the annulus and
ascending aorta, it may be possibleto reduce regurgitation by
narrowing the annulus or by excising a portion of the aortic
root

ONGOING CARE
Monitoring

In patients with severe AR, to select optimal time for surgery

o Clinical folllow-up for symptoms
o Echocardiography at 6-month intervals to assess LV function

Complication

Endocarditis
Congestive heart failure

Prognosis

Operative risk and late mortality depend largely on the stage of

disease and on myocardial function at the time of surgery
o Operative mortality rate in AVR
Isolated AVR or repar : 4-5%
AVR and coronary artery bypass graft: 8%
AVR and mitral valve repair: 7-5%
o Patients with marked cardiac enlargement and prolonged LV
dysfunction
Operative mortality rate approximately 10%
Late mortality rate approximately 5% per year because
of LV failure
Because of very poor prognosis with medical management, even
patients with LV failure should be considered for surgery

Prevention

Avoidance of risks for rheumatic heart disease, including treatment

of streptococcal infections
Avoidance of anoretic drugs associated with heart valve disease
(fenfluramine and dexfenfluramine; no longer marketed in U.S.)

PEARLS

The diagnosis of severe AR can often be made from across the

room, by observing the bobbing of the patients head with each
heartbeat

Acute, severe AR may not be associated with a wide pulse pressure

or long diastolic murmur because of mid-diastolic (preamature)
closure of the mitral valve

INTERNET SITE
Guideline for aortic regurgitation national guideline clearinghouse
Alorithm ACC/ AHA guidelines for valvular heart