Aortic Regurgitation is defined as leakage or incompetence of the aortic
valve apparatus or the dilatation of the valve ring.
Aortic regurgitation can be chronic or acute in origin.
Causes of Chronic Aortic regurgitation are:
• Chronic rheumatic valvular heart disease
• Bacterial endocarditis of bicuspid aortic valve
• Syphilitic aortitis with aortic root dilataion
• Acquired connective tissue disorders like rheumatoid arthritis and
• Congenital connective tissue disorders like Marfan’s syndrome and
Ehlers Danlos syndrome
Causes of acute Aortic regurgitation are:
• Blunt trauma to the chest
• Acute bacterial endocarditis
• Dissection of ascending aorta
• Rupture of ascending aorta aneurysm
• Rupture of sinus of valsalva aneurysm
In chronic rheumatic valvular disease the aortic valve is usually damaged
by chronic inflammation of the valve cusps, leading to in approximation of the
valve and resultant leakage of blood from the aorta to the left ventricular
chamber. In connective tissue diseases myxomatous degeneration of the valves
results in increased pliability of the valves and also excessive redundancy of the
chordae tendinae and the papillary muscles. Aortic regurgitation may also occur
due to dilatation of the valve ring that might occur as a dilatation of the root of
aorta as in syphilitic aortitis, aneurysm of ascending aorta and left ventricular
Leakage of blood from aorta to the left ventricle occurs only during the
early phase of diastole. This is because of the fact that, the left ventricle gets
filled up by the blood received normally from the left atrium thorough the mitral
valve during diastole, and the blood received from the aorta during the AR leak.
Thus the pressure in the aorta and the left ventricle gets equalized during mid-
diastole, earlier than the normal persons; hence the leak also diminishes during
the late diastole.
All these lead to a volume overload of the left ventricle and increasing its
end diastolic volume. Most of this blood is pumped back into the aorta during the
next systole there will be an increase in the stroke volume. This may cause an
ejection systolic murmur even in the absence of any aortic valve stenosis.
The volume over load of the left ventricle leads to left ventricular
hypertrophy, left ventricular dilatation, passive congestion of the left atrium and
the pulmonary veins. Rarely left ventricular failure, pulmonary artery hypertension
and right heart failure may occur late in the course of the disease. In acute aortic
regurgitation compensatory mechanisms are not active and therefore the
increase in end diastole pressure is marked and left ventricular failure also
Patients with chronic aortic regurgitation may remain asymptomatic for
along time. Moderate degree of aortic regurgitation presents with palpitation,
increased fatigability, exertional dyspnoea, and some times chest pain. . Cardiac
failure symptoms are unusual as the initial presentation. If aortic regurgitation
coexists with aortic stenosis or mitral valve disease, the patient may present with
more symptoms at an earlier date.
Patients with isolated aortic regurgitation are moderately built and
moderately nourished. If the regurgitation is due valvular endocarditis the patient
may also present with evidence of pallor, clubbing and other peripheral signs of
The pulse rate and rhythm are usually normal. The character of the pulse
is typically high volume and collapsing. This character is due to three
pathophysiological mechanisms which are present simultaneously a) an
increased stroke volume, b) rapid run off of blood from the aortic circulation and
c) peripheral vasodilatation. On must also remember that high volume collapsing
pulse may also occur in conditions like persistent ductus arteriosus,
arteriovenous fistulas and Paget’s disease of the bone.
The blood pressure is also suggestive of aortic regurgitation. The systolic
pressure is markedly elevated and the diastolic pressure is grossly reduced and
hence the pulse pressure is very high. A typical instance of blood pressure in
aortic regurgitation will be 180/40 mm of Hg. When there is coexisting aortic
stenosis the systolic blood pressure is not elevated to the same extent as in case
of aortic regurgitation.
Jugular venous pressure is not elevated in case of aortic regurgitation
unless there is congestive heart failure. The jugular venous wave pattern is
Apex beat is shifted laterally and downwards due to ventricular dilatation.
The character of the apex is forceful due to the volume overload. A diastolic thrill
is unusual. Left parasternal heave and palpable shock of second heart sound are
present only if there is significant pulmonary artery hypertension. On percussion
of heart borders the cardiomegaly will be evident.
On auscultation the first heart sound is usually normal and the second
heart sound also unaltered. No S3 is heard; S4 may be present. The
characteristic murmur is an early diastolic murmur of grade2-4 intensity, which is
high pitched decrescendo best heard in the second aortic area conducted along
the right sternal border. In syphilitic aortic regurgitation, the murmur is best heard
in the aortic area and conducted along the right sternal border. The aortic
regurgitation murmur is better heard when the patient is sitting up and leaning
forward with the breath held in expiration
An ejection systolic murmur not associated with an ejection click or
conduction to the carotids is heard because of the increased stroke volume due
to increased flow across the aortic valve even without any valvular stenosis. But
if any mount of aortic stenosis coexists with aortic regurgitation, the
characteristics of the systolic murmur will also differ including a thrill and
conduction to the carotids.
The third murmur, which may occur in aortic regurgitation, is an Austin
Flint murmur. This is a mid diastolic rumble heard in the mitral area, due to the
displacement of the anterior mitral valve leaflet by the blood regurgitating from
the aortic valve obstructing the blood flow from left atrium to the left ventricle.
Patients with moderate to severe aortic regurgitation may also have
peripheral signs of aortic regurgitation. These are: Alfred de Musset’s sign (head
nodding), Muller’s sign (pulsations of uvula), Corrigan’s sign (dancing carotids),
Dancing brachial, Traube sign (pistol shot sounds), Durozeiz murmur (diasolic
murmur on compression of femoral artery proximally) Hills sign difference in
systolic Blood pressure between upper limb and lower limb >20 mm of Hg.
ECG will show evidence of left ventricular enlargement and left ventricular
hypertrophy, but without evidence of strain pattern asymmetrical T inversion and
ST depression in V5 and V6
Chest X ray PA view will show cardiomegaly with displacement of apex
downward and outward. Pulmonary venous congestion and pulmonary artery
hypertension may also be present.
Echocardiography will show dilated left atrium and left ventricle. And
Doppler echo will demonstrate the aortic valve leak. ECHO will also demonstrate
the presence of vegetations in case of infective endocarditis.
Cardiac catheterization is diagnostic.
Aortic regurgitation needs to be differentiated from pulmonary
regurgitation in which case signs of pulmonary arterial hypertension and right
ventricular hypertrophy. On has to look for evidence of acquired connective
tissue disorders like rheumatoid arthritis and ankylosing spondylitis. Also look for
evidence of congenital connective tissue disorders like Marfan’s syndrome and
Ehlers Danlos skin. More commonly a rheumatic etiology will be evident if there
is a positive rheumatic history. In that situation the mitral valve is also usually
involved Syphilitic aortic regurgitation is suggested by the conduction of the
murmur along the right sternal border and a positive VDRL and Khan test.
• This includes treatment of cardiac failure like diuretics, vasodilators and ACE
inhibitors and digoxin.
• Restriction of strenuous physical activities and
• Salt restriction.
• Infective endocarditis as a cause of aortic regurgitation requires treatment for
4-6 weeks given after culture and sensitivity test.
Aortic valve replacement is recommended for all patients with severe
chronic aortic regurgitation who develop signs and symptoms of cardiac failure,
either with bioprosthetic valve or a metallic prosthesis. These patients will require
life long anticoagulation.
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