Aortic insufficiency, also known as aortic regurgitation, is the leaking of the aortic
valve of the heart that causes blood to flow in the reverse direction during ventricular
diastole, from the aorta into the left ventricle.
Aortic insufficiency can be due to abnormalities of either the aortic valve or the aortic root.
Causes About half of the cases of aortic insufficiency
are due to the aortic root dilation, which is idiopathic in over 80% of cases, but otherwise
may result from aging, syphilitic aortitis, osteogenesis imperfecta, aortic dissection,
Behçet's disease, reactive arthritis and systemic hypertension.
Aortic root dilation is the most common cause of aortic insufficiency in developed countries.
In about 15% the cause is innate bicuspidal aortic valve, while another 15% cases are
due to retraction of the cusps as part of postinflammatory processes of endocarditis
in rheumatic fever and various collagen vascular diseases.
Rheumatic heart disease is the most common cause of aortic insufficiency in developing
nations.
Additionally, aortic insufficiency has been linked to the use of some medications, specifically
medications containing fenfluramine or dexfenfluramine isomers and dopamine agonists.
Other potential causes that affects the valve directly include the following: Marfan's syndrome,
Ehlers–Danlos syndrome, ankylosing spondylitis, and systemic lupus erythematosus.
In acute cases of aortic insufficiency, the main causes are infective endocarditis, aortic
dissection or trauma.
Physiology In individuals with a normally functioning
aortic valve, the valve is only open when the pressure in the left ventricle is higher
than the pressure in the aorta.
This allows the blood to be ejected from the left ventricle into the aorta during ventricular
systole.
The amount of blood that is ejected by the heart is known as the stroke volume.
Under normal conditions, 50–70% of the blood in a filled left ventricle is ejected into
the aorta to be used by the body.
After ventricular systole, the pressure in the left ventricle decreases as it relaxes
and begins to fill up with blood from the left atrium.
This relaxation of the left ventricle causes a fall in its pressure.
When the pressure in the left ventricle falls below the pressure in the aorta, the aortic
valve will close, preventing blood in the aorta from going back into the left ventricle.
Pathophysiology
In aortic insufficiency, when the pressure in the left ventricle falls below the pressure
in the aorta, the aortic valve is not able to completely close.
This causes a leaking of blood from the aorta into the left ventricle.
This means that some of the blood that was already ejected from the heart is regurgitating
back into the heart.
The percentage of blood that regurgitates back through the aortic valve due to AI is
known as the regurgitant fraction.
For instance, if an individual with AI has a stroke volume of 100 ml and during ventricular
diastole 25 ml regurgitates back through the aortic valve, the regurgitant fraction is
25%.
This regurgitant flow causes a decrease in the diastolic blood pressure in the aorta,
and therefore an increase in the pulse pressure.
Thus, physical examination will reveal a bounding pulse, especially in the radial artery.
Since some of the blood that is ejected during systole regurgitates back into the left ventricle
during diastole, there is decreased effective forward flow in AI.
Note that while diastolic blood pressure is diminished and the pulse pressure widens,
systolic blood pressure generally remains normal or can even be slightly elevated.
This is because sympathetic nervous system and the renin-angiotensin-aldosterone axis
of the kidneys compensate for the decreased cardiac output.
Catecholamines will increase the heart rate and increase the strength of ventricular contraction,
directly increasing cardiac output.
Catecholamines will also cause peripheral vasoconstriction, which causes increased systemic
vascular resistance and ensures that core organs are adequately perfused.
Renin, a proteolytic enzyme, cleaves angiotensinogen to angiotensin I, which is converted to angiotensin
II, which is also a potent vasoconstrictor.
In the case of chronic aortic insufficiency with resultant cardiac remodeling, heart failure
will develop, and it is possible to see systolic pressures diminish.
Aortic insufficiency causes both volume overload and pressure overload of the heart.
The volume overload causes left ventricular hypertrophy.
There is both concentric hypertrophy and eccentric hypertrophy in AI.
The concentric hypertrophy is due to the increased left ventricular pressure overload associated
with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant
fraction.
Hemodynamics The hemodynamic sequelae of AI are dependent
on the rate of onset of AI.
Acute AI and chronic AI will have different hemodynamics and individuals will have different
signs and symptoms.
Acute aortic insufficiency In acute AI, as may be seen with acute perforation
of the aortic valve due to endocarditis, there will be a sudden increase in the volume of
blood in the left ventricle.
The ventricle is unable to deal with the sudden change in volume.
In terms of the Frank-Starling curve, the end-diastolic volume will be very high, such
that further increases in volume result in less and less efficient contraction.
The filling pressure of the left ventricle will increase.
This causes pressure in the left atrium to rise, and the individual will develop pulmonary
edema.
Severe acute aortic insufficiency is considered a medical emergency.
There is a high mortality rate if the individual does not undergo immediate surgery for aortic
valve replacement.
If the acute AI is due to aortic valve endocarditis, there is a risk that the new valve may become
seeded with bacteria.
However, this risk is small.
Acute AI usually presents as florid congestive heart failure, and will not have any of the
signs associated with chronic AI since the left ventricle had not yet developed the eccentric
hypertrophy and dilatation that allow an increased stroke volume, which in turn cause bounding
peripheral pulses.
On auscultation, there may be a short diastolic murmur and a soft S1.
S1 is soft because the elevated filling pressures close the mitral valve in diastole.
Chronic aortic insufficiency If the individual survives the initial hemodynamic
derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy
and dilatation of the left ventricle, and the volume overload is compensated for.
The left ventricular filling pressures will revert to normal and the individual will no
longer have overt heart failure.
In this compensated phase, the individual may be totally asymptomatic and may have normal
exercise tolerance.
Eventually the left ventricle will become decompensated, and filling pressures will
increase.
While most individuals would complain of symptoms of congestive heart failure to their physicians,
some enter this decompensated phase asymptomatically.
Proper treatment for AI involves aortic valve replacement prior to this decompensation phase.
Symptoms Symptoms of aortic insufficiency are similar
to those of heart failure and include dyspnea on exertion, orthopnea and paroxysmal nocturnal
dyspnea.
Palpitations and angina pectoris may also be felt.
In acute cases there may be cyanosis and circulatory shock.
Physical examination
The physical examination of an individual with aortic insufficiency involves auscultation
of the heart to listen for the murmur of aortic insufficiency and the S3 heart sound.
The murmur of chronic aortic insufficiency is typically described as early diastolic
and decrescendo, which is best heard in the third left intercostal space and may radiate
along the left sternal border.
If there is increased stroke volume of the left ventricle due to volume overload, an
ejection systolic 'flow' murmur may also be present when auscultating the same aortic
area.
Unless there is concomitant aortic valve stenosis, the murmur should not start with an ejection
click.
There may also be an Austin Flint murmur, a soft mid-diastolic rumble heard at the apical
area.
It appears when regurgitant jet from the severe aortic insufficiency renders partial closure
of the anterior mitral leaflet.
Peripheral physical signs of aortic insufficiency are related to the high pulse pressure and
the rapid decrease in blood pressure during diastole due to blood returning to the heart
from the aorta through the incompetent aortic valve, although the usefulness of some of
the eponymous signs has been questioned: large-volume, 'collapsing' pulse also known
as: Watson's water hammer pulse
Corrigan's pulse
low diastolic and increased pulse pressure de Musset's sign
Quincke's sign Traube's sign
Duroziez's sign Also, these are usually less detectable in
acute cases.
Less used signs include: Lighthouse sign
Landolfi's sign Becker's sign
Müller's sign Mayne's sign
Rosenbach's sign Gerhardt's sign
Hill's sign - a ≥ 20 mmHg difference in popliteal and brachial systolic cuff pressures,
seen in chronic severe AI.
Considered to be an artefact of sphygmomanometric lower limb pressure measurement.
Lincoln sign Sherman sign
Ashrafian sign Unfortunately, none of the above putative
signs of aortic insufficiency is of utility in making the diagnosis, but they may help
as pointers.
What is of value is hearing a diastolic murmur itself, whether or not the above signs are
present.
Diagnostic evaluation The most common test used for the evaluation
of the severity of aortic insufficiency is transthoracic echocardiography, which can
provide two-dimensional views of the regurgitant jet, allow measurement of velocity using Doppler,
and estimate jet volume.
The findings in severe aortic regurgitation, based on the 2006 American College of Cardiology/American
Heart Association guidelines include: An AI color jet width > 65 percent of the
left ventricular outflow tract diameter Doppler vena contracta width > 0.6 cm
The pressure half-time of the regurgitant jet is < 250 ms
Early termination of the mitral inflow Holodiastolic flow reversal in the descending
aorta.
Regurgitant volume > 60 ml Regurgitant fraction > 50 percent
Regurgitant orifice area > 0.3 cm2 Increased left ventricular size
In acute aortic regurgitation, echocardiography may show early closure of the mitral valve.
Chest X-ray can assist in making the diagnosis, showing left ventricular hypertrophy and dilated
aorta.
ECG typically indicates left ventricular hypertrophy.
Cardiac chamber catheterization assists in assessing the severity of regurgitation and
any left ventricular dysfunction.
Prognosis The risk of death in individuals with aortic
insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2
percent per year.
Risk increases if the ejection fraction decreases or if the individual develops symptoms.
Treatment
Aortic insufficiency can be treated either medically or surgically, depending on the
acuteness of presentation, the symptoms and signs associated with the disease process,
and the degree of left ventricular dysfunction.
Surgical treatment is controversial in asymptomatic patients, however has been recommended if
the ejection fraction falls to 50% or below, in the face of progressive and severe left
ventricular dilatation, or with symptoms or abnormal response to exercise testing.
For both groups of patients, surgery before the development of worsening ejection fraction/LV
dilatation, is expected to reduce the risk of sudden death, and is associated with lower
peri-operative mortality.
Also, surgery is optimally performed immediately in acute cases.
Medical treatment Medical therapy of chronic aortic insufficiency
that is stable and asymptomatic involves the use of vasodilators.
Small trials have shown a short term benefit in the use of ACE inhibitors or angiotensin
II receptor antagonists, nifedipine, and hydralazine in improving left ventricular wall stress,
ejection fraction, and mass.
The use of these vasodilators is only indicated in individuals who suffer from hypertension
in addition to AI.
The goal in using these pharmacologic agents is to decrease the afterload so that the left
ventricle is somewhat spared.
The regurgitant fraction may not change significantly, since the gradient between the aortic and
left ventricular pressures is usually fairly low at the initiation of treatment.
Other rather conservative medical treatments for stable and asymptomatic cases include
low sodium diet, diuretics, digoxin, calcium blockers and avoiding very strenuous activity.
As of 2007, the American Heart Association no longer recommends antibiotics for endocarditis
prophylaxis before dental procedures in patients with aortic insufficiency.
Antibiotic prophylaxis to prevent endocarditis before gastrointestinal or genitourinary procedures
is no longer recommended for any patient with valvular disease.
In mild to moderate cases, echocardiography and cardiac stress test should be followed
up every 1–2 years.
In severe moderate/severe cases, echocardiography with cardiac stress test and/or isotope perfusion
imaging should be performed every 3–6 months.
Surgical treatment The surgical treatment of choice at this time
is an aortic valve replacement.
This is currently an open-heart procedure, requiring the individual to be placed on cardiopulmonary
bypass.
In the case of severe acute aortic insufficiency, all individuals should undergo surgery if
there are no absolute contraindications for surgery.
Individuals with bacteremia with aortic valve endocarditis should not wait for treatment
with antibiotics to take effect, given the high mortality associated with the acute AI.
Instead, replacement with an aortic valve homograft should be performed if feasible.
A percutaneous approach to aortic valve replacement is now feasible, but the main experience has
been in the treatment of aortic stenosis.
Additional images
References
External links Heart Disease and Life After by Richard Hinkle
Additional resource on the Aortic Valve See also
Aortic valve replacement Preload
Afterload