Aortic insufficiency (
AI), also known as
aortic regurgitation (
AR), 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 (the beginning of the aorta).
Etiology
About half of the cases of aortic insufficiency are due to the aortic root dilatation (
annuloaortic ectasia), which is
idiopathic in over 80% of cases, but otherwise occurs with
aging and
hypertension,
Marfan syndrome,
aortic dissection, and
syphilis. 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. Additionally, aortic insufficiency has been linked to the use of some medications belonging to the class of serotonin reuptake inhibitors, specifically medications containing
fenfluramine or
dexfenfluramine isotopes, and
dopamine agonists.
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. After ventricular systole, the pressure in the ventricle decreases, as the ventricle relaxes and gets ready to fill up with blood from the
left atrium. This relaxation of the left ventricle (early ventricular
diastole) causes a fall in the pressure in the left ventricle. When the pressure in the left ventricle falls below the pressure in the
aorta, the
aortic valve will close, preventing blood from going from the aorta back into the left ventricle. The amount of blood that is
ejected by the heart is known as the
stroke volume or
stroke work. Under normal conditions, the entire stroke volume delivers oxygenated blood to the body.
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 (systolic pressure - diastolic pressure).
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.
AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart.
The pressure overload (due to elevated pulse pressure and the systemic effects of neuroendocrine hormones) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the increased left ventricular systolic pressures 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 (rather than the mitral valve being closed at the beginning of systole).
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 (typically after a latency period) 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.
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 S4
heart sound (which would indicate left ventricular filling against a hypertrophied LV wall). The murmur of chronic aortic insufficiency is typically described as early diastolic and decresendo, which is best heard at aortic area when the patient is seated and leans forward with breath held in expiration. The murmur is usually soft and seldom causes thrill. If there is radiation to the right parasternal region, ascending aortic aneurysm has to be excluded.
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 concomittant 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 the AI, although usefulness of some of the eponymous signs has been questioned:
- large-volume, 'collapsing' pulse
- bounding peripheral pulses; also known as Watson's water hammer pulse
- low diastolic and increased pulse pressure
- Corrigan's pulse (rapid upstroke and collapse of the carotid artery pulse)
- de Musset's sign (head nodding in time with the heart beat)
- Quincke's sign (pulsation of the capillary bed in the nail)
- Traube's sign (systolic and diastolic murmurs described as 'pistol shots' heard over the femoral artery when it is gradually compressed)
- Duroziez's sign (a double sound heard over the femoral artery when it is compressed distally)
Rarer signs include:
Unfortunately, none of the above putative signs of aortic insufficiency is of utility in making the diagnosis. 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 the
echocardiogram, which can provide two-dimensional views of the regurgitant jet, and allow measurement of the velocity and volume of the jet.
The echocardiographic findings in severe aortic regurgitation include:
- An AI color jet dimension > 60 percent of the left ventricular outflow tract (LVOT) diameter (may not be true if the jet is eccentric)
- The pressure half-time of the regurgitant jet is < 250 msec
- Early termination of the mitral inflow (due to increase in LV pressure due to the AI.)
- Early diastolic flow reversal in the descending aorta.
- Regurgitant volume > 60 ml
- Regurgitant fraction > 55 percent
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
Indications for surgery for chronic severe aortic insufficiency
| Symptoms
| Ejection fraction
| Other information
|
| NYHA class III - IV
| ≥ 50 %
| |
| NYHA class II
| ≥ 50 %
| Progression of symptoms or worsoning parameters on echocardiography |
| CHA class ≥ II angina
| ≥ 50 %
| |
| Regardless of symptoms
| 25 - 49 %
| |
| Cardiac surgery for other cause (ie: CAD, other valvular disease, ascending aortic aneurysm)
|
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 below 50% or in the face of progressive and severe left ventricular dilatation. For both groups of patients, surgery before the development of worse ejection fracture/LV systolic dilatation, is expected to reduce the risk of sudden death, and is associated with lower peri-operative mortality.
Medical treatment
Medical therapy of chronic aortic insufficiency involves the use of vasodilators. Small trials have shown a short term benefit in the use of
ACE inhibitors,
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.
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. In stead, replacement with an aortic valve homograft should be performed if feasible.
In the future, it is hoped that a percutaneous approach to aortic valve replacement will be feasible.
References
External links
See also
