Aortic insufficiencyAortic 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. The aortic valve separates the left ventricle of the heart (the heart's largest pumping chamber) from the aorta, the large artery that carries oxygen-rich blood out of the left ventricle to the rest of the body. In aortic valve insufficiency, the aortic valve becomes leaky, causing blood to flow backwards into the left ventricle. Aortic valve insufficiency occurs when this valve cannot properly close
after blood that is leaving the heart's left ventricle enters the aorta. With each contraction of the heart more and more blood flows back into the left ventricle, causing the ventricle to become overfilled. This larger-than-normal amount of blood that collects in the left ventricle puts pressure on the walls of the heart, causing the heart muscle to increase in thickness (hypertrophy). If this thickening continues, the heart can be permanently damaged. Aortic valve insufficiency is also know as aortic valve regurgitation because of the abnormal reversed flow of blood leaking through the poorly functioning valve.
Diseases of the aortic valve leaflets that can cause AI include endocarditis, rheumatic heart disease (in individuals with rheumatic fever), and various collagen vascular diseases. Diseases of the aortic root that can cause AI include annuloaortic ectasia (dilatation of the proximal aortic root that occurs with aging and hypertension), Marfan syndrome, aortic dissection, and syphilis. Of all these causes of AI, the most common are endocarditis and annuloaortic ectasia.
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 oxygentaed blood to the body.
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, and therefore an increase in the pulse pressure (systolic pressure - diastolic pressure) and hypertension. Since some of the blood that is ejected during systole regurgitates back during diastole, there is decreased effective forward flow in AI. AI causes both volume overload (elevated preload) and pressure overload (elevated afterload) of the heart. The pressure overload (due to elevated pulse pressure and hypertension) causes left ventricular hypertrophy (LVH). There is both concentric hypertrophy and eccentric hypertrophy in AI. The concentric hypertrophy is due to the hypertension associated with AI, while the eccentric hypertrophy is due to volume overload caused by the regurgitant fraction.
The hemodynamic sequelae of AI are dependant on the rate of onset of AI. Acute AI and chronic AI will have different hemodynamics and individuals will have different signs and symptoms. In acute aortic insufficiency, 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, unable to deal with the sudden change in volume, and will decompensate. The filling pressure of the left ventricle will increase. This causes pressure in the left atrium to rise, and the individual will develop congestive heart failure. 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 may be difficult to diagnose clinically, since the left ventricle had not yet developed the eccentric hypertrophy and dilatation that allow an increased stroke volume and bounding peripheral pulses that are common in chronic AI. 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). If the individual survives the initial hemodynamic derailment that acute AI presents as, the left ventricle adapts by eccentric hypertrophy and dilitation 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. Whlie 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.
The physical examination of an individual with aortic insufficiency involves auscultation of the heart to listen for the murmur of aortic insufficiency and related heart sounds. The murmur of chronic aortic insufficiency is a holodiastolic (lasts all of diastole) decrescendo murmur (starts off loud and becomes soft). 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. 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 typically warranted prior to the ejection fraction falling below 55% or the left ventricular end-systolic dimension falling below 55mm, regardless of symptoms. If either of these thresholds is passed, the prognosis worsens. 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 the use of these pharmacologic agents is to decrease the afterload so that the left ventricle is spared somewhat. 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. 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 circulatory arrest.
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.