aortic stenosis, pathologic narrowing of the aortic valve
Chest radiographs may show cardiac enlargement. Minimal enlargement
and more subtle signs of concentric hypertrophy without dilatation
are present, including mildly enlarged heart size, rounding at the
cardiac apex, and slight backward displacement of the heart as seen
in lateral view.
In later, more severe stages of AS, roentgenographic signs of left
atrial enlargement, pulmonary artery enlargement, right-sided
enlargement, and pulmonary congestion are evident.
Two-dimensional transthoracic echocardiography can confirm the
clinical diagnosis of AS and provide specific data on left
ventricular function. It can show the structure and function of the
other valves as well.
Pathophysiology: When the aortic valve becomes stenotic, resistance
to systolic ejection occurs and a systolic pressure gradient
develops between the left ventricle and the aorta. Stenotic aortic
valves have a decreased aperture that leads to a progressive
increase in left ventricular systolic pressure. This leads to
pressure overload in the left ventricle, which, over time, causes an
increase in ventricular wall thickness (ie, concentric hypertrophy).
At this stage, the chamber is not dilated and ventricular function
is preserved, although diastolic compliance may be affected.
Eventually, however, the left ventricle dilates. This, coupled with
a decrease in compliance, is associated with an increase in left
ventricular end-diastolic pressure, which is increased further by a
rise in atrial systolic pressure. A sustained pressure overload
eventually leads to myocardial decompensation. The contractility of
the myocardium diminishes, which leads to a decrease in cardiac
output. The elevated left ventricular end-diastolic pressure causes
a corresponding increase in pulmonary capillary arterial pressures
and a decrease in ejection fraction and cardiac output. Ultimately,
congestive heart failure (CHF) develops
Mortality/Morbidity: Sudden cardiac death occurs in 3-5% of
patients with AS. Adults with AS have a 9% mortality rate per year.
Once symptoms develop, the incidence of sudden death increases to
15-20%, with average survival duration of less than 5 years.
Patients with exertional angina or syncope survive an average of 3
years. After the development of left ventricular failure, life
expectancy is slightly greater than 1 year.
The development of any of the three classic symptoms (shortness of
breath, syncope and angina) indicates aortic stenosis severe enough
to be treated with valve replacement surgery. Valve replacement, the
only treatment for aortic stenosis, involves major open-heart
surgery. Since patients with aortic stenosis often also have
blockages in the coronary arteries (coronary artery disease),
surgeons typically treat any significant blockages by performing a
bypass operation at the same time. Thus, most patients who will
undergo valve replacement surgery are first referred for cardiac
catheterization to detect blockages in the coronary arteries.
Valve Replacement Surgery
Replacement of the aortic valve requires open-heart surgery, in
which the sternum (breast bone) is split down the middle, allowing
access to the heart. The heart is actually stopped during critical
parts of the operation, and a special machine pumps oxygenated blood
throughout the body. A small part of the heart is then opened, the
diseased valve is removed, and a new valve is sewn in.
There are three basic types of valves used to replace the diseased
heart valve. A porcine valve is made of tissue from a pig (Figure
1). The advantage of a porcine valve is that it poses no significant
risk for blood clots on the valve; thus, patients do not need blood
thinner medication. The disadvantage is that after approximately ten
years some of these valves degenerate and must be replaced.
A mechanical valve is fashioned from metal and synthetic materials.
The most commonly used mechanical valve, St. Jude's valve (Figure
2), consists of two semicircular discs that open with each
contraction of the left ventricle and close when the ventricle
relaxes. The advantage of a mechanical valve is that it is quite
durable, often lasting more than 20 years. The disadvantage is that
there is a small potential for a blood clot to form on the valve.
This blood clot can break off, travel to the brain, and cause a
stroke. To prevent this complication, patients who receive
mechanical heart valves are treated with warfarin (Coumadin®), a
blood thinner that decreases the chance for blood clot formation.
A homograft valve is an aortic valve that has been taken from a
human organ donor. These valves are not associated with a
significant risk of blood clot formation and, thus, do not require
blood thinner therapy. Although no long-term follow-up data are yet
available, it is thought that these valves may be quite durable.
There have been significant advances in the way valve replacement
surgery is now performed, and in most patients the risks for major
complications are acceptably low, approximately 3% to 5% in
otherwise relatively healthy patients. Major complications include
bleeding, infection, kidney failure, stroke, heart attack, and
X-ray showing Mitral Stenosis