C h a p t e r 1 9
Disorders of Cardiac Function
463
apparatus as the leaflets prolapse. Two-dimensional and
Doppler echocardiography is used to diagnose mitral
valve prolapse.
The treatment of mitral valve prolapse focuses on
the relief of symptoms and the prevention of compli-
cations.
38
Persons with palpitations and mild tachyar-
rhythmias or increased adrenergic symptoms, and
those with chest discomfort, anxiety, and fatigue often
respond well to therapy with beta blockers. In many
cases, the cessation of stimulants such as caffeine, alco-
hol, and cigarettes may be sufficient to control symp-
toms. Although infective endocarditis is an uncommon
complication in persons with a murmur, antibiotic pro-
phylaxis may be recommended before extensive den-
tal or surgical procedures associated with bacteremia.
Transient ischemic attacks occur more frequently in per-
sons with mitral valve prolapse. Therefore, daily aspirin
therapy is recommended in persons with documented
events who have a sinus rhythm and no atrial thrombi.
Persons with severe valve dysfunction may require valve
surgery.
Aortic Valve Disorders
The aortic valve, which is located between the left ven-
tricle and aorta, has three cuplike cusps and sometimes
is referred to as the
aortic semilunar valve
because its
leaflets are crescent or moon shaped. The aortic valve
has no chordae tendineae. Although their structures are
similar, the edges of the aortic valve leaflets are thicker
than those of the mitral valve, particularly at the middle
of the leaflet (see Chapter 17, Fig. 17-10). The mecha-
nism of action of the aortic valve is also different from
that of the mitral valve. During ventricular systole when
the ventricles contract and blood is being ejected into the
aorta, the cusps of the valve are flattened against the aor-
tic wall and blood rushes past them; when the ventricles
relax and the blood (no longer propelled forward by the
pressure of ventricular contraction) begins to flow back-
ward toward the heart, it fills the cusps and this closes
the valve.
An important feature of the aortic valve is the loca-
tion of the orifices for the two main coronary arteries,
which are located behind the valve and at right angles
to the direction of blood flow. It is the lateral pressure in
the aorta that propels blood into the coronary arteries.
During the ejection phase of the cardiac cycle, the lateral
pressure is diminished by conversion of potential energy
to kinetic energy as blood moves forward into the aorta.
This process is grossly exaggerated in aortic valve steno-
sis because of the high flow velocities.
Aortic Valve Stenosis.
Aortic valve stenosis is charac-
terized by narrowing of the valve orifice with increased
resistance to ejection of blood from the left ventricle
into the aorta (see Fig. 19-15). The most common
causes of aortic valve stenosis are congenital valve
malformations and acquired calcification of a normal
aortic valve. Congenital malformations may result
in unicuspid, bicuspid, or misshapen valve leaflets.
Acquired aortic stenosis is usually the consequence of
calcification associated with age-related degenerative
changes or the normal “wear and tear” of either pre-
viously normal aortic valves or congenitally bicuspid
valves with which approximately 1% of the popula-
tion are born.
9
The incidence of acquired aortic valve
stenosis is increasing with the rising average age of the
population.
6,40
The progression of calcific aortic stenosis is usu-
ally slow and varies widely among individuals. It usu-
ally becomes clinically evident in the sixth and seventh
decades in persons with bicuspid aortic valves, and not
until the eighth and ninth decades in those with pre-
viously normal valves. Valve changes range from mild
thickening without obstruction to severe calcification
with impaired leaflet motion and obstructed left ven-
tricular outflow.
41
Processes in the development of cal-
cific aortic valve disease have been shown to be similar
to those in CAD. Both conditions are more common in
men, older persons, and persons with hypercholester-
emia, and both derive in part from an active inflamma-
tory process.
40
Early lesions of aortic sclerosis show focal subendo-
thelial plaquelike lesions, similar to the initial phases of
an atherosclerotic lesion. Aortic sclerosis is distinguished
from aortic stenosis by the degree of valve impairment.
In aortic sclerosis the valve leaflets are abnormally thick-
ened, but the obstruction to outflow is minimal, whereas
in aortic stenosis the functional area of the valve has
decreased enough to cause measurable obstruction to
outflow. Calcification of the aortic valve progresses
from the base of the cusps to the leaflets. This reduces
leaflet motion and effective valve area, but without com-
missural fusion. As calcification progresses, the leaflets
become more rigid, there is worsening of obstruction to
left ventricular outflow, and fusion of the commissures
leads to aortic stenosis.
Because aortic stenosis usually develops gradually,
the left ventricle has time to adapt. With increased
systolic pressure from obstruction, the left ventricular
wall becomes thicker, or hypertrophies, but a normal
chamber volume is maintained. With this increase in
wall thickness, called concentric remodeling, the left
ventricular ejection fraction is maintained within nor-
mal limits. Hemodynamic variables remain stable even
though the valve opening area is reduced to half of its
normal size. However, an additional reduction in the
valve opening area from one half to one fourth of its
normal size produces severe obstruction to flow and a
progressive increase in the pressure overload on the left
ventricle. At this point, the increased work of the heart
begins to exceed the coronary blood flow reserve, caus-
ing both systolic and diastolic dysfunction and signs of
heart failure.
38,40,41
Aortic stenosis is usually first diagnosed with aus-
cultation of a loud systolic ejection murmur or a single
or paradoxically split-second heart sound. Eventually,
the classic symptoms of advanced aortic stenosis
such as angina, syncope, and heart failure develop,
although more subtle signs of a decrease in exercise
tolerance or exertional dyspnea should be monitored
closely. Angina occurs in approximately two thirds of
