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Background: With the increase in age of the United States population, disease
processes in elderly individuals have become a major point of interest among health
care professionals. Valvular aortic stenosis (AS) is no exception to this trend because
senile degenerative AS currently is the leading indication for aortic valve replacement
(AVR). Obviously, accurate diagnosis and efficient treatment of this clinical entity are
becoming increasingly more important. Two-dimensional (2D) and Doppler
echocardiographic methods have become invaluable tools for estimating the degree of
stenosis and hence, for assisting in management guidance in most patients. Magnetic
resonance imaging (MRI) has also proven useful in evaluating aortic valve stenosis, but
its accessibility and practicality has limited its use. The favorable long-term outcome
following aortic valve (AV) surgery and the relatively low operative risk emphasize the
importance of an accurate and timely diagnosis.
In infants and children with congenital AS, the increase in obstruction occurs gradually
because the valve orifice shows little change as the child grows. Similarly, left
ventricular (LV) obstruction usually develops and increases gradually over a long period
of time in adults. The progressive LV outflow obstruction results in increased LV mass
by parallel replication of sarcomeres producing concentric hypertrophy at the expense
of cavity size. This increase in wall thickness is a compensatory mechanism to
normalize LV wall stress. Indeed, wall thickness appears to be a critical determinant of
ventricular performance in patients with AS; an inverse relationship exists between LV
wall stress and ejection fraction (EF). Inadequate development of hypertrophy,
depression of myocardial contractility, or a combination of these factors usually leads to
impairment of ventricular performance.
LV systolic function usually is well preserved, and cardiac output (CO) is maintained for
many years despite a large pressure gradient across the AV without a reduction in
resting CO, LV dilatation, or development of symptoms. Although an elevated left
ventricular end-diastolic pressure (LVEDP) may be an indicator of impending LV failure,
it often reflects diminished compliance of a hypertrophic LV wall.
In patients with severe AS, the left atrial (LA) pressure waveform usually demonstrates
a large a wave because of a combination of vigorous contraction of a hypertrophic left
atrium and reduced LV compliance. Atrial contraction plays a particularly important role
in mitral valve conductance and filling of the left ventricle in AS. It raises LVEDP while
preventing a concomitant elevation of mean LA pressure. This prevents pulmonary
venous and capillary pressures from rising to levels that would normally produce
pulmonary congestion, while at the same time elevating LVEDP sufficiently to ensure
effective LV contraction. Therefore, development of atrial fibrillation in AS is often
catastrophic to the maintenance of normal forward stroke volume.
Although the CO at rest is normal in most patients with severe AS, it often fails to rise
significantly during exercise. Late in the course of the disease, the CO, stroke volume,
and the left ventricle and aorta pressure gradient all decline, whereas the mean left
atrium, pulmonary capillary wedge, pulmonary artery, right ventricle systolic and
diastolic, and right atrial (RA) pressures rise, often sequentially. AS intensifies the
severity of existing mitral regurgitation (MR) by increasing the ventricular pressure
gradient responsible for driving blood from the left ventricle to the left atrium.
Coronary blood flow at rest is increased in absolute terms but is normal when corrected
for LV mass. However, myocardial blood flow reserve often is reduced. Increased LV
mass, increased LV systolic pressure, and prolongation of the systolic ejection phase all
elevate the myocardial oxygen requirement, especially in the subendocardial region.
Myocardial perfusion also is compromised by the relative decline in myocardial capillary
density and by a reduced diastolic transmyocardial (coronary) perfusion gradient due to
elevated LVEDP. Therefore, the subendocardium is susceptible to low nutrient flow, and
this underperfusion results in myocardial ischemia.
Frequency:
History: In AS of adults, a long latent period exists during which the LV outflow
obstruction and the pressure load on the myocardium gradually increase while patients
remain asymptomatic.
• The classic symptom triad of AS includes angina pectoris, syncope, and heart
failure, which most commonly manifest after the sixth decade of life.
o Exertional dyspnea is the most common initial complaint, even with normal
LV systolic function, and it relates to abnormal LV diastolic function.
• Calcific AS may cause emboli of calcium in various organs, including the heart,
kidney, and brain.
• Because resting CO usually is well maintained for many years in patients with
severe AS, marked fatigability, debilitation, peripheral cyanosis, and other
manifestations of a low CO usually are not prominent until quite late in the natural
history of the disease.
Physical: In severe AS, the carotid arterial pulse is small and rises slowly (pulsus
parvus et tardus); however, in elderly individuals, it may not be present despite severe
stenosis because of a more rigid aorta. A lag time may be present between the apical
impulse and the carotid impulse. Systolic hypertension can coexist with AS, but a
systolic blood pressure higher than 200 mm Hg is rare in patients with critical AS. In
advanced-stage AS, both systolic blood pressure and pulse pressure are decreased.
• Pulsus alternans can occur with the onset of LV dysfunction. The jugular venous
pulse may show prominent a waves reflecting reduced RV compliance
consequent to hypertrophy of the interventricular septum. The v wave also may
become prominent as pulmonary hypertension leads to RV failure and tricuspid
regurgitation.
• S1 usually is normal or soft. The aortic component of the second heart sound, A2,
usually is diminished or absent because the AV is calcified and immobile and/or
aortic ejection is prolonged or buried in the prolonged systolic ejection murmur.
Paradoxical splitting of the S2 also occurs because of late closure of A2; its
absence usually excludes severe AS. P2 also may be accentuated when LV
failure leads to secondary pulmonary hypertension.
• The intensity of the systolic murmur does not correspond to the severity of AS,
rather, the timing of the peak and the length or duration of the murmur
corresponds to the severity of AS. The more severe the stenosis, the longer the
duration of the murmur and the more likely it peaks at mid-to-late systole.
• When the left ventricle fails and CO falls, the murmur becomes softer and can
even disappear. The slow rising pulse becomes difficult to recognize. Atrial
fibrillation with short R-R intervals also can decrease the murmur intensity or
make it appear absent. In an elderly person with symptoms of CHF and a soft
systolic ejection murmur, noninvasive evaluation for AS is needed because
occult AS may be a cause of intractable heart failure. Embolization from a
calcified or infected AV that results in unilateral vision loss, focal neurological
signs, and myocardial infarction can be the first signs of AV pathology.
Causes: Most cases of AS are due to the obstruction at the valvular level. Common
causes are summarized in Table 1. Valvular AS can be either congenital or acquired.
Imaging Studies:
• Echocardiography
Indication Class
Diagnosis and assessment of severity of AS I
Assessment of LV size, function, and/or hemodynamics I
Reevaluation of patients with known AS with changing symptoms or I
signs
Assessment of changes in hemodynamic severity and ventricular I
function in patients with known AS during pregnancy
Reevaluation of asymptomatic patients with severe AS I
Reevaluation of asymptomatic patients with mild-to-moderate AS IIa
and evidence of LV dysfunction or hypertrophy
Routine reevaluation of asymptomatic adult patients with mild AS III
who have stable physical signs and normal LV size and function
Other Tests:
• Electrocardiogram
o Although the ECG findings may be entirely normal, the principal finding is
left ventricular hypertrophy (LVH), which is found in 85% of patients with
severe AS; however, its absence does not preclude critical AS. The
correlation between absolute voltages in precordial leads and the severity
of obstruction, unlike in children with congenital AS, is poor in adults.
o The rhythm usually is normal sinus. Atrial fibrillation is uncommon and can
be seen at late stages or as a consequence of coexistent MV disease or
hyperthyroidism.
• Chest roentgenogram
o The cardiac size often is normal, with rounding of the LV border and apex
despite significant AS. Poststenotic dilatation of the ascending aorta is
common.
o Cardiomegaly is a late feature of severe isolated AS. The left atrium may
be slightly enhanced, and pulmonary venous hypertension may be seen.
• Exercise stress testing usually is not needed in patients with severe AS. It may
precipitate ventricular tachyarrhythmias, including ventricular fibrillation.
However, closely monitored exercise stress testing may be of value to assess
exercise capacity in asymptomatic patients and can be used during
measurements of pulmonary capillary wedge pressure upon exercise. Abnormal
results may prove greater disability than the patient could admit.
o The measured AVA does not change and the mean pressure gradient
increases significantly with an intravenous dobutamine infusion in patients
with an initially low-pressure gradient but severe AS. In contrast, a marked
increase in both the SV and the measured AVA usually occurs in patients
who have a low CO due to concomitant myocardial dysfunction rather than
due to severe AS alone.
Procedures:
• Cardiac catheterization
o In general, if clinical findings are not consistent with Doppler
echocardiogram results, cardiac catheterization is recommended for
further hemodynamic assessment. ACC/AHA recommendations for
cardiac catheterization in AS are summarized in Table 4.
o Measuring the left ventricular end-diastolic volume (LVEDV) and ESV and
calculating the EF also can quantitate the status of LV systolic pump
function. However, EF may underestimate LV performance in the
presence of the increased afterload associated with severe AS. Aortic root
angiogram may show thickening and doming of the AV as well as a
poststenotic dilatation of the aortic root.
Indication Class
Coronary angiography before AVR in patients at risk for CAD I
Assessment of severity of AS in symptomatic patients when AVR is I
planned or when noninvasive tests are inconclusive or a
discrepancy exists in the clinical findings regarding severity of AS
or the need for surgery
Assessment of severity of AS before AVR when noninvasive tests IIb
are adequate and concordant with clinical findings and coronary
angiography is not needed
Assessment of LV function and severity of AS in asymptomatic III
patients when noninvasive tests are adequate
Medical Care: The primary management of symptomatic patients with valvular AS is
interventional. Medical treatment essentially is reserved for patients who have
complications of AS such as heart failure, infective endocarditis, or arrhythmias.
• Digitalis can be used as an inotropic agent and also to control the ventricular rate
in cases with atrial fibrillation. Diuretics may be used for pulmonary congestive
symptoms, and vasodilators may be used for heart failure and for hypertension.
Both classes of agents should be used with caution to avoid critically reducing
preload in a patient with significant AS and a hypertrophic noncompliant LV. The
same precaution also is valid for beta-blockers and calcium channel blockers.
The age of patients undergoing AVR is rising steadily because the incidence of calcific
AS increases as the age of the population increases. The percentage of patients older
than 70 years who undergo AVR and have functional class III or IV is very high. Early
detection and close follow-up of patients with AS, along with a low threshold for the
intervention decision, reduces the operative risk and improves the duration and quality
of life. Once symptoms develop, intervention is needed.
o The best results from valvuloplasty are obtained in patients with congenital
commissural bicuspid AVs, where a 60-70% reduction in gradient and a
60% increase in AVA can be expected. It is recommended for patients
with gradients higher than 50-60 mm Hg and/or a valve area of less than
0.5 cm2/m2, even in asymptomatic patients, because of the low risk
associated with balloon valvuloplasty, the high desire for unrestricted or
minimally limited lifestyle in younger populations, and the incidence of
certain rare cases of sudden cardiac death. The risk rate of causing
significant AR is 10%.
o In critically ill patients, the mortality rate associated with the procedure is
3-7%. Another 6% develop serious complications including perforation,
myocardial infarction, and severe AR.
Indication Class
A bridge to surgery in hemodynamically unstable patients who are IIa
at high risk for AVR
Palliation in patients with serious comorbid conditions IIb
Patients who require urgent noncardiac surgery IIb
As an alternative to AVR III
Indication Class
Symptomatic patients with severe AS I
Patients with severe AS undergoing I
coronary artery bypass surgery
Patients with severe AS undergoing surgery on the aorta or other I
heart valves
Patients with moderate AS undergoing coronary artery bypass IIa
surgery or surgery on the aorta or other heart valves
Asymptomatic patients with severe AS and the following:
Activity: Patients with mild AS can lead a normal life. In cases of moderate AS,
moderate-to-severe physical exertion and competitive sports should be avoided.
o In patients with mild AS, yearly history and physical examination and
echocardiograms every 5 years are appropriate.
o The medical treatment options are limited in symptomatic patients who are
not candidates for surgical intervention. In cases of pulmonary congestion,
digitalis, diuretics, and ACE inhibitors might be used cautiously, whereas
beta-blockers might be used if the predominant symptom is angina. In any
case, excessive decrease in preload should be avoided. Onset of atrial
fibrillation often requires prompt cardioversion.
Complications:
• Heart failure
• Conduction defects
• Infective endocarditis
• Calcific embolization
Medical/Legal Pitfalls:
• In cases where the patient refuses AV replacement surgery, the patient needs to
have a full understanding of the potential implications (including sudden cardiac
death) of his or her decision.
• If, on the other hand, the patient does agree with surgery, again the patient
needs to understand its possible consequences, including perioperative death,
the need for lifelong anticoagulation depending on the type of prosthesis, the
need for bacterial endocarditis prophylaxis, and the risk of prosthesis malfunction
with potential need for reoperation at a higher operative risk.
• Discussion and careful documentation of these issues not only would help
patients become familiar with their condition and therapeutic options, but also
would help to avoid misunderstandings and potential litigation.