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Aortic Stenosis

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.

Pathophysiology: The pathophysiologic mechanisms that are operative in patients with

AS include an increase in afterload, progressive hypertrophy of the left ventricle, and a
decrease in systemic and coronary flow as consequences of valve obstruction.

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.

Additionally, functional MR as a consequence of LV dilatation in late stages of AS may

superimpose the hemodynamic changes associated with this lesion on those produced
by AS. Consequent to secondary pulmonary hypertension, bulging of the hypertrophied
interventricular septum into the right ventricular (RV) cavity, or both, the RA a wave
becomes prominent. LVEDV usually remains normal or low until quite late in the course;
however, LV mass increases in response to LV chronic pressure overload, resulting in
an elevated LV mass-to-volume ratio.

Another consequence to the pathophysiologic response to AS, LV diastolic function,

commonly is abnormal, resulting in elevated LV filling pressures, which is reflected onto
the pulmonary circulation. Diastolic dysfunction occurs as a consequence of both
impaired LV relaxation and decreased LV compliance that is caused by increased
afterload, a thick noncompliant LV, and relative myocardial ischemia. Chamber stiffness
can revert toward normal as LV hypertrophy regresses following relief of valvular
obstruction, and in some patients, muscle stiffness also may revert to normal. Extensive
myocardial fibrosis develops with long-standing hypertrophy, which may not disappear
despite regression of hypertrophy.

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.


• In the US: Aortic sclerosis (considered a precursor of calcific degenerative AS)

increases with age and is present in 29% of individuals older than 65 years and
in 37% of individuals older than 75 years. In elderly persons, the prevalence of
AS is between 2% and 9%.

Mortality/Morbidity: The natural history of AS is well known. Patients with severe AS

may be asymptomatic for many years despite the presence of severe left ventricular
outflow tract (LVOT) obstruction. The peak AV systolic pressure gradient can exceed
150 mm Hg, and peak LV pressure can reach 300 mm Hg with normal end-diastolic
volume (EDV) and end-systolic volume (ESV). In one series, 40% of patients with
severe AS treated medically survived 5 years, whereas the 10-year survival rate was
20%. In another series of patients with significant AS treated medically, the 5-year
survival rate was 64%. With the appearance of symptoms, a rapidly progressive
downhill course is observed. Onset of angina and syncope is associated with an
average survival of 2-3 years, whereas the onset of congestive heart failure (CHF) is
associated with an average survival of 1-1.5 years.

• Among symptomatic patients with moderate-to-severe AS treated medically,

mortality rates from the onset of symptoms were approximately 25% at 1 year
and 50% at 2 years. More than 50% of deaths were sudden. Death in general,
including sudden death, occurs primarily in symptomatic patients.

• Asymptomatic patients, even with critical AS, have an excellent prognosis

regarding survival, with an expected death rate of less than 1% per year; only 4%
of sudden cardiac deaths in severe AS occur in asymptomatic patients.

• Although the obstruction tends to progress more rapidly in patients with

degenerative calcific AV disease than in those with congenital or rheumatic
disease, predicting the rate of progression in individual patients is not possible.
Therefore, careful clinical follow-up is mandatory in all patients with moderate-to-
severe AS. Catheterization and echocardiographic studies suggest that the valve
area may decline 0.1-0.3 cm2 per year; the systolic pressure gradient across the
valve can increase by as much as 10-15 mm Hg per year. A higher rate of
progression is observed in elderly patients with coronary artery disease (CAD)
and chronic renal insufficiency.

Race: No racial predilection is associated with congenital or acquired AS.

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 In patients in whom the AV obstruction remains unrelieved, the onset of

these symptoms predicts a poor outcome. The approximate time interval
from the onset of symptoms to death is 2 years for heart failure, 3 years
for syncope, and 5 years for angina.

o Exertional dyspnea is the most common initial complaint, even with normal
LV systolic function, and it relates to abnormal LV diastolic function.

o Angina pectoris occurs in approximately two thirds of patients with critical

AS, of which 50% have significant CAD. Because angina commonly is
precipitated by exertion and relieved by rest, it often simulates symptoms
of CAD. Angina results from a concomitant increased oxygen requirement
by the hypertrophic myocardium and diminished oxygen delivery
secondary to the excessive compression of coronary vessels and relative
subendocardial myocardial ischemia. Of course, angina also can result
from coexistent CAD.

o The cause of syncope is multifactorial. It often occurs upon exertion when

the arterial systolic blood pressure drops because of systemic
vasodilatation in the presence of a fixed forward stroke volume. Exertional
hypotension also may manifest as blackout spells, lightheadedness, or
dizziness upon effort. It also may be caused by atrial or ventricular
tachyarrhythmias, commonly with premonitory symptoms.

o Syncope at rest may be due to transient ventricular tachycardia from

which the patient recovers spontaneously. Episodes of atrial fibrillation
with precipitous decline in CO or transient AV block due to extension of
the calcification of the valve into the conduction system also can be
culprits. Another cause of syncope is abnormal vasodepressor reflexes
caused by increased LV intracavitary pressure (vasodepressor syncope),
which is probably a common mechanism in patients with severe AS.

• Paroxysmal nocturnal dyspnea, orthopnea, and pulmonary edema usually are

late-occurring symptoms of heart failure.

• Gastrointestinal bleeding, idiopathic or due to small bowel angiodysplasia or

other vascular malformations, is present at a higher than expected frequency in
patients with calcific AS; it usually resolves following AV surgery.

• Risk of infective endocarditis is higher in younger patients with mild valvular

deformity than in older patients with degenerated calcified AVs, but it can occur
in both. It can occur frequently at any age with hospital-acquired Staphylococcus
aureus bacteremia, which frequently results in aortic valve replacement.

• 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.

• Atrial fibrillation, pulmonary hypertension, and systemic venous hypertension in

patients with isolated AS are preterminal findings.

• Sudden cardiac death is rare and usually occurs in symptomatic patients.

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

• At the apex, a precordial a wave often is visible and palpable. A hyperdynamic

LV is unusual and suggests concomitant aortic regurgitation (AR) or MR. A
systolic "thrill" may be present at the second right intercostal space or at the
suprasternal notch and usually indicates a mean AV gradient higher than 50 mm
Hg. The thrill is best felt while the patient is leaning forward. On occasion, it can
be transmitted to the carotids.
• Rarely, RV failure with systemic venous congestion, hepatomegaly, and edema
precede LV failure. This probably is due to the bulging of the interventricular
septum into the right ventricle, with impedance in filling, elevated jugular venous
pressure, and a prominent a wave (Bernheim effect).

• 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 presence of an ejection sound is dependent on the mobility of the valve

cusps and disappears when they become immobile and severely calcified. Thus,
it is common in children and young adults with congenital AS but rare in elderly
individuals with acquired calcific AS with rigid valves. This sound occurs
approximately 40-60 milliseconds after the onset of S1 and frequently is heard
best with the diaphragm of the stethoscope along the mid-lower left sternal
border; it often is well transmitted to the apex and may be confused with a split
S1. In contrast to a pulmonic ejection sound, the aortic ejection sound usually
does not vary with respiration.

• A prominent S4 usually is present due to forceful atrial contraction and presystolic

partial closure of the mitral leaflets. Presence of an S4 in a young patient with AS
indicates significant AS, but with AS in an elderly person, this is not necessarily

• The classic crescendo-decrescendo systolic murmur of AS is best heard at the

second intercostal space in the right upper sternal border; it is harsh and rasping
at the base and radiates to both carotid arteries. However, it may be more
prominent at the apex in elderly persons with calcific AS due to radiation of the
high-frequency components of the murmur to the apex (Gallavardin
phenomenon) leading to its misinterpretation as a murmur of MR. Accentuation
of the AS murmur following a long R-R interval (as in atrial fibrillation or following
a premature beat) distinguishes it from the MR murmur, which usually does not
change. Nevertheless, coexistent MR can be present, due to progressive LV
dilatation, CAD, or mitral annular calcification. A high-pitched decrescendo
diastolic murmur secondary to aortic regurgitation is common in many patients
with dominant AS.

• 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.

• The murmur of valvular AS is augmented by the inhalation of amyl nitrite upon

squatting or in a postpremature beat; the murmur intensity is reduced during
Valsalva strain, which usually increases in hypertrophic obstructive

• 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.

• Congenital valvular aortic stenosis

o Congenitally unicuspid, bicuspid, tricuspid, or even quadricuspid valves

may be the cause of AS. In neonates and infants younger than 1 year, a
unicuspid valve can produce severe obstruction and is the most common
anomaly in patients with fatal valvular AS.

o In general, unicuspid valves are most frequent in cases of symptomatic

AS in patients younger than 15 years. In adults, congenital AS usually is
due to a bicuspid valve but usually does not cause significant narrowing of
the aortic orifice during childhood because most of the bicuspid valves are
not stenotic at birth. Their altered architecture induces turbulent flow with
continuous trauma to the leaflets, ultimately resulting in fibrosis, increased
rigidity and calcification of the leaflets, and narrowing of the aortic orifice.
Regurgitation is common and may be an indicator of acute or healed
infective endocarditis.

o These anatomical/pathological changes are very similar to those observed

in senile degenerative calcific stenosis of a tricuspid AV, except that in
congenital AS in a bicuspid valve, these changes occur several decades
earlier. Congenitally malformed tricuspid AVs with unequally sized cusps
and some commissural fusion also can cause turbulent flow leading to
fibrosis and, ultimately, to calcification and stenosis. Clinical
manifestations of congenital AS in adults usually occur after the fourth
decade of life.

• Acquired valvular aortic stenosis

o The main causes of acquired AS include rheumatic heart disease and

senile degenerative calcification.

o In rheumatic AS, the underlying process includes progressive fibrosis of

the valve leaflets with varying degrees of commissural fusion, often with
retraction of the leaflet edges and, in certain cases, calcification. As a
consequence, the rheumatic valve often is regurgitant and stenotic.
Coexistent mitral valve disease is common. This form of AS is uncommon
in the United States.

o Degenerative (senile) calcific AS involves progressive calcification of the

leaflet bodies resulting in limitation of the normal cusp opening during
systole. This represents a consequence of long-standing hemodynamic
stress on the valve and currently is the most frequent cause of AS
requiring AV surgery. It usually occurs in individuals older than 75 years.
Cellular aging and degeneration have been implicated. Diabetes mellitus
and hypercholesterolemia are risk factors for the development of this
lesion. The calcification may involve the mitral annulus or extend into the
conduction system, resulting in atrioventricular or intraventricular
conduction defects.
 The pathophysiologic changes are preceded by structural changes
in the valvular apparatus. Recent histopathologic studies have
provided important insight into the pathogenesis of calcific AS. The
available data suggest that the development and progression of
calcific AS are due to an active disease process at the cellular and
molecular level that shows many similarities with atherosclerosis,
ranging from endothelial dysfunction to, ultimately, calcification.
 These similarities between calcific AV disease and atherosclerosis
at tissue level imply that they may share similar association with
clinical risk factors. Indeed, the Cardiovascular Health Study has
suggested that calcific AV disease is associated with older age,
male sex, serum LDL and Lp(a) levels, systemic arterial
hypertension, diabetes mellitus, and smoking.
 The early lesion in the pathogenesis of degenerative calcific AV
disease is focal endothelial thickening on the aortic side of the
cusps that is initiated by endothelial disruption due to increased
mechanical stress and decreased shear stress. These lesions
consist of intracellular and extracellular lipids (mainly LDL and Lp[a]
with evidence of lipoprotein oxidation), inflammatory cells (mainly
macrophages with some foam cells and few T lymphocytes),
extracellular matrix, and microscopic calcification associated with
active production of osteopontin protein by a subset of
macrophages. The upregulated matrix metalloproteinase
expression induces remodeling of the extracellular matrix via
cytokine stimulation. Phenotypically altered fibroblasts and HLA-DR
also accumulate in the abnormal region of the AV.
 Another important finding is the presence of angiotensin-converting
enzyme and angiotensin II, which suggests a potential role of the
renin-angiotensin system in the lesion pathogenesis. After initial
inflammatory changes, calcification predominates later in the
process. The extension of the lesion into adjacent fibrosa of the
cusps leads to disruption of the normal collagen fiber architecture
that provides tensile strength to valve leaflets, resulting in

o Coexistent coronary artery calcification is also common and has been

found to be correlated with aortic-valve calcium based on electron beam
computed tomography (EBCT) findings, also called Ultrafast CT. Calcific
AS is also observed in end-stage renal disease. Rheumatoid involvement
of the valve (ie, systemic lupus erythematosus, rheumatoid arthritis) can
result in nodular thickening of the valve cusps and involvement of the
proximal part of the aorta but is a rare cause of AS.

• Other infrequent causes of AS include obstructive vegetations, homozygous type

II hyperlipoproteinemia, Paget disease, Fabry disease, ochronosis, and
• The likely cause of AS depends on the age of the patient at presentation. In
patients who develop symptoms in their teens and early twenties, the cause
usually is a congenitally unicuspid or fused bicuspid AV. If symptoms arise
between the fifth and seventh decade, the culprit is either a calcified bicuspid AV
or it is degenerative in nature. Nowadays, the most common presentation is an
elderly patient with senile degenerative AV with calcific deposits at the base of
the cusps in the absence of commissural fusion.

Table 1. Common Reasons of Aortic Stenosis Requiring Surgery

Age <70 years (n=324) Age >70 years (n=322)

Bicuspid AV (50%) Degenerative (48%)
Postinflammatory (25%) Bicuspid (27%)
Degenerative (18%) Postinflammatory (23%)
Unicommissural (3%) Hypoplastic (2%)
Hypoplastic (2%)
Indeterminate (2%)

Imaging Studies:

• Echocardiography

o Two-dimensional Doppler echocardiography is the imaging modality of

choice to help diagnose and estimate the severity of AS and localize the
level of obstruction. American College of Cardiology/American Heart
Association (ACC/AHA) recommendations for echocardiography in AS are
summarized in Table 2.

o In valvular AS, the etiology (bicuspid, rheumatic, or senile degenerative)

may be assessed from the parasternal short-axis view. LV size, mass, and
function should be evaluated in each patient. Although the presence of AS
is readily diagnosed on 2D echocardiography (doming), severity of AS
cannot be judged based on the 2D-echocardiographic images alone.
Doppler echocardiography is an excellent tool for assessing the severity of
AS. Using the modified Bernoulli equation, a maximum instantaneous and
mean AV gradient can be derived from the continuous-wave Doppler
velocity across the AV. To avoid underestimating the AV gradient, the
Doppler beam should be kept as parallel as possible to the stenotic jet.

o In a laboratory with experienced personnel, Doppler-derived AV gradients

are accurate and reproducible and correlate well with those obtained with
hemodynamically measured pressures during cardiac catheterization. In a
patient with clinical findings of severe AS and a Doppler-derived mean
gradient greater than 50 mm Hg, no other hemodynamic information is
needed to assess the severity of AS.

o AV gradient depends not only on the severity of obstruction but also on

aortic flow. In patients with low CO, the stenosis still may be severe, with a
mean gradient less than 50 mm Hg. To overcome this problem, 2D-
Doppler echocardiography also can provide a reliable estimation of aortic
valve area (AVA) by the continuity equation, where LVOT indicates LV
outflow tract and TVI indicates time velocity integral. The continuity
equation is AVA = LVOT area multiplied by LVOT TVI/AV TVI. In
experienced hands, this formula is more accurate than the Gorlin formula
in patients with low CO states. The echocardiographic criteria for
assessment of AS severity are outlined in Table 3.

o The major limitation of Doppler echocardiography in estimating the

severity of AS is underestimation of the gradient if the beam is not parallel
to the AS velocity jet. Thus, in a patient with clinical features of severe AS
but echo/Doppler findings of mild-to-moderate AS, further evaluation with
repeat Doppler or catheterization is required. Very rarely, Doppler may
overestimate the mean gradient in cases of severe anemia (hemoglobin
<8 g/dL), a small aortic root, or sequential stenoses in parallel (coexistent
LVOT and valvular obstruction). Furthermore, echocardiographic
calculation of AVA with the continuity equation is highly dependent on
accurate measurement of the diameter of the LVOT. In cases with poor
transthoracic images, transesophageal echocardiography (TEE) may be
used to measure the mean and peak gradient and a planimeter may be
used to measure the AVA.

Table 2. ACC/AHA Recommendations for Echocardiography in Aortic


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
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

Table 3. Criteria for Determining Severity of Aortic Stenosis

Severity Mean gradient (mm Hg) Aortic valve area (cm2)

Mild <25 >1.5
Moderate 25-50 1-1.5
Severe >50 <1
(or <0.5 cm2/m2 body surface area)
Critical >80 <0.7
• Radionuclide ventriculography may provide information on LV function, including
LV ejection fraction, ESV, and EDV.

• Electron beam computed tomography (EBCT): This essentially focuses on the

calcium score of the AV and seeks correlation between the amount of calcium
and severity of the AV disease. A good correlation between the EBCT calcium
score and the actual amount of calcium of the explanted AV was shown in 30
patients with various degrees of AS. An AV calcium score of 1100 Agatston units
or more (corresponding to 650 mg of calcium) has provided the highest sum of
sensitivity and specificity (93% and 82%, respectively) for diagnosis of severe AS
(AVA <1 cm2). Because the calcium score was easily reproducible, it has the
potential to be a valuable tool for detection of disease progression and for
assessment of the effect of medical treatment in a more sensitive manner.

• Multislice computed tomography: Three-dimensional volume quantification of AV

calcification using this method demonstrated a close nonlinear relationship to
echocardiographic parameters of severity of AS. This method is not yet clinically

• Cardiac magnetic resonance imaging: Comparison of the AV TVI and AVA

measurements via echocardiography/Doppler and cardiac magnetic resonance
imaging has shown excellent correlation. This method is not yet clinically

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 T-wave inversion and ST-segment depression in leads with predominantly

positive QRS complexes are common. ST depression exceeding 0.3 mV
in patients with AS indicates LV strain and suggests that severe LVH is
present. Occasionally, a septal pseudoinfarct pattern can be seen. LA
enlargement with preterminal negative p wave in V1 is noted in 80% of
severe isolated cases of AS. The QRS vector may be directed posteriorly
and superiorly in the left sagittal plane, and counterclockwise rotation with
major forces being in the left posterior quadrant may be present in the
transverse plane.

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

o Extension of calcification into the conduction system can cause

atrioventricular or intraventricular block in 5% of cases. Approximately
10% of all cases of left anterior fascicular block are secondary to calcified
AV disease. Ambulatory ECG monitoring frequently shows complex
ventricular arrhythmias, particularly in cases with myocardial dysfunction.

• 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

o On lateral view, AV calcification is found in almost all adults with

hemodynamically significant AS. Although its absence on fluoroscopy in
individuals older than 35 years rules out severe valvular AS, its presence
does not prove severe obstruction in individuals older than 60 years.

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.

• Ambulatory ECG recordings may be necessary in the occasional patients in

whom tachyarrhythmia or silent ischemia is suspected.

• Provocative testing is used in cases when the severity of the AS is uncertain or in

the presence of heart failure because of a small stroke volume (SV) and a small
mean AV gradient (low-gradient AS).

o The AVA is determined to be small even using Doppler echocardiography.

o Infusion of an inotropic agent such as dobutamine, which results in an

increase in SV and heart rate, usually is helpful in establishing the correct

o Measuring CO and LV and aortic pressures simultaneously both before

and during dobutamine infusion is important.

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.


• 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 Measurement of simultaneous LV and aortic pressures or pullback

techniques may be used to estimate the peak pressure gradient. The
pullback method is inaccurate in patients with irregular rhythm or low CO
states. Using femoral artery pressure during a simultaneous measurement
technique provides inaccurate results because the difference between
central aortic pressure and femoral artery pressure may be significant. At
the time of catheterization, CO should be assessed for the calculation of
AVA, preferably by the Fick principle.

o The thermodilution technique has limited accuracy in patients with

irregular rhythm or low output states. Coexistent MR or AR may cause
errors in calculation of the valve area when using the Gorlin equation, in
which SEP indicates systolic ejection period, PG indicates the pressure
gradient, and HR indicates heart rate (AVA = 1000 x CO/44 x SEP x HR x
the square root of PG or simplified AVA = CO/square root of PG).

o Exclusion of CAD by coronary angiography is needed in all patients older

than 35 years who are being considered for valve surgery. It also should
be performed in patients younger than 35 years if they have LV systolic
dysfunction, symptoms/signs suggestive of CAD, or 2 or more risk factors
for premature CAD, excluding sex. Generally, the incidence of associated
CAD has been reported to be 50% in individuals older than 50 years.

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.

Table 4. Recommendations for Cardiac Catheterization in Aortic Stenosis

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.

• Endocarditis prophylaxis is recommended in all patients regardless of the

etiology or the patient's age and surgical status. The risk of valve-ring abscess is
highest of all of the valve lesions.

• Recently, several small observational studies suggested that HMG-CoA

reductase inhibitor use can reduce AV leaflet calcification and delay the
progression of AS severity. Some of these studies attributed this effect to the
consequence of lowering of serum LDL levels; in others, the effect was
independent of serum LDL levels. Although these retrospective studies are
promising for a potential role of these drugs in the management of calcific AV
disease, no data are currently available from prospective, randomized, placebo-
controlled trials to recommend their routine use. In similar observational studies,
use of ACE inhibitors was associated with slower calcium accumulation in AV;
however, no hemodynamic benefit was seen during the same period. A recent
randomized clinical trial of atorvastatin versus placebo showed no difference in
AVA or pressure gradients.

Surgical Care: The primary management of symptomatic patients with valvular AS is

interventional. The timing of intervention is determined by the severity of the stenosis,
the age of the patient, and the presence of symptoms. In asymptomatic patients with
severe AS, follow-up is needed every 6 months. The natural history suggests that
patients with a mean gradient of less than 25 mm Hg have a 20% chance of requiring
intervention in 15 years. Overall, 40% of those in the medically treated group require
intervention in 15 years, although in certain cases, progression to severe AS may be

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.

• Percutaneous balloon valvuloplasty was introduced approximately 10 years ago.

Generally, it is used as a palliative measure in critically ill patients who are not
surgical candidates or as a bridge in critically ill patients before they undergo

o ACC/AHA recommendations for aortic balloon valvotomy in adults with AS

are summarized in Table 5. In cases of congenital AS without calcified
unicuspid or bicuspid AV in children, adolescents, and young adults,
percutaneous balloon valvuloplasty is an accepted alternative to surgical
valvotomy and carries a risk of 1%, but its value is limited in adults with
calcific AS. The high rate of restenosis and the absence of a mortality
benefit preclude its use as a definitive treatment method in these cases.
However, a recent study investigated the long-term outcome of balloon
valvuloplasty in patients with severe AS, including repeat procedures to
maintain symptom relief and survival impact. In 212 patients with severe
AS who were not operative candidates, repetitive balloon valvuloplasty
emerged as a viable strategy to maintain clinical improvement and
provided a median survival of 3 years.

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 Restenosis is common, particularly in patients with unicuspid valves or

with valves affected by severe dysplasia (>60% at 6 mo, virtually 100% at
2 y). More than mild AR poses a contraindication for this procedure.

o Valvuloplasty also can be performed in patients with severe CHF or

cardiogenic shock (1) as a bridge to valve replacement as a palliative
measure, (2) for patients with other comorbid conditions with a very short
life expectancy, (3) for those who refuse surgery, (4) for those with heart
failure who need an urgent major noncardiac surgical procedure, or (5) in
pregnant patients with critical AS.

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.

Table 5. Recommendations for Aortic Balloon Valvotomy in Adults With

Aortic Stenosis

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

• Aortic valve replacement

o ACC/AHA recommendations for AV replacement in patients with valvular
AS are summarized in Table 6. In most adults with calcific AS and in those
patients with calcified, bicuspid, severely stenotic AVs, AVR is the surgical
treatment of choice. It is recommended if hemodynamic evidence of
severe obstruction and symptoms due to AS are present. It also is
recommended in asymptomatic patients with LV dysfunction. AVR should
be performed in all symptomatic patients with severe AS regardless of LV
function. Even in the presence of LV dysfunction, survival is better with
surgical treatment than with medical treatment.

o Prior to AV surgery, complete hemodynamic assessment of AS with either

Doppler or catheterization is required. Assessment of LV function and MV
disease also is required. If significant MR is present, the degree of
regurgitation should be evaluated intraoperatively after replacement of the
AV to determine the need for MV repair or replacement, unless intrinsic
disease of the MV apparatus is present. Coronary angiography is needed
in all patients aged 35-40 years and in those patients with risk factors for

o Successful AVR produces substantial clinical and hemodynamic

improvement in patients with AS, including octogenarians. The choice of
prosthesis is determined by the anticipated longevity of the patients and
their ability to tolerate anticoagulation.
o Postoperatively, end-diastolic pressure and ESV drop significantly, and
symptoms of elevated LA pressure and ischemia improve. Improvement in
EF invariably occurs over the following 6 months, and increased LV mass
tends to decrease within 18 months postoperatively.
o The surgical mortality risk in patients with normal LV systolic function and
no other comorbid conditions is less than 5%. Risk factors for increased
operative mortality include (1) high New York Heart Association (NYHA)
class (25-30% mortality in patients with class IV), (2) preoperative LV
systolic dysfunction (strongest predictor of postoperative LV dysfunction),
(3) age (up to 30% mortality in patients >80 y but is not a contraindication
for AVR), and (4) the presence of associated AR.
o The skill level of the surgical team cannot be ignored.
o Whenever possible, AVR and coronary artery bypass graft (CABG) should
be performed at the same time. The increase in operative mortality is
negligible compared to AVR alone. Risk factors for late death include
preoperative NYHA class and LV systolic function, preoperative ventricular
arrhythmias, concomitant AR, atrial fibrillation, and CAD, particularly a
history of myocardial infarction. Overall, the 5-year survival rate in all
adults after AVR is 80-94%, whereas 10-year survival rate is 68-89%.

Table 6. Recommendations for Aortic Valve Replacement in Aortic


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:

LV systolic dysfunction IIa

Abnormal response to exercise (eg, hypotension) IIa
Ventricular tachycardia IIb
Marked or excessive LVH (>15 mm) IIb
Valve area <0.6 cm2 IIb
Prevention of sudden death in asymptomatic patients with none of III
the findings listed under asymptomatic patients with severe AS

o The Ross procedure is another option in young patients as an initial

procedure or for reoperation after prior valvotomy. In this procedure, the
patient's own pulmonary valve and main pulmonary artery are
transplanted to the aortic position, with reimplantation of coronary arteries.
A homograft is placed in the pulmonary position. Its durability is better
than with tissue valves, and anticoagulation is not required. This
procedure is technically demanding.
o Despite the proven efficacy of surgical valve replacement, it still carries
high operative mortality and morbidity rates in the growing population of
elderly patients with significant comorbidities. Recently, percutaneous AV
replacement using the antegrade transseptal and retrograde arterial
approaches has been introduced as an alternative to surgical AV
replacement in a subset of patients with AS who are at high surgical risk.
In the first reported human case, using the transcatheter technique with
antegrade transseptal approach, a trileaflet bovine pericardial valve
mounted within a balloon-expandable stent was successfully deployed
with significant hemodynamic improvement. In another case, a retrograde
arterial approach was successfully used because the antegrade approach
was complicated by guidewire injury to the mitral valve. Although
percutaneous AV replacement may be an exciting alternative to the
standard surgical approach, this approach has thus far raised more
questions than it has provided answers.

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.

Treatment of valvular AS is interventional. When intervention is not an option, signs of

heart failure must be treated with inotropic therapy, diuretics, and nitrates. Drug therapy
essentially is reserved for bacterial endocarditis prophylaxis.

Drug Category: Antibiotics -- For endocarditis prophylaxis during

dental/oral/respiratory tract and gastrointestinal/gastrourinary (GI/GU) procedures.
Amoxicillin (Amoxil, Trimox) -- Interferes with
synthesis of cell wall mucopeptides during
Drug Name active multiplication, resulting in bactericidal
activity against susceptible bacteria.
Used as prophylaxis in minor procedures.
2 g PO 1 h before the procedure; alternatively,
Adult Dose 3 g PO 1 h before procedure followed by 1.5 g
6 h after initial dose
Pediatric Dose 50 mg/kg PO 1 h before procedure
Contraindications Documented hypersensitivity
Interactions Reduces efficacy of oral contraceptives
B - Usually safe but benefits must outweigh
the risks.
Adjust dose in renal impairment; may enhance
chance of candidiasis
Ampicillin (Marcillin, Omnipen) -- For
prophylaxis in patients undergoing surgical
Drug Name
procedures. Coadministered with gentamicin
for prophylaxis.
2 g PO/IV/IM 30 min prior to procedure and 1
Adult Dose
g 6 h after first dose
Pediatric Dose 50 mg/kg IV/IM 30 min prior to procedure
Contraindications Documented hypersensitivity
Probenecid and disulfiram elevate levels;
allopurinol decreases effects and has additive
effects on ampicillin rash; may decrease
effects of oral contraceptives
B - Usually safe but benefits must outweigh
the risks.
Adjust dose in renal failure; evaluate rash and
differentiate from hypersensitivity reaction
Clindamycin (Cleocin) -- Useful in patients
Drug Name allergic to penicillin who require antibiotic
prophylaxis prior surgical procedures.
600 mg PO/IV 1 h prior to procedure and 150
Adult Dose
mg PO/IV 6 h after first dose
Pediatric Dose Not established
Documented hypersensitivity; regional
Contraindications enteritis, ulcerative colitis, hepatic impairment,
antibiotic-associated colitis
Increases duration of neuromuscular blockade
induced by tubocurarine and pancuronium;
erythromycin may antagonize effects;
antidiarrheals may delay absorption
B - Usually safe but benefits must outweigh
the risks.
Adjust dose in severe hepatic dysfunction; no
adjustment necessary in renal insufficiency;
Precautions associated with severe and possibly fatal
colitis by allowing overgrowth of Clostridium
Vancomycin (Vancocin) -- Potent antibiotic
directed against gram-positive organisms and
active against Enterococcus species. Useful to
treat septicemia and skin structure infections.
Indicated for patients who cannot receive or
have failed to respond to penicillins and
Drug Name cephalosporins or have infections with
resistant staphylococci.
Use creatinine clearance to adjust dose in
patients diagnosed with renal impairment.
Used in conjunction with gentamicin for
prophylaxis in penicillin-allergic patients
undergoing surgical procedures.
Surgical procedures: 1 g IV, infused over 1 h,
one hour prior to the procedure, plus 1.5
Adult Dose
mg/kg gentamicin infused over 1 h, one hour
prior to surgery
Surgical procedures: 20 mg/kg IV 1 h prior to
Pediatric Dose procedure, alternatively, 20 mg/kg plus 2
mg/kg 1 h prior to surgery
Contraindications Documented hypersensitivity
Erythema, histaminelike flushing, and
anaphylactic reactions may occur when
administered with anesthetic agents; taken
concurrently with aminoglycosides, risk of
Interactions nephrotoxicity may increase above that with
aminoglycoside monotherapy; effects in
neuromuscular blockade may be enhanced
when coadministered with nondepolarizing
muscle relaxants
C - Safety for use during pregnancy has not
been established.
Caution in renal failure and neutropenia; red
man syndrome is caused by an IV infusion that
is too rapid (dose given over a few minutes)
but rarely happens when dose given as 2-h
administration or as PO or IP administration;
red man syndrome is not an allergic reaction
Drug Name Gentamicin (Garamycin) -- Aminoglycoside
antibiotic for gram-negative coverage. Used in
combination with both an agent against gram-
positive organisms and one that covers
Used in conjunction with ampicillin or
vancomycin for prophylaxis in surgical
1.5 mg/kg IV with 1-2 g ampicillin 30 min prior
Adult Dose
to procedure; not to exceed 80 mg
2 mg/kg IV with ampicillin (50 mg/kg) 30 min
Pediatric Dose
prior to procedure
Documented hypersensitivity; non–dialysis-
dependent renal insufficiency
Coadministration with other aminoglycosides,
cephalosporins, penicillins, and amphotericin
B may increase nephrotoxicity;
aminoglycosides enhance effects of
neuromuscular blocking agents, thus,
prolonged respiratory depression may occur;
coadministration with loop diuretics may
increase auditory toxicity of aminoglycosides;
possible irreversible hearing loss of varying
degrees may occur (monitor regularly)
C - Safety for use during pregnancy has not
been established.
Narrow therapeutic index (not intended for
long-term therapy); caution in renal failure (not
Precautions on dialysis), myasthenia gravis, hypocalcemia,
and conditions that depress neuromuscular
transmission; adjust dose in renal impairment
Erythromycin (EES, E-Mycin, Eryc) -- Used for
Drug Name prophylaxis in penicillin-allergic patients
undergoing surgical procedures.
1 g PO 1-2 h before procedure, followed by
Adult Dose
500 mg 6 h after initial dose
20 mg/kg PO 2 h prior to procedure, followed
Pediatric Dose
by 10 mg/kg 6 h after initial dose
Documented hypersensitivity; hepatic
Coadministration may increase toxicity of
theophylline, digoxin, carbamazepine, and
cyclosporine; may potentiate anticoagulant
effects of warfarin; coadministration with
lovastatin and simvastatin increases risk of
B - Usually safe but benefits must outweigh
the risks.
Caution in liver disease; estolate formulation
may cause cholestatic jaundice; adverse GI
Precautions effects are common (give doses pc);
discontinue use if nausea, vomiting, malaise,
abdominal colic, or fever occur
Cefazolin (Ancef) -- First-generation
semisynthetic cephalosporin that arrests
Drug Name bacterial cell wall synthesis, inhibiting bacterial
growth. Primarily active against skin flora,
including S aureus.
Adult Dose 1 g IV/IM within 30 min of procedure
Pediatric Dose 25 mg/kg IV/IM within 30 min of procedure
Contraindications Documented hypersensitivity
Probenecid prolongs effect; coadministration
with aminoglycosides may increase renal
toxicity; may yield false-positive results for
urine-dip test for glucose
B - Usually safe but benefits must outweigh
the risks.
Adjust dose in renal impairment;
superinfections and promotion of
nonsusceptible organisms may occur with
prolonged use or repeated therapy
Cephalexin (Keflex) -- First-generation
cephalosporin that arrests bacterial growth by
inhibiting bacterial cell wall synthesis.
Drug Name Bactericidal activity against rapidly growing
organisms. Primary activity against skin flora;
used for skin infections or prophylaxis in minor
Adult Dose 2 g PO 1 h before procedure
Pediatric Dose 50 mg/kg PO 1 h before procedure
Contraindications Documented hypersensitivity
Coadministration with aminoglycosides
increases nephrotoxic potential
B - Usually safe but benefits must outweigh
the risks.
Precautions Adjust dose in renal impairment
Cefadroxil (Duricef) -- First-generation
cephalosporin that arrests bacterial growth by
inhibiting bacterial cell wall synthesis.
Drug Name Bactericidal activity against rapidly growing
organisms. Primary activity against skin flora;
used for skin infections or prophylaxis in minor
Adult Dose 2 g PO 1 h before procedure
Pediatric Dose 50 mg/kg PO 1 h before procedure
Contraindications Documented hypersensitivity
Coadministration with furosemide or
Interactions aminoglycosides may increase nephrotoxicity;
probenecid prolongs effects
B - Usually safe but benefits must outweigh
the risks.
Adjust dose in renal impairment;
superinfections and promotion of
nonsusceptible organisms may occur with
prolonged use or repeated therapy
Azithromycin (Zithromax) -- Inhibits bacterial
growth, possibly by blocking dissociation of
Drug Name
peptidyl t-RNA from ribosomes, causing RNA-
dependent protein synthesis to arrest.
Adult Dose 500 mg PO 1 h before procedure
Pediatric Dose 15 mg/kg PO 1 h before procedure
Documented hypersensitivity; hepatic
impairment; do not administer with pimozide
May increase toxicity of theophylline, warfarin,
and digoxin; effects are reduced with
coadministration of aluminum and/or
magnesium antacids; nephrotoxicity and
neurotoxicity may occur when coadministered
with cyclosporine
B - Usually safe but benefits must outweigh
the risks.
Bacterial or fungal overgrowth may result with
prolonged antibiotic use; may increase hepatic
enzymes and cholestatic jaundice; caution in
patients with impaired hepatic function,
prolonged QT intervals, or pneumonia; caution
in hospitalized, elderly, or debilitated patients
Clarithromycin (Biaxin) -- Inhibits bacterial
growth, possibly by blocking dissociation of
Drug Name
peptidyl t-RNA from ribosomes, causing RNA-
dependent protein synthesis to arrest.
Adult Dose 500 mg PO 1 h before procedure
Pediatric Dose 15 mg/kg PO 1 h before procedure
Documented hypersensitivity; coadministration
of pimozide
Interactions Toxicity increases with coadministration of
fluconazole, astemizole, and pimozide;
clarithromycin effects decrease and adverse
GI effects may increase with coadministration
of rifabutin or rifampin; may increase toxicity of
anticoagulants, cyclosporine, tacrolimus,
digoxin, omeprazole, carbamazepine, ergot
alkaloids, triazolam, and HMG CoA-reductase
inhibitors; cardiac arrhythmias may occur with
coadministration of cisapride; plasma levels of
certain benzodiazepines may increase,
prolonging CNS depression; arrhythmias and
increase in QTc intervals occur with
disopyramide; coadministration with
omeprazole may increase plasma levels of
both agents
C - Safety for use during pregnancy has not
been established.
Coadministration with ranitidine or bismuth
citrate is not recommended with CrCl <25
mL/min; give half dose or increase dosing
Precautions interval if CrCl <30 mL/min; diarrhea may be
sign of pseudomembranous colitis;
superinfections may occur with prolonged or
repeated antibiotic therapies

Further Outpatient Care:

• Follow-up of asymptomatic patients

o The frequency of the follow-up visits in asymptomatic patients is

determined by the severity of AS and by the presence of comorbid

o In patients with mild AS, yearly history and physical examination and
echocardiograms every 5 years are appropriate.

o Patients with moderate or severe AS should be examined twice yearly and

whenever they develop symptoms attributable to AS.

o In patients with moderate AS, echocardiograms should be performed

every 2 years, whereas in asymptomatic patients with severe AS, yearly
echocardiograms are recommended.

• Follow-up of symptomatic patients

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.

o Following AV replacement, every patient should undergo

echocardiographic examination after recovery. Thereafter, an examination
is recommended whenever new symptoms develop that are attributable to
a potential valvular dysfunction.

o Patients with mechanical valves should receive lifelong anticoagulation

with warfarin and should undergo periodic screening of their
anticoagulation status.
In/Out Patient Meds:

• All patients with AS require antibiotic prophylaxis against infective endocarditis

and also against recurrent rheumatic carditis if the valve lesion has a rheumatic


• Sudden cardiac death

• Heart failure

• Conduction defects

• Infective endocarditis

• Calcific embolization

Medical/Legal Pitfalls:

• Patients with severe valvular AS should receive appropriate counseling regarding

their conditions, including restriction of physical activity and the need for surgery,
if appropriate. Physicians should document these points in patients' records.

• 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.

Caption: Picture 1. Calcific aortic stenosis (parasternal long-axis and short-axis


Caption: Picture 2. Stenotic aortic valve (macroscopic appearance).