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Aortic valve stenosis
The aortic valve is a flap-like opening located between the left
side of the heart and the aorta. The aorta is the main artery
carrying blood from the heart. Blood is pumped by the left
ventricle across the aortic valve into the aorta and the
arteries of the body. Aortic stenosis causes restricted systolic
opening of the valve leaflets, with a mean transvalvular
pressure gradient of at least 5-10 mmHg. When the degree of
narrowing becomes significant enough to impede the flow of blood
from the left ventricle to the arteries, heart problems develop.
In the Euro Heart Survey on Valvular Heart Disease, aortic valve
stenosis was the most common valve abnormality. Aortic valve
sclerosis is commonly defined as a focal or diffuse thickening
of the aortic cusps with calcific nodules generally at the base
of leaflets and transvalvular velocity at Doppler still in the
normal range (Vmax <2 m/s).
Rheumatic valve disease has declined dramatically in the
United States during the past 50 years, and isolated rheumatic
aortic valve is unusual in any event. With our aging population,
calcific aortic stenosis accounts for the vast majority of
aortic valve disease. In the elderly, mild thickening and/or
calcification of a trileaflet aortic valve without restricted
leaflet motion (ie, aortic sclerosis) affects about 25% of the
population > 65 years of age. Calcific aortic stenosis, however,
affects approximately 2% to 3% of those > 75 years. Thus not all
patients with aortic sclerosis will go on to develop obstructive
aortic valve disease.
The approximate overall incidence of an anatomic bicuspid
aortic valve is 1% to 2% of the population. Of these
individuals, most will go on to present with aortic stenosis,
while a minority will develop a regurgitant lesion.
Particularly, the aortic valve sclerosis (aortic valve
thickening and calcification without pressure gradient) seem to
affect about one fourth of adults over 65 years of age, while
the aortic valve stenosis is present in 2?9% of general
population over 65 years of age; an increased prevalence of both
sclerosis and stenosis with aging (48% and 4% in those over 85
years) is observed.
The relative frequency of the postinflammatory disease (i.e.
post-rheumatic) decreased from 30% to 18% and the relative
frequency of the bicuspid aortic valve changed from 37% to 33%;
in contrast, the relative frequency of degenerative-calcific
aortic stenosis (an "atherosclerotic" form of disease, see
below) increased from 30% to 46%. These differences were
striking in subjects older than 70 years.
Aortic stenosis due to bicuspid valves affects males three
times more often than females, but late-life calcific disease of
a trileaflet valve involves both sexes equally.
Aortic stenosis can occur at any age (because the causes are
different) but is usually asymptomatic until middle or old age.
Until few years ago, aortic stenosis was considered a
physiologic process related to aging without clinical relevance.
However, aortic valve sclerosis is not observed in about 50% of
people over 80 years old.
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Causes and risk factors
A number of conditions contribute towards aortic stenosis.
Three conditions that are known to cause aortic stenosis are:
1. Calcification of a bicuspid valve
Bicuspid aortic valve is the most common cause of aortic
stenosis in patients under age 65. Normal aortic valves have
3 thin leaflets called cusps. About 2% of people are born
with aortic valves that have only 2 cusps (bicuspid valves).
Although bicuspid valves usually do not impede blood flow
when the patients are young, they do not open as widely as
normal valves with 3 cusps. The turbulent blood flow causes
excessive wear and tear leading to calcification, scarring,
and reduced mobility of the valve leaflets over time. About
10% of bicuspid valves become significantly narrowed,
resulting in the symptoms and heart problems of aortic stenosis.
2. Senile calcific aortic stenosis
The most common cause of aortic stenosis in patients 65
years and over is called "senile calcific aortic stenosis."
With aging, protein collagen of the valve leaflets is
destroyed, and calcium is deposited on the leaflets. Once
valve leaflet mobility is reduced by calcification,
turbulence across the valve increases, causing scarring,
thickening, and stenosis of the valve. Why this aging
process progresses to cause significant aortic stenosis in
some patients but not in others is not known.
3. Rheumatic fever
Rheumatic fever rarely causes isolated aortic stenosis. Rheumatic fever is a condition resulting from untreated
infection by group A streptococcal bacteria. Damage to valve
leaflets from rheumatic fever causes increased turbulence
across the valve and more damage. The narrowing from
rheumatic fever occurs from the fusion of the commissures of
the valve leaflets. Rheumatic aortic stenosis usually occurs
with some degree of aortic regurgitation. Under normal
circumstances, the aortic valve closes to prevent blood in
the aorta from flowing back into the left ventricle. In
aortic regurgitation, the diseased valve allows leakage of
blood back into the left ventricle as the ventricular
muscles relax after pumping. These patients also have some
degree of rheumatic damage to the mitral valve.
Subvalvular aortic stenosis
Hypertrophic obstructive cardiomyopathy
Valvular aortic stenosis results in chronic left ventricular
pressure overloading. At any stage of life, however, the natural
history of aortic stenosis largely reflects the functional
integrity of the mitral valve. As long as adequate mitral valve
function is maintained, the pulmonary bed is protected from the
systolic pressure overloading imposed by aortic stenosis. In
contrast to mitral valve disease where the pulmonary circuit is
directly involved, compensatory concentric left ventricular
hypertrophy allows the pressure overloaded ventricle to maintain
stroke volume with modest increases in diastolic pressure, and
patients can remain asymptomatic for many years.Eventually, left ventricular hypertrophy results in either
diastolic dysfunction with the onset of congestive symptoms or
myocardial oxygen needs in excess of supply with the onset of
Most patients with calcific aortic stenosis report knowing of a
cardiac murmur for many years. Common symptoms of aortic
stenosis include: coughing at night; fainting, especially with
physical activity; fatigue; shortness of breath that worsens at
night or with exertion; angina; and, visual impairments. Some
patients may also experience exertional syncope, probably
reflecting the inability to increase cardiac output and maintain
blood pressure in response to vasodilation. Vasodepressor
syncope, however, may be an operative mechanism in a portion of
these syncopal episodes.
On physical examination, the harsh systolic diamond shaped
(crescendo-decrescendo) murmur of aortic stenosis, loudest at the base of the heart and radiating to the
carotids, is often, but not always, prominent. Low output
states, obesity, or chronic lung disease may mask the findings.
The murmur may radiate toward the cardiac apex, in which case
the harsh component is lost; this finding may be mistaken for a
second murmur. Other hallmarks of significant aortic valve
stenosis include a single (pulmonic) component of the second
heart sound and a sustained left ventricular apical impulse with
a fourth heart sound. The slowly rising, low volume carotid
arterial pulses of severe aortic stenosis may be noted in
younger patients, but changes in arterial compliance often mask
these findings in the elderly.
Patients with typical findings of aortic stenosis should have a
detailed history-taking session with inquiry into habitual
activity levels and any changes in exercise tolerance. The onset
of any of the classic symptoms of left ventricular outflow
obstruction, namely angina, syncope, or heart failure, in a
patient with valvular aortic stenosis indicates advanced valve
disease and should be carefully and promptly evaluated. The
severity of symptoms is not always related to the severity of
the disease. In fact, people sometimes die suddenly from aortic
stenosis without having had symptoms. Symptoms usually occur
when the aortic valve area narrows to less than 1 square
centimeter. Critical aortic stenosis is present when the valve
area is less than 0.7 square centimeters.
The electrocardiogram often shows changes of left ventricular
hypertrophy. In rare instances, electrical conduction
abnormality can also been seen.
The chest X-ray is seldom helpful, although occasionally heavy
calcification of the valve or post-stenotic ascending aortic
dilation may be seen.
With its widespread availability, two-dimensional and Doppler
echocardiography has become the study of choice in the
evaluation of patients with suspected valvular disease.
Echocardiography allows assessment of the anatomy of the valve
as well as chamber size and ventricular function. Doppler
studies permit estimation of pressure gradients, as well as
aortic valve area by employing the continuity equation.
With good quality echocardiography, cardiac catheterization is
usually not required for diagnosis of patients with aortic
stenosis. However, a cardiac catheterization is the gold
standard in evaluating aortic stenosis. A pre-operative coronary
angiography is generally performed in men over 40 years old and
women over 50.
Patients with (predominant) aortic stenosis fall into one of
four categories of severity:
- valve area > 1.2 cm2??????????.mild
- valve area 1.0 to 1.2 cm2????????.moderate
- valve area 0.7 to 1.0 cm2????????.severe
- valve area < 0.7 cm2??????????.critical
Asymptomatic patients with mild to moderate aortic stenosis
should have medical follow-up with regular inquiry as to changes
in exercise tolerance or other symptoms. Serial
echocardiographic examination should be based on an
understanding of the natural history of the lesion, as outlined
below. Patients should avoid strenuous activity, and
particularly avoid post-prandial exertion. Infective
endocarditis precautions following American Heart Association
guidelines must be emphasized at each visit.
Hypertension occurs in about 20% to 30% of patients with mild to
moderate aortic stenosis and should be managed with angiotensin-converting
enzyme inhibitors or angiotensin receptor blockers titrated
slowly. Selected patients may be given modest doses of
A supervised exercise tolerance test may provide helpful
objective assessment in patients with echocardiographic evidence
of moderate aortic stenosis who report atypical symptoms, who
minimize complaints, or who are sedentary and therefore might
not experience exercise intolerance. Functional limitation with
inability to exercise to levels greater than 6 metabolic
equivalents (METs) may, in some cases, be viewed as a "symptom."
Stress testing is not advocated for patients with very severe
left ventricular outflow obstruction.
2. Valve replacement
Symptomatic patients, ie, those with angina, syncope, dyspnea,
with moderate, severe, or critical aortic stenosis should
undergo valve replacement. Indications for aortic valve surgery
include moderate aortic stenosis in patients requiring coronary
bypass grafting and/or any other cardiac surgery,
exercise-induced hypotension, and asymptomatic severe aortic
stenosis with evidence of left ventricular dysfunction. Smoking
cessation and diabetic control are mandatory after the
replacement. Dental care should be completed with antibiotic
prophylaxis before surgery.
The advantages and drawbacks of mechanical versus
bioprosthetic valves should be discussed with the patient and
his or her family. Often the choice of prosthesis is
straightforward, but younger patients in particular may have
special needs, which should be addressed Bioprosthetic valves
offer the advantage of not requiring long-term oral
anticoagulation, but have the drawback of relatively limited
durability. In contrast, mechanical valves offer long-term
durability, but require lifelong warfarin therapy. The generally
accepted risk of serious bleeding with warfarin is on the order
of 3% per year. Childbearing in women and vigorous sports
activities in men are contra-indications to chronic oral
anticoagulation with warfarin, and may figure importantly in the
choice of valves. In general, bioprosthetic valves are preferred
in patients over the age of 60 years and mechanical valves under
the age of 50. Homograft aortic valve replacement with a
cryopreserved cadaveric valve may offer specific advantages in
patients with infective endocarditis or with disease of the
aortic root. If significant narrowing of the coronary arteries
is found, coronary artery bypass graft surgery (CABG) can be
performed during aortic valve replacement surgery.
3. Balloon valvuloplasty
Balloon valvuloplasty is a technique that lowers the pressure
across the valve by slightly enlarging the opening. This is
usually done when someone is not stable enough for corrective
Current evidence indicates that calcific aortic stenosis
progresses, on the average, at a rate of about 0.1 cm2 per year
decline in valve area. To date, no medical therapy exists for
the treatment of degenerative aortic stenosis. The possible
impact of 'secondary prevention' measures, particularly lipid
lowering with HMG-CoA reductase inhibitors (statins), on the
progression of aortic stenosis is under investigation.
Successful replacement of the valve restores normal blood
flow. The long-term outcome is usually very good. Artificial
valves wear out over a period of years. Their function is
monitored, and the valves are replaced as necessary. A
prosthetic heart valve commits a patient to continued infective
endocarditis prophylaxis, regular cardiac follow-up, and often
to continued medical therapy, including anticoagulation with
warfarin for those with mechanical prostheses. Re-operation may
be required for malfunction of the prosthetic valve. In
addition, a small but not insignificant subset of patients may
require implantation of a permanent pacemaker after valve
Prognosis and survival
Serious long-term effects of aortic stenosis without timely
- congestive heart failure
- coronary heart disease
- enlargement of the left ventricle
- pulmonary edema
- sudden death (occurs in less than 1%)
With surgery, the patient can expect to live a normal life
with necessary precautions as explained above.