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AORTIC STENOSIS

BY
EPIFANI D. ARMEDILLA
OBJECTIVES
Review the anatomy and physiology of the
cardiovascular system
Describe the pathophysiology of aortic
stenosis
Identify the causes of aortic stenosis
Recognize the signs and symptoms of aortic
stenosis
Discuss the imaging studies used in detecting
the severity of aortic stenosis
Review the treatment for aortic stenosis
The Cardiovascular System
AORTIC STENOSIS

Obstruction of blood flow


across the aortic valve during
left ventricular systole
AORTIC STENOSIS
Causes of Aortic Stenosis
Congenital
Rheumatic fever
Degenerative calcification of the aortic
cusps most common
Obstructive infective vegetations
Pagets disease of the bone
Systemic lupus erythematous
Rheumatoid disease
Irradiation
Congenital AS
Calcified AS
Senile or degenerative AS
Aortic Stenosis
Clinical Findings in Aortic
Stenosis
Typical murmur and thrill for slightly narrowed,
thickened, or roughened valves
Systolic ejection murmur at the aortic area
transmitted to the neck and apex for mild or
moderate cases
Palpable left ventricular heave or thrill, a weak to
absent aortic second sound, or reversed splitting
of the second sound are present in severe cases
of AS because of prolonged ejection time
S4 is common and reflects increased atrial
contribution to ventricular filling
Symptoms of Aortic Stenosis
AS is asymptomatic until the valve orifice
has narrowed to approximately 0.5 cm/m
body surface area of adults
Patients remain asymptomatic for a long
period of time
The condition is first diagnosed based on
detection of a systolic murmur on
auscultation that can be explained by the
gradual process of obstruction
Three Cardinal Symptoms of
AS
Exertional dyspnea
Exertional angina
Exertional syncope
Exertional Dyspnea
Is a result of elevation of the pulmonary
capillary pressure secondary to reduced
compliance and/or LV dilatation
Exertional Angina
Usually develops later and reflects an
imbalance between the augmented
myocardial oxygen requirements and
reduced oxygen availability
Exertional Syncope
Caused by arrhythmias (usually ventricular
tachycardia and bradycardias), hypotension, or
decreased cerebral perfusion resulting from
increased blood flow to exercising muscles
without compensatory increase in cardiac output
Imaging Studies
ECG
Chest radiography
Echocardiography
Dobutamine echocardiography
Cardiac catheterization
ECG
LV hypertrophy classic finding
Other nonspecific changes are left
atrial enlargement, left axis deviation,
and left bundle-branch block
Not a reliable test because of the
wide variations seen in AS and other
cardiac conditions
ECG LV Hypertrophy
Large S wave in V1
Large R wave in V5
Chest Radiograph
Normal or enlarged
cardiac silhouette
Calcification of
aortic valve
Dilatation and
calcification of
ascending aorta

Arrow points out dilated shadow


of the ascending aorta
Echocardiography
Useful in assessing the
severity of AS, the
degree of coexisting
aortic regurgitation, LV
size and function
Helpful in estimating
pulmonary systolic
pressure and in
identifying other
cardiac abnormalities
TEE displays the
obstructive orifice
extremely well
TEE
Dobutamine
Echocardiography
Indicated in patients with moderate aortic
stenosis and LV dysfunction to predict the
reversibility of LV dysfunction after AVR
Pts. With AS, LV dysfunction, and relatively
low gradients have better outcome when
management decisions are based on the
results of dobutamine echocardiogram
(Schwammenthal, et al, 2001)
Cardiac Catheterization
Indicated for hemodynamic evaluation whenever
there is discrepancy between the clinical picture and
echocardiography
Indicated for young, asymptomatic patients with
noncalcific congenital AS, to define the severity of
obstruction to LV outflow
Indicated for patients in whom it is suspected that
the obstruction to LV outflow may not be at the
aortic valve but rather in the sub or supra-valvular
regions
Also indicated to evaluate the coronaries in AS
patients at risk for coronary artery disease
Grading of Aortic Stenosis
The aortic valve area must be reduced
to one-fourth of its normal size before
significant changes in the circulation
occur
AS is graded based on the aortic valve
area
Mild - >1.5 cm
Moderate 1.1 to 1.5 cm
Severe - <0.75 to 1 cm
Management of Aortic
Stenosis
Pharmacological
Management
Medical treatment has no role in
preventing the progression of the
disease process
But with the onset of LV systolic
dysfunction, the use of inotropic
agent may be advocated
Surgical Management
AVR is indicated for symptomatic
patients
AVR improves survival in patients with
depressed as well as normal LV function
The risks of surgery and prosthetic
valve complications outweigh the
benefits of preventing sudden cardiac
death and prolonged survival in
asymptomatic patient
Types of Valves
Bioprosthesis
(Porcine)
Mechanical (St.
Jude) Porcine valve
Homograft
Bioprosthesis vs. Mechanical
Valves
Bioprosthesis valves are less durable than mechanical
valves and begin to deteriorate after 5-6 years; usually do
not require long-term coagulation
Mechanical valves are durable but require lifelong
anticoagulation to control thromboembolism
Mechanical valve was associated with significantly lower 15
year mortality compared with bioprosthesis valve (66% vs.
79%) (Hammermeister, et al, 2000).
Mechanical valves are less obstructive than stented
bioprosthesis valves of the same size (Bech-Hanssen, et al,
1999).
Despite a better survival rate with mechanical valve, the
choice of valve should be tailored to the patients needs.
References
Alpert, J. T. (Ed.). (2001). The AHA Clinical Cardiac Consult. Philadelphia: Lippincott Williams &
Wilkens.
Bech- Hassen, O., Caidahl, K., Wall, B., Myken, P., Lason, S., & Wallentin, I. (1999). Influence of
aortic valve replacement, prosthesis type, and size of functional outcome and ventricular
mass in patients with aortic stenosis. Journal of Thoracic Cardiovascular Surgery. 118(1):57-
65.
Braunwald, E., Fauci, A. S., Kasper, D. L., Hauser, S. L., Longo, D. L., & Jameson, J. L. (2001).
Harrisons 15th Edition Principles of Internal Medicine. New York: McGraw-Hill.
Hammersmeister, K., Sethi, G. K., Henderson, W. G., Grover, F. L., Oprian, C., & Rahimtoola, S.
H. (2000). Outcome 15 years after valve replacement with a mechanical versus a bioprosthetic
valve: Final report of the Veterans Affairs Ramdomized trials. Journal of American Cardiology.
36:1152-1158.
Martin, L. & Coulden, R. (1999). Cardiac radiology: valvular heart disease.
disease. Clinics of North
America. 37(2):319-338.
Munt, B. (1999). Physical examination in valvular aortic stenosis: correlation with stenosis
severity and prediction of clinical outcome. American Heart Journal. 137(2):298-306.
Nowrangi, S. K., Connolly, H. M., Freeman, W. K., & Click, R. L. (2001). Impact of intraoperative
transesophageal echocardiography among patients undergoing aortic valve replacement for
aortic stenosis. Journal of American Society of Echocardiography. 14(9):863-6.
Otto, C. M. (1999). Valvular Heart Disease. Philadelphia: W. B. Saunders Company.
Tierney, Jr., L. M., McPhee, S. J., & Papadakis, M. A. (2002). Current Medical Diagnosis &
Treatment: 2002. (41st Ed.). New York: Lange Medical Books/McGraw-Hill.
THE END

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