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
Paget’s 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 cm²/m² 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
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
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 cm²
Moderate – 1.1 to 1.5 cm²
Severe - <0.75 to 1 cm²
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)
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 patient’s 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). Harrison’s 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. 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.
