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Transcript
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 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 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 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 Porcine valve Bioprosthesis vs. Mechanical Valves Bioprosthesis valves are less durable than mechanical valves and begin to deteriorate after 5-6 years; usually do not require longterm 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. 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