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Aortic stenosis
- 1. AORTIC VALVE –ANATOMY & AORTIC STENOSIS
- 2. STRUCTURE OF AORTICVALVE • 3 SEMILUNAR CUSPS
- 3. • Cusps areattached directly to the vessel wall • Nodule • Lunule • Aortic sinuses - coronary arteries arise from anterior and left posterior aortic sinuses
- 4. • Structure ofaortic valve
- 5. • Narrowing ofthe valve orifice due to fusion of cusps is known as – stenosis • Dilatation of the valve orifice or stiffening of the cusps causes imperfect closure of valves leading to back flow of blood – incompetence or regurgitation
- 6. AORTIC STENOSIS • Occursin one fourth of all patients with chronic valvular heart disease • 80% of adult patients with symptomatic AS are male
- 7. CAUSES Infants, children, adoloscents •Congenital aortic stenosis • Congenital subvalvular aortic stenosis • Congenital supravalvular aortic stenosis
- 8. Young adults tomiddle aged • Calcification and fibrosis of congenitally bicuspid aortic valve • Rheumatic aortic stenosis Middle aged to elderly • Senile degenerative aortic stenosis • Calcification of bicuspid valve • Rheumatic aortic stenosis
- 9. • Congenital (bicuspid,unicuspid) • Degenerative calcific • Rheumatic fever • Radiation
- 10. Pathogeensis • Initially cardiacoutput is maintained by steady increase in pressure gradient across aortic valve • LV hypertrophy and coronary blood flow inadequate to supply the myocardium- angina • LV failure and pulmonary edema
- 11. Symptoms • Cardinal symptomsare angina,breathlessness and syncope • Mild or moderate stenosis: usually asymptomatic • Exertional dyspnoea • Angina • Exertional syncope • Sudden death • Episodes of acute pulmonary edema
- 12. Signs • Ejection systolicmurmur • Pulsus parvus et tardus • Slow rising carotid pulse • A thrill or anacrotic shudder over carotid arteries • a wave in the jvp is accentuated • Thrusting apex beat • Narrow pulse pressure • Signs of pulmonary venous congestion
- 13. • LV impulseis usually displaced laterally • Double apical impulse (with a palpable S4)
- 14. • Auscultation oEjection systolicmurmur oParadoxical splitting of S2 oS4 is audible at the apex
- 16. Investigations ECG Left ventricular hypertrophy– ST segment depression and T wave inversion (LV strain) in lead I and aVL Left bundle branch block Chest X ray May be normal; sometimes enlarged left ventricle and dilated ascending aorta on postero-anterior view, calcified valve on lateral view
- 17. Echocardiogram Calcified valve withrestricted opening, hypertrophied left ventricle Doppler Measurement of severity of stenosis(systolic gradient across the aortic valve) Detection of associated aortic regurgitation Cardiac catheterisation Mainly to identify associated coronary artery disease May be used to measure gradient between left ventricle and aorta
- 18. Natural history • Averagetime to death after the onset of various symptoms • Angina – 3 years • Syncope – 3 years • Dyspnoea – 2 years • Congestive heart failure – 1.5 to 2 years
- 19. Medical treatment • Nitroglycerin •Beta blockers , ACE inhibitors • Statins
- 20. • Surgical –aortic valve replacement • Percutaneous balloon aortic valvuloplasty • Children and young adults • Bridge to operation • Percutaneous aortic valve replacement
- 21. Aortic stenosis inoldage • Most common form of valve disease affecting very old • Syncope, angina, heart failure • Because of increasing stiffening in the central arteries, low pulse pressure and a slow rising pulse may not be present • Trans catheter aortic valve implantation (TAVI) • Biological valve is preferable
- 22.