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Aortic Stenosis

Aortic Stenosis

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Aortic Stenosis

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  1. Aortic Stenosis Dr. s.a. moezzi seidali@ yahoo.com

  2. C D

  3. Definition Aortic Stenosis is the narrowing of the aortic valve opening caused by failure of the valve leaflets to open normally. Concentric LVH then develops due to an increase in LV pressure.

  4. Causes of Aortic Stenosis • Supravalvular • Subvalvular • discrete • tunnel • Valvular • congenital (1-30yrs old) • bicuspid (40-60yrs old) • rheumatic (40-60yrs old) • senile degenerative (>70yrs old)

  5. Supravalvular • congenital abnormality in which ascending aorta superior to the aortic valve is narrowed • rarest site of AS • either a single discrete constriction or a long tubular narrowing

  6. Supravalvular cont • On physical exam - thrill felt on palpation of right carotid but not left • On 2D echo - visualization of narrowed ascending aorta

  7. Suprvalvular cont • Associations: • Elfin facies • Hypercalcemia • Peripheral pulmonic stenosis

  8. Subvalvular AS • Discrete seen in 10% of all pts with AS • can be secondary to a subvalvular ridge that extends into LVOT or to a tunnel-like narrowing of the outflow tract • Aortic regurgitation frequently accompanies

  9. Subvalvular cont • Echo - visualization of a narrowing or discrete subvalvular ridge extending into the LVOT and a high-velocity turbulence on continuous wave doppler • If site of obstruction is not visualized on transthoracic echo, TEE is indicated

  10. Subvalvular vs HCM • Dx of subvalvular AS needs to be differentiated from dynamic outflow obstruction of HCM b/c tx differs • Discrete subvalvular - some recommend resection in all pts with moderate or higher to relieve degree of LVOT obstruction and prevent progressive AR

  11. Valvular • Accounts for most cases • Cause of valve abnormality depends on age at presentation • Teens to early 20’s - congenitally unicuspid or fused bicuspid valve • 40’s to 60’s - calcified bicuspid or rheumatic disease • 70’s and beyond - senile degeneration of valve with calcific deposits

  12. Pathophysiology • In adults with AS, obstruction develops gradually, usually over years • LV adapts to systolic pressure overload through a hypertrophic process that results in increased LV wall thickness (normal chamber volume maintained) • Eventually, LV cannot compensate for the long-standing pressure overload and ventricular dilation and progressive decrease in systolic function

  13. Pathophysiology 1. increase in afterload 2. decrease in systemic & coronary blood flow from obstruction 3. progressive hypertrophy

  14. Pathophysiology • Depressed contractile state of the myocardium may also cause low EF • Difficult to determine whether low EF is secondary to this or to excessive afterload • When caused by depressed contractility, corrective surgery is less beneficial.

  15. More Pathophysiology • Exertional dyspnea is common, even when LVSF is preserved • Diastolic dysfunction is common and result in increased LV filling pressures that are reflected onto pulmonary circulation • Diastolic dysfunction occurs from prolonged ventricular relaxation and decreased compliance and is caused by myocardial ischemia, a thick non-compliant ventricle, and increased afterload

  16. Aortic Valve Variations • A – Normal Valve • B – Congenital AS • C – Rheumatic AS • D – Bicuspid AS • E – Senile AS

  17. Tricuspid Aortic ValveDegeneration • Senile Degeneration 2° to calcifications • Most common cause of AS age > 70 • Risk factors include DM & Cholesterol • Pathophysiology of degeneration is unknown

  18. Bicuspid Aortic Valve • Most common congenital heart anomaly • Most common cause of AS age < 70 • 50% develop mild AS by age 50 • Increased incidence in Turners Syndrome

  19. Congenital AS • Fusion of valve leaflets before birth • More hypertrophy yet patients almost never develop heart failure symptoms • 15% encounter sudden death

  20. Rheumatic Fever • Currently less common in the U.S. • Still prevalent in other countries • Almost alwaysin combination with mitral valve abnormality

  21. Other Causes • SLE • Severe Familial Hypercholesterolemia • Fabry’s Disease • Ochronosis • Paget’s Disease of the Bone

  22. Signs & Symptoms • Classic Triad • DOE 2° to CHF (50%) • Angina (35%) • Effort Syncope (15%) • Onset of symptoms heralds a dramatic  in mortality rate if AVR is not performed

  23. Source: Am J Geriatr Cardiol 12(3):178-182, 2003

  24. Signs & Symptoms (cont.) • Other more rare initial findings include • Embolization from a calcified aortic valve resulting in unilateral vision loss, focal neurologic deficit, & MI • Heyde’s Syndrome- angiodysplasia due to von Willebrand deficiency which can lead to GIB if AVR is not performed

  25. DOE 2° to CHF (50%) • CHF can cause • Dyspnea on Exertion • Orthopnea • Paroxysmal Nocturnal Dyspnea • Diastolic CHF (early) • 2° to wall thickness & collagen deposition in walls which leads to ventricular wall stiffness • Systolic CHF (late) • Due to LV dilation

  26. Angina (35%) • 2° to myocardial ischemia (O2 demand exceeds supply) • Frequently occurs in AS in the absence of CAD • Concentric LVH develops 2° to the pressure overload of AS… …The Law of Laplace

  27. Law of Laplace LV Wall Stress = Pressure x Radius 2 x Thickness Wall Stress = O2 Demand X HR Hence, Wall Stress  O2 Demand

  28. Effort Syncope (15%) • Secondary to inadequate cerebral perfusion • During exercise TPR  so that more blood can get to the muscles, but CO cannot  in the case of AS MAP(or BP) = CO x TPR • Exercise can also cause both ventricular & supraventricular arrhythmias • 2° Afib or calcification of the conduction system can lead to AV block • Atrial kick is very important because A>E, therefore patients with AS who develop Afib can become severely symptomatic

  29. Coagulation Abnormalities • In most pts with severe AS, impaired platelet fxn and decreased levels of von Willebrand factor are noted • Severity of coagulation problem correlates with degree of AS • Associated with clinical bleeding in 20% of patients • Resolves after valve replacement

  30. Physical Exam • Dampened upstroke of carotid artery • Sustained bifid LV impulse • Single or split S2 • Late peaking systolic ejection murmur (may be heard with same intensity at apex and base) • The severity more related with timing of peak and duration than loudness

  31. Auscultation: Murmurs • Systolic Ejection Murmur • Located at the RUSB radiating to carotids • As dz worsens, murmur peaks progressively later (intensity, possible thrill) • Severe AS, murmur may  as CO falls hence intensity is not a predictor of severity • Gallivardin’s Phenomenon when AS is heard at the apex and may even sound holosystolic

  32. Common Murmurs and Timing (click on murmur to play) Systolic Murmurs • Aortic stenosis • Mitral insufficiency • Mitral valve prolapse • Tricuspid insufficiency Diastolic Murmurs • Aortic insufficiency • Mitral stenosis S1 S2 S1

  33. Physical Findings S1 S2 S1 S2 Mild-Moderate Severe

  34. Auscultation: Heart Sounds • Paradoxic Splitting of S2 • Absent/Soft A2 which leads to a soft S2 • S4 in early AS due to LVH/diastolic CHF • S3 in late AS due to systolic CHF • Ejection click with bicuspid valve

  35. Carotid Upstroke • Low blood volume & delay in reaching its peak • “Pulsus parvus et tardus” probably the single best way to estimate the severity of AS at the bedside • In elderly patients, stiff carotids may falsely normalize the upstroke

  36. Apical Impulses • PMI usually not displaced due to concentric LVH • PMI abnormally forceful & sustained in nature • PMI laterally displaced in AS when severe CHF has developed

  37. Heart Failure • Right Heart Failure • Edema • Congestive hepatomegaly • JVD • Left Heart Failure • Rales in lungs

  38. Diagnostics • EKG • CXR • ECHO • Cardiac Catheterization

  39. EKG • Nonspecific for AS • LVH • LAE • LBBB • ST/T wave changes • if A fib is present, concomitant mitral valve disease or thyroid disease should be suspected

  40. CXR • May have normal sized heart • Calcification of aortic valve • Pulmonary congestion • Post-stenotic dilatation of the aorta

  41. Class 1 Echo recommendations • Echocardiography is recommended for diagnosis and severity of AS • Echocardiography is recommended in patients with AS for assessment of LV wall thickness, size, and function • Echocardiography is recommended in patients with known AS and changing symptoms • Echocardiography is recommended for assessment of changes in hemodynamic severity and LV function in pts with known AS during pregnancy • Transthoracic echocardiography is recommended for re-evaluation of asymptomatic patients: • severe AS - yearly; • moderate AS - every 1-2 years; • mild AS - every 3-5 years

  42. Doppler • Modified Bernoulli equation (delta P=4v2), a maximal instantaneous and mean aortic valve gradient can be derived from continous pulse wave doppler velocity across aortic valve. • The accuracy of the above relies on the fact that Doppler beam is parallel to the stenotic jet