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Aortic Stenosis Dr. s.a. moezzi seidali@ yahoo.com CD 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. 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) 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 Supravalvular cont On physical exam - thrill felt on palpation of right carotid but not left On 2D echo - visualization of narrowed ascending aorta Suprvalvular cont Associations: Elfin facies Hypercalcemia Peripheral pulmonic stenosis 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 tunnellike narrowing of the outflow tract Aortic regurgitation frequently accompanies 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 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 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 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 Pathophysiology 1. increase in afterload 2. decrease in systemic & coronary blood flow from obstruction 3. progressive hypertrophy 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. 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 noncompliant ventricle, and increased afterload Aortic Valve Variations A – Normal Valve B – Congenital AS C – Rheumatic AS D – Bicuspid AS E – Senile AS Tricuspid Aortic Valve Degeneration Senile Degeneration 2° to calcifications Most common cause of AS age > 70 Risk factors include DM & Cholesterol Pathophysiology of degeneration is unknown 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 Congenital AS Fusion of valve leaflets before birth More hypertrophy yet patients almost never develop heart failure symptoms 15% encounter sudden death Rheumatic Fever Currently less common in the U.S. Still prevalent in other countries Almost always in combination with mitral valve abnormality Other Causes SLE Severe Familial Hypercholesterolemia Fabry’s Disease Ochronosis Paget’s Disease of the Bone Signs & Symptoms Classic Triad DOE 2° to CHF (50%) 2. Angina (35%) 3. Effort Syncope (15%) 1. Onset of symptoms heralds a dramatic in mortality rate if AVR is not performed Source: Am J Geriatr Cardiol 12(3):178-182, 2003 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 DOE 2° to CHF (50%) CHF can cause Diastolic CHF (early) Dyspnea on Exertion Orthopnea Paroxysmal Nocturnal Dyspnea 2° to wall thickness & collagen deposition in walls which leads to ventricular wall stiffness Systolic CHF (late) Due to LV dilation 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 Law of Laplace LV Wall Stress = Pressure x Radius 2 x Thickness Wall Stress = O2 Demand X HR Hence, Wall Stress O2 Demand 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 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 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 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 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 Physical Findings S1 S2 Mild-Moderate S1 S2 Severe 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 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 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 Heart Failure Right Heart Failure Edema Congestive hepatomegaly JVD Left Heart Failure Rales in lungs Diagnostics EKG CXR ECHO Cardiac Catheterization 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 CXR May have normal sized heart Calcification of aortic valve Pulmonary congestion Post-stenotic dilatation of the aorta 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 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 More Doppler Data Aortic valve gradients depend on severity of obstruction and on flow. Pt may have low cardiac output and gradient less than 40mm Hg, but still have severe stenosis. Aortic valve area (AVA) is used to overcome this limitation Doppler info ECHO (cont.) Criteria for determining severity of AS G (mmHg) AVA (cm2) Mild < 25 > 1.5 Moderate 25-40 1-1.5 Severe 40-80 0.7-1 Critical >80 <0.7 Dobutamine Echocardiography Indicated in patients with moderate aortic stenosis and LV dysfunction (relatively low gradient AS ) to predict the reversibility of LV dysfunction after AVR management decisions are based on the results of dobutamine echocardiogram Hemodynamics Class 1 Indications for Cardiac Catheterization Coronary angiography is recommended before AVR in pts with AS at risk for CAD Cardiac cath for hemodynamic measurements is recommended for assessment of severity of AS in symptomatic pts when noninvasive tests are inconclusive or there is a discrepancy between noninvasive tests and clinical findings Coronary angiography is recommended before AVR in pts with AS for whom a pulmonary autograft (Ross procedure) is contemplated and if the origin of the coronary arteries is not identified by noninvasive techniques Cardiac Catheterization (cont.) The Gorlin formula is used to calculate the aortic valve area AVA = CO/SEP x HR 44.3G AVA = CO / G or simply… Cardiac MRI & AS CMR Evaluation of Aortic Stenosis • Safe • Minimally invasive • Absence of ionizing radiation • Absence of nephrotoxic contrast agents • Morphology + physiology • Simultaneous cardiac evaluation Natural History After symptoms occur in a pt with severe AS, rapidly progressive downhill course 2 to 3 year mortality of 50% Therefore, recommendations support AV replacement in all pts with severe AS and symptoms In young, healthy pts, very low perioperative mortality of 1-2% Asymptomatic AS Controversial recommendations regarding valve replacement Some studies have shown increased mortality in asymptomatic pts while others have shown similar mortality to agematched normal adults Frequent reassessment for symptoms Treatment The only effective treatment is relief of the mechanical obstruction via… Surgical AVR Aortic Valve Debridement Pharmacologic Therapy Aortic Balloon Valvuloplasty Medical Therapy Antibiotic prophylaxis is NOT recommended in all pts with AS for prevention of infective endocarditis. Pts with associated systemic HTN should be treated cautiously with appropriate antihypertensives (preload dependence) Statins have been studied to see if they cause regression or delayed progression of leaflet calcification (need more data) AVR Surgery Mortality rate is 2-3% Indicated for ALL symptomatic patients Usually not indicated for asymptomatic patients In Congenital AS surgery is recommended when gradient reaches 75mmHg AVR in Advanced Disease Still beneficial No in mortality EF may immediately double & eventually normalize LVH may regress AVR Contraindications Most patients with a low transvalvular gradient (<30mmHg) & far advanced heart failure do not improve post AVR Aortic Balloon Valvuloplasty Beneficial in congenital AS No regression of LVH in adults Gradient reduced by only 50% 50% AS recurrence after 6mo Same mortality rate as AVR Palliative measure for those who cannot have AVR or are awaiting AVR Antibiotic prophylaxis is no longer indicated in patients with aortic stenosis for prevention of infective endocarditis. Severe MS MVP Aortic coarctation Class 1 Recommendations for Aortic Valve Replacement in AS • AVR is indicated for symptomatic pts with severe AS • AVR is indicated for pts with severe AS undergoing CABG • AVR is indicated for pts with severe AS undergoing surgery on aorta or other heart valves • AVR is recommended for pts with severe AS and LV systolic dysfunction (EF<50%) Aortic Valve Surgery Options AVR include: with mechanical or bioprosthetic valve AVR with allograft (homograft) Pulmonic vavle autotransplantation (Ross) Aortic valve repair LV to descending aorta shunt Types of AVR Elderly Patients Pts >80years, operative mortality as high as 30%. Percutaneous aortic balloon valvuloplasty is an alternative to valve replacement introduced in ‘80s. Inflating one or more large balloons across the aortic valve from a percutaneous route, a modest decrease in gradient and improvement in symptoms
