Aortic Stenosis:: Updates in Diagnosis & Management
Aortic Stenosis:: Updates in Diagnosis & Management
Aortic Stenosis:: Updates in Diagnosis & Management
Learning Objectives
Following the presentation the participant should be able to:
Define aortic stenosis based on echocardiographic guidelines Explain primary causes and risk factors Identify the demographics Discuss optimal management including timing of valvular surgery
Aortic Valve
Valvular
congenital (1-30yrs old) bicuspid (40-60yrs old) rheumatic (40-60yrs old) senile degenerative (>70yrs old)
This is the aortic valve viewed from the outflow side, i.e. from the aorta. Blood flows up through the valve from the left ventricle, pushing the cusps out of the way. Two of the three cusps are clearly visible in this view.
Schematic of AV
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
Dx should be suspected in young pt with LVOT murmur On physical exam - thrill felt on palpation of right carotid but not left On 2D echo - visualization of narrowed ascending aorta On Doppler - provides info on magnitude of obstruction
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 tunnel-like 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 20s - congenitally unicuspid or fused bicuspid valve 40s to 60s - calcified bicuspid or rheumatic disease 70s 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 longstanding 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 non-compliant ventricle, and increased afterload
Angina
Exertional angina may occur in absence of epicardial coronary artery obstruction Pathophysiology here is related to mismatch of myocardial oxygen supply and demand due to
high diastolic pressures decreased myocardial perfusion gradient increased myocardial mass
Critical AS
In critical AS, with onset of systemic hypotension (either from medications or vasovagal reaction), coronary artery perfusion may decrease. This increased myocardial oxygen supply/demand mismatch and results in myocardial ischemia This reduces forward cardiac output, aortic diastolic pressure decreases, which further decreases coronary perfusion.
Clinical Presentation
Asymptomatic but heart murmur detected on physical exam May have any one or all three exertional dyspnea, angina, syncope Occasionally pt with end stage aortic stenosis and LV dysfunction present with anasarca and cardiac cachexia
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
Echocardiography
2D and Doppler echo are imaging modalities of choice to diagnose and estimate severity of AS 2D can identify location In pts with valvular, the cause may be assessed in parasternal short-axis view Doppler excellent for assessment of severity
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
Doppler info
Hemodynamics
AVA cont
Echo and doppler estimate aortic valve area by the continuity equation AVA = LVOTarea X LVOTtvi AVtvi AV = aortic valve flow velocity TVI = time-velocity integral Doppler echo may underestimate AV gradient
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
Calcific Aortic Stenosis Note that there are three distinct cusps in this valve, and that the free edges of the cusps appear normal. Heaped up calcific deposits extend from the cusps into the sinuses of Valsalva. This calcification prevents normal opening of the valve. Calcification of the aortic valve may be a result of rheumatic heart disease. The gross appearance illustrated here, however, is characteristic of degenerative ("wear and tear") calcific aortic stenosis in an elderly individual. Bicuspid aortic valves (a congenital abnormality) also tend to calcify, but usually at an earlier age than normal three-cusped valves.
CT Dx of AS
CT Evaluation of Aortic Stenosis
Excellent Assessment of Calcification
May establish stenosis severity Cannot establish insufficiency Good evaluation of mechanical prostheses Evaluates coronary anatomy in patients undergoing valve surgery
This enhanced CT image puts you inside the aorta, looking down at the aortic valve. You can clearly see the three valve leaflets, currently closed.
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)
Types of AVR
Examples of replacement aortic valves: a) shows an aortic homograft, b) and c) show a xenograft, d) shows a ball and cage valve, e) shows a tilting-disk valve, f) shows a bi-leaflet valve
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
Balloon Valvuloplasty
Follow-up has demonstrated a high rate of re-stenosis (>60% at 6 months and nearly 100% at 2 years), with no decrease in mortality rate after procedure Therefore, now only has a role in critically ill elderly pts who are not candidates for surgery or as a bridge in critically ill pts before AV replacement
References
Bonow RO, Carabello BA, Chatterjee K, de Leon AC Jr., Faxon DP, Freed MD, Gaasch WH, Lytle BW, Nishimura RA, OGara PT, ORourke RA, Otto CM, Shah PM, Shanewise JS. ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: a report of the American College of Cardiology/America Heart Association Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Valvula Heart Disease). American Heart Association Web Site. Available at: http://www.americanheart.org. Circulation. Rosenhek R, Klaar U, Schemper M, et al. Mild and moderate aortic stenosis. Natural history and risk stratification by echocardiography. Eur Heart J 2004;25:199 205. Cosmi JE, Kort S, Tunick PA, et al. The risk of the development of aortic stenosis in patients with benign aortic valve thickening. Arch Intern Med 2002;162:23457. Stewart BF, Siscovick D, Lind BK, et al. Clinical factors associate with calcific aortic valve disease: Cardiovascular Health Study. J Am Coll Cardiol 1997;29:6304.