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... College of Cardiology/American Heart Association Tas

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Title: ... College of Cardiology/American Heart Association Tas


1
Aortic Stenosis When the Window of Opportunity
is Closing
  • CPT Bradley K. Harrison, MD
  • 2009 USAFP Annual Meeting
  • 1545-1630, 04 April 2009

2
Objectives
  • Review the pathophysiology and classic
    presentations of aortic stenosis
  • Understand when to refer for diagnostic testing
    and/or consultation
  • Comprehend the definitive management of aortic
    stenosis
  • Review literature in reference to medical
    management

3
Case Presentation
  • 66 y/o male presents for a physical.
  • Wife mentions decreased amount of physical
    activity over 2 yearsattributed to getting
    older.
  • Smoker (40 pack/year), sedentary
  • BP 139/85, HR 88, RR 13, T 99.0
  • 2/6 late-peaking systolic ejection murmur, heard
    at the right upper sternal border radiating to
    the neck

4
Aortic Stenosis (AS)
  • Active, inflammatory process associated with
    cardiovascular risk factors
  • Age, sex, cholesterol, blood pressure, diabetes,
    metabolic syndrome, smoking
  • Increased risk of death from cardiovascular
    causes1 (even in absence of CAD)
  • Histopathologic changes in valve leaflets similar
    to other atherosclerotic diseases2

5
Aortic Stenosis (cont.)
  • Key initiating factor likely mechanical stress
  • The most important cardiac valve disease in
    developed countries
  • Affecting 3-5 of persons gt65 years old
  • 1-2 with bicuspid aortic valve
  • AS develops with age (Senile aortic stenosis)

6
Recently In the News
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9
Compensatory Mechanisms
  • Adaptive and maladaptive
  • Progressive worsening of left ventricular outflow
    obstruction leads to hypertrophy
  • Compensatory hypertrophy required to maintain
    wall stress (afterload)
  • Augmented preload with increased atrial kick
    preserve LV systolic function

10
Heart Failure
  • Changes in LV function may no longer be adequate
    to overcome the outflow obstruction
  • Hypertrophic remodeling leads to diastolic
    dysfunction
  • Afterload excess results in decreased ejection
    fraction systolic dysfunction
  • 50 presentation
  • 50 die in 2 years

11
Angina
  • Progressive LV hypertrophy from aortic stenosis
    leads to increased myocardial oxygen needs3
  • Hypertrophy may compress the coronary arteries
  • Reduced diastolic filling may result in classic
    angina, even in the absence of coronary artery
    disease4
  • 35 presentation
  • 50 die in 5 years

12
Syncope
  • Cardiac output no longer increases with exercise5
  • A drop in systemic vascular resistance that
    normally occurs with exertion may lead to
    hypotension and syncope6
  • 15 presentation
  • 50 die in 3 years

13
Signs
  • Harsh, crescendo-decrescendo systolic murmur that
    is loudest over the 2nd right intercostal space
    and radiates to the carotid arteries
  • Increased incidence of atherosclerosis and
    hypertension may mask the classic carotid
    findings
  • It is difficult to rule out AS with physical
    examination findings alone
  • Physical examination does not correlate with
    severity

14
Murmur
  • 2/6 systolic murmur
  • Older patients with vague complaints and
    asymptomatic patients undergoing preoperative
    medical assessment
  • 3/6 systolic murmur
  • ACC/AHA guidelines recommend echocardiography in
    asymptomatic patients with a grade 3/6 or louder
    systolic murmur7

15
Symptoms
  • Classic symptoms of AS
  • Dyspnea and other symptoms of heart failure
  • Angina
  • Syncope
  • Indicate hemodynamically significant AS and is a
    critical point for management decisions
  • Non-classic symptoms of AS
  • May present as a decrease in exertional tolerance
    without recognizing the classic symptoms

16
Case 66 y/o male
  • Decreased activity, getting older
  • Remains asymptomatic
  • Refer for echocardography
  • Ejection fraction 50
  • Peak transaortic flow velocity 4.0 m/s
  • Aortic valve area 1.0 cm2

17
Diagnostic Testing
  • Doppler echocardiography is the recommended
    initial test for patients with classic symptoms
    of AS7
  • Estimates aortic jet velocity, mean gradiant, and
    aortic valve area
  • Echocardiography is well validated and compares
    with cardiac catheterization
  • Provides information regarding LV function and
    coexisting abnormalities of other valves

18
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19
Classifications of Severity7
20
Severity
  • Normal
  • Jet velocity lt2.5 m/s
  • Valve area 3-4 cm2
  • Mild-to-Moderate
  • Jet velocity 3-4 m/s
  • Valve area 1-1.5 cm2

21
Treatment
  • Aortic valve replacement is the only effective
    treatment for hemodynamically significant AS
  • No prospective randomized trials comparing
    medical versus surgical treatment
  • The effect of aortic valve replacement on
    survival, Circulation 1982

22
Survival among Patients with Severe Symptomatic
Aortic Stenosis Who Underwent Valve Replacement
and Similar Patients Who Declined to Undergo
Surgery10
23
Treatment-Symptomatic
  • Mortality increases dramatically
  • Overall survival of 2-3 years without surgical
    treatment
  • 10-year survival rate after aortic valve
    replacement almost identical to that in age- and
    sex-matched persons11
  • Well-accepted recommendation that aortic valve
    replacement should be performed promptly in
    symptomatic patients7

24
Treatment-Symptomatic (cont.)
  • Surgery has an average perioperative mortality
    rate of 48
  • Risk of prosthetic valve failure of 1 per year9
  • Mechanical valve
  • Durability versus Anticoagulation (INR 2-3)
  • Biological valve
  • Xenograft
  • Allograft/homograft
  • Ross procedure

25
Treatment-Asymptomatic
  • Aortic valve replacement recommended for
    asymptomatic patients with severe AS accompanied
    by LV dysfunction (EFlt50)12
  • Watchful waiting recommended in most asymptomatic
    patients, even severe AS
  • Survival in patients with watchful waiting is
    comparable
  • Surgical risk (4) outweighs the approximately
    1-2 annual risk of sudden death in asymptomatic
    patients

26
Asymptomatic?
  • Important to distinguish patients who may have a
    decreased routine activity level
  • ACC/AHA guidelines recommend exercise stress
    testing be performed under the direct observation
    of an experienced cardiologist7
  • Safe in mild to moderate AS
  • Aortic valve replacement should be considered13
  • Symptoms occur at lt80 of predicted maximum heart
    rate

27
Asymptomatic-Other Considerations14
  • High risk of developing symptoms
  • Very severe AS (lt0.6 cm or 5 m/s)
  • More rapid increase in aortic jet velocity over
    time (0.3 m/s or more per year)
  • Severe valve calcification
  • Patients who do not live near a medical care
    facility
  • Predicted operative mortality rate 1 (70 years
    or younger without comorbidities)

28
Monitoring
  • Watchful waiting is appropriate in most
    asymptomatic patients
  • Serial echocardiography (ACC/AHA guidelines7)
  • Annually Severe AS
  • 1-2 years Moderate AS
  • 3-5 years Mild AS
  • Symptoms are best indicator of hemodynamic
    significance
  • Patients should be educated about their
    importance and promptly reported to their
    physician

29
Referral
  • Cardiology referral is recommended
  • All patients with symptomatic AS
  • AS accompanied by LV dysfunction
  • Asymptomatic patients with very severe or rapidly
    progressive calcification
  • Cardiology referral should be considered in
    patients with subtle or atypical presentations
  • Decreased exercise tolerance

30
Medical Management
  • No medical treatments have been proven to delay
    the progression of aortic valve disease or to
    improve survival
  • Many patients have concurrent cardiac conditions
  • Hypertension (40)
  • Atrial fibrillation (5)
  • Coronary artery disease

31
Coronary Risk Reduction16
  • Smoking cessation
  • Aspirin prophylaxis in adults with 10-year risk
    of cardiovascular disease 6
  • Participation in regular exercise
  • Mild AS should not be restricted from physical
    activity
  • Asymptomatic with moderate to severe AS should
    avoid competitive or vigorous activities, other
    exercise is safe7,17

32
Statins?
  • Can statins slow the progression of AS?
  • Initial observational studies (retrospective or
    case-control) suggested a significantly lower
    rate of progression18
  • Randomized prospective study (SALTIRE) showed no
    statistical difference19
  • Intensive Lipid Lowering with Simvastatin and
    Ezetimibe in Aortic Stenosis (SEAS)20

33
SEAS20
  • Randomized, double-blind, placebo controlled,
    N1873
  • 1 composite of major cardiovascular events
  • 2 aortic-valve stenosis, ischemic cardiovascular
    events
  • 45-85y, asymptomatic, mild-to-moderate (2.5-4
    m/s)
  • Excluded for CAD or equivalent

34
SEAS20
  • Progression of AS
  • Placebo 3.71, increase of 0.62
  • S E 3.69, increase of 0.61
  • Aggressive lipid lowering does not effect
    hemodynamic progression

35
SEAS20
36
Not Atherosclerosis?
  • Calcific aortic stenosis is not atherosclerosis
  • Tissue calcification more severe
  • Mechanism is increased leaflet stiffness
  • Not plaque rupture
  • Severity of CAD and valve disease not related

37
Case 66 y/o male
  • While in primary care office
  • BP 139/85
  • Start ACE inhibitor
  • Start Aspirin
  • Smoker
  • Encourage smoking cessation
  • Statin?
  • Framingham Risk (Chol 200, HDL 40) 19
  • Stress test?

38
Antibiotic Prophylaxis
  • Recommended for patients who have undergone
    aortic valve replacement
  • No longer recommended for patients with acquired
    valve diseases21

39
Case 66 y/o male
  • Experienced cardiologist performed exercise
    stress testing
  • Earlier-than-predicted fatigue/dyspnea (gt80
    predicted maximum heart rate)
  • Referred for aortic valve replacement

40
Challenges
  • Valve diseases progress over decades
  • Clinical trials only a few years
  • End points difficult to assess
  • Subjective
  • Therapies affect other cardiovascular outcomes
  • Ideal endpoint is valve tissue changes

41
Future Implications
  • Mutations in NOTCH1 gene
  • Phenotypic transformation to end stage severe
    valve calcification?
  • Cellular and molecular pathways must mediate
    disease progression

42
Conclusion
  • 3 classic symptoms heart failure, syncope,
    angina
  • Indications for referral and/or consultation
  • Definitive management of aortic stenosis

43
References
  • Cosmi JE, Kort S, Tunick PA, et al. The risk of
    the development of Aortic Stenosis in patient
    with benign aortic valve thickening. Arch
    Intern Med 20021622345-7.
  • Otto CM, Kuusisto J, Reichenback DD, et al.
    Characterization of the early lesion of
    degenerative valvular aortic stenosis
    histological and immunohistochemical studies.
    Circulation 199490844-53.
  • Johnson LL, Sciacca RR, Ellis K, et al. Reduced
    left ventricular myocardial blood flow per unit
    mass in aortic stenosis. Circulation
    197857(3)582-590.
  • Marcus ML, Doty DB, Hiratzka LF, et al. Decreased
    coronary reserve a mechanism for angina pectoris
    in patients with aortic stenosis and normal
    coronary arteries. N Eng J Med 1982307(22)1362-1
    366.
  • Bache RJ, Wang Y, Jorgensen CR. Hemodynamic
    effects of exercise in isolated valvular aortic
    stenosis. Circulation 197144(6)1003-1013.
  • Kulbertus HE. Ventricular arrhythmias, syncope
    and sudden death in aortic stenosis. Eur Heart J
    19889(suppl E)51-52.
  • Bonow RO, Carabello BA, Kanu C, et al. ACC/AHA
    2006 guidelines for the management of patients
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  • Ambler G, Omar RZ, RoystonP, et al. Prediction of
    operative mortality after valve replacement
    surgery. Circulation 2005112(2)224-231.
  • Pellikka PA, Sarano ME, Nishimura RA, et al.
    Outcome of 622 adults with asymptomatic,
    hemodynamically significant aortic stenosis
    during prolonged follow-up. Circulation
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    effect of aortic valve replacement on survival.
    Circulation 1982661105-1110.
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44
References (cont.)
  • Vaquette B, Corbineau H, Laurent M, et al. Valve
    replacement in patients with critical aortic
    stenosis and depressed left ventricular function
    predictors of operative risk, left ventricular
    function recovery, and long-term outcome. Heart
    200591(10)1324-1329.
  • Das P, Rimingtom H, Chambers J. Exercise testing
    to stratify risk in aortic stenosis. Eur Heart J
    200526(13)1309-1313.
  • Rosenhek R, Binder T, Porenta G, et al.
    Predictors of outcome in severe, asymptomatic
    aortic stenosis. N Engl J Med 2000343(9)611-617.
  • Antonini-Canterin F, Huang G, Cervesato E, et al.
    Symptomatic aortic stenosis does systemic
    hypertension play an additional role?
    Hypertension 200341(6)1268-1272.
  • U.S. Preventative Services Task Force. Guide to
    clinical preventative services. 3rd ed.
    2000-2002. http//www.ahrq.gov/clinic/prevnew.htm.
    Accessed March 16, 2009.
  • Bonow RO, Cheitlin MD, Crawford MH, et al. Task
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    Cardiol 200545(8)1334-1340.
  • Rosenhek R, Rader F, Loho N, et al. Statins but
    not angiotensin-converting enzyme inhibitors
    delay progression of aortic stenosis. Circulation
    2004110(10)1291-1295.
  • Cowell SJ, Newby DE, Prescott RJ, et al. for the
    Scottish Aortic Stenosis and Lipid Lowering
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  • Rossebo AB, Pedersen TR, Boman K, et al. for the
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