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Aortic Stenosis

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Causes of Aortic Stenosis Supravalvular Subvalvular discrete tunnel Valvular congenital (1-30yrs old) bicuspid (40-60yrs old) rheumatic (40-60yrs old) ... – PowerPoint PPT presentation

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Title: Aortic Stenosis


1
Aortic Stenosis
  • Dr. s.a. moezzi
  • seidali_at_ yahoo.com

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C D
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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.

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Causes of Aortic Stenosis
  • Supravalvular
  • Subvalvular
  • discrete
  • tunnel
  • Valvular
  • congenital (1-30yrs old)
  • bicuspid (40-60yrs old)
  • rheumatic (40-60yrs old)
  • senile degenerative (gt70yrs old)

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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

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

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Suprvalvular cont
  • Associations
  • Elfin facies
  • Hypercalcemia
  • Peripheral pulmonic stenosis

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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

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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

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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

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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

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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

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

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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.

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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

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

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Tricuspid Aortic Valve Degeneration
  • Senile Degeneration 2 to calcifications
  • Most common cause of AS age gt 70
  • Risk factors include DM ?Cholesterol
  • Pathophysiology of degeneration is unknown

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

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

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

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Other Causes
  • SLE
  • Severe Familial Hypercholesterolemia
  • Fabrys Disease
  • Ochronosis
  • Pagets Disease of the Bone

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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

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Source Am J Geriatr Cardiol 12(3)178-182, 2003
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Signs Symptoms (cont.)
  • Other more rare initial findings include
  • Embolization from a calcified aortic valve
    resulting in unilateral vision loss, focal
    neurologic deficit, MI
  • Heydes Syndrome- angiodysplasia due to von
    Willebrand deficiency which can lead to GIB if
    AVR is not performed

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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

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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

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Law of Laplace
  • LV Wall Stress Pressure x Radius
  • 2 x Thickness
  • Wall Stress O2 Demand X HR
  • Hence, Wall Stress ? O2 Demand

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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 AgtE,
    therefore patients with AS who develop Afib can
    become severely symptomatic

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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

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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

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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
  • Gallivardins Phenomenon when AS is heard at the
    apex and may even sound holosystolic

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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
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Physical Findings
S1 S2 S1
S2 Mild-Moderate
Severe
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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

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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

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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

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

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Diagnostics
  • EKG
  • CXR
  • ECHO
  • Cardiac Catheterization

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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

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

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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

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Doppler
  • Modified Bernoulli equation (delta P4v2), 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

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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

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Doppler info
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ECHO (cont.)
  • Criteria for determining severity of AS

G (mmHg) AVA (cm2)
Mild lt 25 gt 1.5
Moderate 25-40 1-1.5
Severe 40-80 0.7-1
Critical gt80 lt0.7
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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

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Hemodynamics
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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
    non-invasive 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

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Cardiac Catheterization (cont.)
  • The Gorlin formula is used to calculate the
    aortic valve area
  • AVA CO/SEP x HR or simply
  • 44.3?G
  • AVA CO / ?G

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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
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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

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Asymptomatic AS
  • Controversial recommendations regarding valve
    replacement
  • Some studies have shown increased mortality in
    asymptomatic pts while others have shown similar
    mortality to age-matched normal adults
  • Frequent reassessment for symptoms

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Treatment
  • The only effective treatment is relief of the
    mechanical obstruction via
  • Surgical AVR
  • Aortic Valve Debridement
  • Pharmacologic Therapy
  • Aortic Balloon Valvuloplasty

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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)

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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

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AVR in Advanced Disease
  • Still beneficial
  • No ? in mortality
  • EF may immediately double eventually normalize
  • LVH may regress

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AVR Contraindications
  • Most patients with
  • a low transvalvular gradient (lt30mmHg)
  • far advanced heart failure
  • do not improve post AVR

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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

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Antibiotic prophylaxis
  • is no longer indicated in patients with aortic
    stenosis for prevention of infective
    endocarditis.
  • Severe MS
  • MVP
  • Aortic coarctation

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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 (EFlt50)

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Aortic Valve Surgery
  • Options include
  • AVR with mechanical or bioprosthetic valve
  • AVR with allograft (homograft)
  • Pulmonic vavle autotransplantation (Ross)
  • Aortic valve repair
  • LV to descending aorta shunt

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Types of AVR
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Elderly Patients
  • Pts gt80years, 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

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