Transcript Aortic Stenosis

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
44.3G
 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