Aortic stenosis

Aortic stenosis by Dr WALINJOM

1. Aortic Stenosis
Dr Walinjom Joshua.
Cardiology Resident
Supervisor
Dr Boombhi / Pr Kingue

2. PLAN
Introduction
Epidemiology
Anatomy
Cause / Pathophysiology
Clinical Presentation
Workup
Treatment
2

3. Introduction
Aortic stenosis (AS) is narrowing of the
aortic valve, obstructing blood flow from
the left ventricle to the ascending aorta
during systole.
3

4. Epidemiology
In recent population-based
echocardiographic studies, 1% to 2% of
persons age 65 or older and 12% of persons
75 or older had calcific aortic stenosis
4

5. Epidemiology
The rate of progression from aortic sclerosis
to stenosis is 1.8% to 1.9% per year.
Among those older than 75, 3.4% (95%
confidence interval [CI] 1.1% to 5.7%) have
severe AS
5

6. Epidemiology
The rate of progression from aortic sclerosis
to stenosis is 1.8% to 1.9% per year.
Among those older than 75, 3.4% (95%
confidence interval [CI] 1.1% to 5.7%) have
severe AS
6

7. Anatomy
7

8. Anatomy
8

9. Anatomy
9

10. Anatomy
10

11. Anatomy
11

12. Anatomy
12

13. Anatomy
13

14. Causes and Pathology
Valvular AS has three principal causes:
1.congenital bicuspid valve with superimposed
calcification,
2.calcification of a normal trileafletvalve, and
3.rheumatic disease
14

15. Causes and Pathology
Valvular AS has three principal causes:
1.congenital bicuspid valve with superimposed
calcification,
2.calcification of a normal trileafletvalve, and
3.rheumatic disease
15

16. Causes and Pathology
In addition,
congenital valve stenosis manifesting in
infancy or childhood
Rarely, AS is caused by severe
atherosclerosis of the aorta and aortic valve
this form of AS occurs most frequently in
patients with severe hypercholesterolemia and
is observed in children with homozygous type
II hyperlipoproteinemia 16

17. Causes and Pathology
Hypertension is a major cause of Aortic
stenosis
Hypertension has been shown to be
independently associated with degenerative
calcific aortic valve sclerosis and stenosis in
elderly population.
HTA -Wall shear stress –Aortic sclerosis –
valve calcification. 17

18. Causes and Pathology
Rheumatoid involvement of the valve is a
rare cause of AS and results in nodular
thickening of the valve leaflets and
involvement of the proximal portion of the
aorta.
Ochronosis(accumulation of homogentisic
acid in connective tissues -Arthrits) with
alkaptonuria is another rare cause of AS.18

19. Causes and Pathology
19

20. Causes and Pathology
Rheumatoid involvement of the valve is a
rare cause of AS and results in nodular
thickening of the valve leaflets and
involvement of the proximal portion of the
aorta.
Ochronosis(accumulation of homogentisic
acid in connective tissues -Arthrits) with
alkaptonuria is another rare cause of AS.20

21. Causes and Pathology
Fixed obstruction to left ventricular (LV)
outflow also may occur above the valve
(supravalvular stenosis) or below the valve
(discrete subvalvular stenosis)
21

22. Causes and Pathology
Congenital Aortic Valve Disease
Congenital malformations of the aortic valve
may be unicuspid, bicuspid, or tricuspid, or the
anomaly may manifest as a dome-shaped
diaphragm.
22

23. Causes and Pathology
Dynamic subaortic obstruction may be caused
by hypertrophic cardiomyopathy
23

24. Causes and Pathology
Calcific Aortic Valve Disease
Calcific (formerly “senile” or “degenerative”) aortic
valve disease affecting a congenital bicuspid or
normal trileaflet valve is now the most common cause
of AS in adults.
24

25. Associations in Observational and Epidemiologic Studies of
Clinical Risk Factors and CalcificAorticValve Disease (CAVD)
25

26. Causes and Pathology
Calcific Aortic Valve Disease
Aorticsclerosis, identified by either
echocardiography or computed tomography
(CT), is the initial stage of calcific valve disease
and, even in the absence of valve obstruction
or known cardiovascular disease, is associated
with an increased risk of myocardial infarction
(MI) and cardiovascular and all-cause mortality
26

27. Causes and Pathology
Calcific Aortic Valve Disease
Aorticsclerosis, identified by either
echocardiography or computed tomography
(CT), is the initial stage of calcific valve disease
and, even in the absence of valve obstruction
or known cardiovascular disease, is associated
with an increased risk of myocardial infarction
(MI) and cardiovascular and all-cause mortality
27

28. Causes and Pathology
Calcific Aortic Valve Disease
Although calcific AS once was considered to
represent the result of years of normal
mechanical stress on an otherwise normal
valve (“wear and tear”), it is now clear that an
active biology underlies the initiation and
progression of calcificaorticvalve disease
28

29. Causes and Pathology
29

30. Causes and Pathology
Calcific Aortic Valve Disease
Although calcific AS once was considered to
represent the result of years of normal
mechanical stress on an otherwise normal
valve (“wear and tear”), it is now clear that an
active biology underlies the initiation and
progression of calcificaorticvalve disease
30

31. Causes and Pathology
Calcific Aortic Valve Disease
Normal valve leaflets are comprised of the
fibrosa (facing the aorta), ventricularis (facing
the ventricle), and spongiosa (located between
the fibrosa and ventricularis)
Valve interstitial cells(VICs) are the most
predominant cell type; endothelial and smooth
muscle cells are also present
31

32. Causes and Pathology
Calcific Aortic Valve Disease
Through a complex interplay of molecular
events, the pliable, flexible valve becomes stiff
and immobile, characterized grossly by fibrosis
and calcification.
The process is initiated by lipid infiltration and
oxidative stress, which attract and activate
inflammatory cells and promote the elaboration
of cytokines.
32

33. Causes and Pathology
Calcific Aortic Valve Disease
VICs undergo osteogenic reprogramming that
promotes the mineralization of the extracellular
matrix and the progression of fibrocalcific
remodeling of the valve.
33

34. Causes and Pathology
Calcific Aortic Valve Disease
34

35. Causes and Pathology
Calcific Aortic Valve Disease
Familial clustering of calcific AS also has been
described, suggesting a possible genetic
predisposition to valve calcification
Genetic polymorphisms have been linked to the
presence of calcific AS, including those
involving the vitamin D receptor, interleukin
(IL)-10 alleles, estrogen receptor, transforming
growth factor (TGF)-ß receptor, and the
apolipoprotein E4 allele
35

36. Causes and Pathology
Rheumatic Aortic Stenosis
Rheumatic AS results from adhesions and
fusions of the commissures and cusps and
vascularization of the leaflets of the valve ring,
leading to retraction and stiffening of the free
borders of the cusps.
Calcific nodules develop on both surfaces, and
the orifice is reduced to a small, round or
triangular opening.
36

37. Causes and Pathology
Rheumatic Aortic Stenosis
37

38. Causes and Pathology
Rheumatic Aortic Stenosis
Rheumatic AS results from adhesions and
fusions of the commissures and cusps and
vascularization of the leaflets of the valve ring,
leading to retraction and stiffening of the free
borders of the cusps.
Calcific nodules develop on both surfaces, and
the orifice is reduced to a small, round or
triangular opening.
38

39. Causes and Pathology
Rheumatic Aortic Stenosis
As a consequence, the rheumatic valve often is
regurgitant as well as stenotic. Patients with
rheumatic AS invariably have rheumatic
involvement of the mitral valve.
With the decline in rheumatic fever in
developed nations, rheumatic AS is decreasing
in frequency, although it continues to be a
major problem on a worldwide basis.
39

40. Age < 70 years
(n=324)
Age >70 years
(n=322)
1. Bicuspid AV(50%) Degenerative(48%)
(Hypertension)
2. Rheumatic(25%) Bicuspid(27%)
3. Degenerative(18%)Rheumatic(23%)
4. Unicommissural(3%)Hypoplastic(2%)
5. Hypoplastic(2%)
6. Indeterminate(2%)
Causes

42. Calcific Aortic
Stenosis
Nodularcalcificmassesonaortic
sideof cusps.
No commissuralfusion.
Freeedgesofcuspsarenot
involved.
Stellate-shaped systolicorifice.

43. Parasternal long
axis view showing
echogenic and
immobile aortic
valve.

44. Parasternalshort-axis
viewshowingcalcified
aorticvalveleaflets.
Immobilityofthecusps
resultsinonlyaslitlike
aorticvalveorificein
systole

45. Bicuspid Aortic
valve
Fusionofthe
rightandleft
coronarycusps(80%).
Fusionoftheright
andnon-coronary
cusps(20%).

46. Two cusps are seen in systole with only two
commissures framing an elliptical systolic
orifice.
Diastolic images may mimic a tricuspid valve
when a raphe is present.

48. Parasternal long-axis echo
may Showan asymmetric
closure linesystolic doming
Diastolicprolapse of the cusps
In children, valve may beStenoticwithout extensive
calcification.

49. In adults, stenosis typically is due to calcific
changes, which often obscures the number of
cusps, making determination of bicuspid vs.
tricuspid valve difficult.

50. Rheumatic Aortic
Stenosis
Characterized by
Commissural fusion
Triangular systolic orifice
thickening & calcification
Accompanied by rheumatic mitral valve
changes.

51. Parasternal short axis view showing
commissural fusion, leaflet thickening and
calcification, small triangular systolic orifice

52. Subvalvularaortic
stenosis
Thin discrete membrane consisting of
endocardial fold and fibrous tissue.
A fibromuscular ridge.
Diffuse tunnel-like narrowing of the LVOT.
Accessory or anomalous mitral valve tissue.

53. Supravalvular Aortic
stenosis
Type I -Thick, fibrous ring above the aortic valve
with less mobility and has the easily identifiable
'hourglass' appearance of the aorta.

54. Type II -Thin, discrete fibrous membrane
located above the aortic
valve.
The membrane usually mobile and may
demonstrate doming during systole.
Type III -Diffuse narrowing.

55. Pathophysiology
Valve Obstruction
In adults with calcific AS, a significant burden
of leaflet disease is present before obstruction
to outflow develops.
However, once even mild obstruction is
present, hemodynamic progression occurs in
almost all patients, with the interval from mild
to severe obstruction ranging from less than 5
to more than 10 years
55

56. Pathophysiology
Valve Obstruction
56

57. Pathophysiology
Valve Obstruction
In adults with calcific AS, a significant burden
of leaflet disease is present before obstruction
to outflow develops.
However, once even mild obstruction is
present, hemodynamic progression occurs in
almost all patients, with the interval from mild
to severe obstruction ranging from less than 5
to more than 10 years
57

58. Pathophysiology
Valve Obstruction
Stages of ValvularAortic Stenosis(AS)
From Nishimura RA, Otto CM, Bonow RO, etal
58

59. Pathophysiology
Valve Obstruction
Stages of ValvularAortic Stenosis(AS)
From Nishimura RA, Otto CM, Bonow RO, etal
59

60. Pathophysiology
Valve Obstruction
Stages of ValvularAortic Stenosis(AS)
From Nishimura RA, Otto CM, Bonow RO, etal
60

61. Pathophysiology
Valve Obstruction
Stages of ValvularAortic Stenosis(AS)
From Nishimura RA, Otto CM, Bonow RO, etal
61

62. Pathophysiology
Valve Obstruction
Stages of ValvularAortic Stenosis(AS)
From Nishimura RA, Otto CM, Bonow RO, etal
62

63. Pathophysiology
Valve Obstruction
The degree ofstenosisassociated with
symptom onset varies among patients,
however, and no single number defines severe
or critical AS in an individual patient.
63

64. Pathophysiology
Hypertrophic Myocardial Remodeling
Maintenance of cardiac output in the face of an
obstructedaorticvalve imposes a chronic
increase in LV pressure
In response, the ventricle typically undergoes
hypertrophic remodeling characterized by
myocyte hypertrophy and increased wall
thickness
64

65. Pathophysiology
Hypertrophic Myocardial Remodeling
65

66. Pathophysiology
Hypertrophic Myocardial Remodeling
Based on LaPlace law, LV remodeling reduces
wall stress (afterload) and is considered one of
the important compensatory mechanisms to
maintain LV ejection performance, which is
directly affected by afterload
66

67. Pathophysiology
Hypertrophic Myocardial Remodeling
increased LV hypertrophic remodeling is
associated with more severe ventricular
dysfunction and heart failure (HF) symptoms,
as well as higher mortality
hypertrophic remodeling in patients with AS is
determined by several factors other than the
severity of valve obstruction, including sex,
genetics, vascular load, and metabolic
abnormalities
67

68. Pathophysiology
Hypertrophic Myocardial Remodeling
increased LV hypertrophic remodeling is
associated with more severe ventricular
dysfunction and heart failure (HF) symptoms,
as well as higher mortality
hypertrophic remodeling in patients with AS is
determined by several factors other than the
severity of valve obstruction, including sex,
genetics, vascular load, and metabolic
abnormalities
68

69. Pathophysiology
Left Ventricular Diastolic Function
Hypertrophic remodeling also impairs diastolic
myocardial relaxation and increases stiffness
Higher cardiomyocyte stiffness, increased
myocardial fibrosis, advanced-glycation end
products, and metabolic abnormalities each
contribute to increased chamber stiffness and
higher end-diastolic pressures.
69

70. Pathophysiology
Left Ventricular Diastolic Function
Hypertrophic remodeling also impairs diastolic
myocardial relaxation and increases stiffness
Higher cardiomyocyte stiffness, increased
myocardial fibrosis, advanced-glycation end
products, and metabolic abnormalities each
contribute to increased chamber stiffness and
higher end-diastolic pressures.
70

71. Pathophysiology
Left Ventricular Diastolic Function
Atrial contraction plays a particularly important
role in filling of the left ventricle in AS because
it increases LV end-diastolic pressure without
causing a concomitant elevation of mean left
atrial pressure.
71

72. Pathophysiology
Left Ventricular Diastolic Function
This “booster pump” function of the left atrium
prevents the pulmonary venous and capillary
pressures from rising to levels that would
produce pulmonary congestion, while
maintaining LV end-diastolic pressure at the
elevated level necessary for effective
contraction of the hypertrophied left ventricle.
72

73. Pathophysiology
Left Ventricular Diastolic Function
Loss of appropriately timed, vigorous atrial
contraction, as occurs in atrial fibrillation (AF)
or atrioventricular dissociation, may result in
rapid clinical deterioration in patients with
severe AS.
73

74. Pathophysiology
Left Ventricular Diastolic Function
After surgical relief of AS, diastolic dysfunction
may revert toward normal with regression of
hypertrophy, but some degree of long-term
diastolic dysfunction typically persists.
74

75. Pathophysiology
Left Ventricular SystolicFunction
Left ventricular systolic function, as measured
by the ejection fraction (EF), remains normal
until late in the disease process in most
patients with AS.
Nonetheless, more subtle systolic dysfunction
can be detected as reduced longitudinal
systolic strain before a reduction in the EF
75

76. Pathophysiology
Left Ventricular Systolic Function
The development and severity of systolic
dysfunction is the result ;
the severity of valve obstruction,
metabolic abnormalities,
vascular load,
inadequate hypertrophy (given the
inverse correlation between wall stress and
systolic performance),
maladaptive hypertrophy (resulting in
impaired contractility),
ischemia, and fibrosis.
76

77. Pathophysiology
Myocardial Fibrosis
Cardiac fibrosis is an emerging risk factor for
adverse clinical outcomes in patients with AS
As a part of the hypertrophic remodeling
process, diffuse and replacement myocardial
fibrosis (not fibrosis from prior MI) may
develop.
77

78. Pathophysiology
Left Ventricular SystolicFunction
Importantly, patients with severe fibrosis,
despite a normal EF, are more likely to have
worse preoperative HF symptoms and less
likely to experience improvement in symptoms
midterm after valve replacement, compared to
those with no or minimal fibrosis before valve
replacement
78

79. Pathophysiology
Pulmonary and Systemic Vasculature
The hypertrophied and pressure overloaded left
ventricle transmits increased pressure to the
pulmonary vasculature, which leads to
pulmonary hypertension in many patients with
AS, becoming severe in 15% to 20%.
pulmonary hypertension is associated with
increased postoperative mortality
79

80. Pathophysiology
Pulmonary and Systemic Vasculature
The hypertrophied and pressure overloaded left
ventricle transmits increased pressure to the
pulmonary vasculature, which leads to
pulmonary hypertension in many patients with
AS, becoming severe in 15% to 20%.
pulmonary hypertension is associated with
increased postoperative mortality
80

81. Pathophysiology
Myocardial Ischemia
In patients with AS, the hypertrophied left
ventricle, increased systolic pressure, and
prolongation of ejection all elevate myocardial
oxygen (O2) consumption.
81

82. Pathophysiology
Myocardial Ischemia
At the same time, even in the absence of
epicardial coronary disease, decreased
myocardial capillary density in the
hypertrophied ventricle, increased LV end-
diastolic pressure, and a shortened diastole all
serve to decrease the coronary perfusion
pressure gradient and myocardial blood flow.
82

83. Pathophysiology
Myocardial Ischemia
Together, this creates an imbalance between
myocardial O2 supply and demand, with the
ischemia most pronounced in the
sub-endocardium.
83

84. Pathophysiology
Myocardial Ischemia
Exercise or other states of increased O2
demand may exacerbate this imbalance and
cause angina indistinguishable from that
caused by epicardial coronary obstruction.
84

85. Clinical Presentation
Symptoms
The cardinal manifestations of acquired AS are
exertional dyspnea,
angina, syncope, and
ultimately HF.
85

86. Clinical Presentation
Symptoms
Symptoms typically begin at age 50 to 70 years
with bicuspid aortic valve stenosis and
in those older than 70 with calcific stenosis of a
trileaflet valve,
although even in this age group approximately
40% of patients with AS have a congenital
bicuspid valve
86

87. Clinical Presentation
Symptoms
The most common clinical presentation in
patients with a known diagnosis of AS who are
followed prospectively is a gradual decrease in
exercise tolerance, fatigue, or dyspnea on
exertion
87

88. Clinical Presentation
Symptoms
The mechanism of exertional dyspnea may be
LV diastolic dysfunction, with an excessive rise
in end-diastolic pressure leading to pulmonary
congestion
Alternatively, exertional symptoms may be a
result of the limited ability to increase cardiac
output with exercise.
88

89. Clinical Presentation
Symptoms
More severe exertional dyspnea, with
orthopnea,
paroxysmal nocturnal dyspnea, and
pulmonary edema,
reflects various degrees of pulmonary venous
hypertension
intervention typically is undertaken before this
disease stage.
89

90. Clinical Presentation
Symptoms
Angina is a frequent symptom of patients with
severe AS and usually resembles the angina
observed in patients with coronary artery
disease (CAD) in that it is usually precipitated
by exertion and relieved by rest
90

91. Clinical Presentation
Symptoms
In patients with CAD, angina is caused by a
combination of epicardial coronary artery
obstruction and the O
2imbalance characteristic
of AS.
Very rarely, angina results from calcific emboli
to the coronary vascular bed.
91

92. Clinical Presentation
Symptoms
Syncopemost often is caused by the reduced
cerebral perfusion that occurs during exertion
when arterial pressure declines because of
systemic vasodilation and an inadequate
increase in cardiac output related to
valvularstenosis.
92

93. Clinical Presentation
Symptoms
Syncopemost often is caused by the reduced
cerebral perfusion that occurs during exertion
when arterial pressure declines because of
systemic vasodilation and an inadequate
increase in cardiac output related to
valvularstenosis.
93

94. Clinical Presentation
Symptoms
Syncopealso has been attributed to
malfunction of the baroreceptor mechanism in
severe AS, as well as to a vasodepressor
response to a greatly elevated LV systolic
pressure during exercise
Exertional hypotension also may be manifested
as “graying-out spells” or dizziness on effort
94

95. Clinical Presentation
Symptoms
Syncopeat rest may be caused by transient
AF with loss of the atrial contribution to LV
filling, which causes a precipitous decline in
cardiac output, or to transient atrioventricular
(AV) block caused by extension of the
calcification of the valve into the conduction
system.
95

96. Clinical Presentation
Symptoms
Gastrointestinal (GI) bleeding may develop in
patients with severe AS, often associated with
angiodysplasia (most frequently of the right
colon) or other vascular malformations
This complication arises from shear stress–
induced platelet aggregation with a reduction
in high-molecular-weight multimers of von
Willebrand factor and increases in proteolytic
subunit fragments
96

97. Clinical Presentation
Symptoms
Infective endocarditis has been documented
in patients withaorticvalve disease,
particularly in younger patients with a
bicuspid valve.
Cerebral emboli resulting in stroke or
transient ischemic attacks (TIAs) may be
caused by microthrombi on thickened
bicuspid valves.
97

98. Clinical Presentation
Symptoms
Calcific AS rarely may cause embolization of
calcium to various organs, including the
heart, kidneys, and brain.
98

99. Clinical Presentation
Physical Examination
The key features of the physical examination in
patients with AS are
palpation of the carotid upstroke,
evaluation of the systolic murmur,
assessment of splitting of the second heart
sound (S2),
signs of HF
99

100. Clinical Presentation
Physical Examination
The carotid upstroke directly reflects the
arterial pressure waveform. The expected finding
with severe AS is a
slow-rising, late-peaking, low-amplitude carotid
pulse, theparvusand tarduscarotid impulse.
When present, this finding is specific for severe
AS.
100

101. Clinical Presentation
Physical Examination
Also with severe AS, radiation of the murmur to
the carotid arteries may result in a palpablethrill
or carotid shudder.
101

102. Clinical Presentation
Physical Examination
Auscultation
The ejection systolic murmur of AS typically is
late-peaking and heard best at the base of the
heart, with radiation to the carotids.
Cessation of the murmur before A
2is helpful in
differentiation from a pansystolic mitral murmur.
102

103. Clinical Presentation
Physical Examination
Auscultation
In patients with calcifiedaorticvalves, the
systolic murmur is loudest at the base of the
heart,
but high-frequency components may radiate
to the apex—the so-calledGallavardin
phenomenon,in which the murmur may be so
prominent that it is mistaken for the murmur of
mitral regurgitation (MR)
103

104. Clinical Presentation
Physical Examination
Auscultation
In general, a louder and later-peaking murmur
indicates more severestenosis.
However, although a systolic murmur of grade 3
intensity or greater is relatively specific for severe
AS, this finding is insensitive, and many patients
with severe AS have only a grade 2 murmur
104

105. Clinical Presentation
Physical Examination
Auscultation
When the left ventricle fails and stroke volume
falls, the systolic murmur of AS becomes softer;
rarely, it disappears altogether.
105

106. Clinical Presentation
Physical Examination
Auscultation
With severe AS, S
2may be single because
calcification and immobility of theaorticvalve
make A
2inaudible, (2) closure of the pulmonic
valve (P
2) is buried in the
prolongedaorticejection murmur, or (3)
prolongation of LV systole makes A
2coincide with
P
2.
-Paradoxical splitting is also seen
106

107. Clinical Presentation
Dynamic Auscultation
Auscultation
The intensity of the systolic murmur varies from
beat to beat when the duration of diastolic filling
varies, as in AF or after a premature contraction.
This characteristic is helpful in differentiating AS
from MR, in which the murmur usually is
unaffected.
107

108. Clinical Presentation
Dynamic Auscultation
Auscultation
The murmur of valvular AS is augmented by
squatting, which increases stroke volume. It is
reduced in intensity during the strain of the
Valsalva maneuver and on standing, both of
which reduce transvalvular flow.
108

109. Diagnostic Testing
109

110. Diagnostic Testing
Echocardiography.
110

111. Echocardiography.
1. valve calcification.
111

112. Echocardiography.
2. LVOT diameter
112

113. Echocardiography.
2. LVOT diameter
113

114. Echocardiography.
3. Measure ascending aorta
114

115. Echocardiography.
3. Measure ascending aorta
115
1= 34mm +/-0.3
2= 29mm +/-0.3
3= 30mm +/-0.3

116. Echocardiography.
3. Measure ascending aorta
116

117. Echocardiography.
3. Aortic orifice planimetry
117

118. Echocardiography.
3. Analyse en doppler pulse
118

119. Echocardiography.
3. PW doppler
119

120. Echocardiography.
3. CW doppler
120

121. Echocardiography.
3. CW doppler
121

122. Echocardiography.
3. contiuity equation
122

123. Echocardiography.
In AF
123

124. Echocardiography.
In AF
124

125. Echocardiography.
Velocity ratio
125

126. Echocardiography.
Aortic Valve resistance
126

127. Echocardiography.
TEE
127

128. Echocardiography.
TEE
128

129. Echocardiography.
Stress Echo
129

130. Echocardiography.
Dilation of ascending aorta , LA
130

131. Echocardiography.
Dilation of ascending aorta , LA
131

132. Echocardiography.
Severity of AS
132

133. Echocardiography.
Low gradient AS with normal EF
133

134. Echocardiography.
Low gradient AS with Reduced EF
134

135. Echocardiography.
Dobutamine Echo
135

136. Echocardiography.
Dobutamine Echo
136

137. Exercise Stress Testing
Exercise testing may be helpful in apparently
asymptomatic patients to unmask symptoms or
demonstrate limited exercise capacity or an
abnormal BP response.
Exercise stress testing should be absolutely
avoided in symptomatic patients
137

138. Cardiac Computed Tomography
CT is also a routine part of the preprocedural
evaluation of patients having AVR, principally to
look for a porcelain aorta, as well as determine
appropriate valve sizing and assess aortic and
peripheral vascular anatomy when a
transcatheter approach is considered.
138

139. Cardiac Computed Tomography
CT is also a routine part of the preprocedural
evaluation of patients having AVR, principally to
look for a porcelain aorta, as well as determine
appropriate valve sizing and assess aortic and
peripheral vascular anatomy when a
transcatheter approach is considered.
139

140. Cardiac Computed Tomography
CT is useful for evaluating aortic dilation in
patients with evidence or suspicion of aortic
root disease on echocardiography or chest
radiography, particularly those with a bicuspid
valve
140

141. Cardiac Catheterization
Cardiac catheterization is now recommended
only when noninvasive tests are inconclusive,
when clinical and echocardiographic findings
are discrepant, and for coronary angiography
before surgical intervention
141

142. Cardiac Magnetic Resonance
Imaging
CMR is useful for assessing LV volume,
function, and mass, especially in settings where
this information cannot be obtained readily
from echocardiography
142

143. Positron Emission Tomography
(PET) identifies active tissue calcification and
predicts change in aortic valve calcification on
follow-up CT 1 to 2 years later
143

144. Positron Emission Tomography
144

145. Treatment
145

146. Treatment
1. Medical Management
Medical therapy has not been shown to affect
disease progression in patients with AS
treatment of hypertension
Angiotensin-converting-enzyme (ACE) inhibitors
or angiotensin receptor blockers (ARBs) may
preferentially considered.
146

147. Treatment
Medical Management
heart failure -diuretics.
phosphodiesterase type 5 inhibition -improve
pulmonary and systemic hemodynamics
147

148. Treatment
Surgical Management
148

149. Balloon Aortic Valvuloplasty
In selected cases, it might be reasonable as a
bridge to definitive treatment with AVR in
unstable patients or as a palliative procedure in
patients who are not candidates for AVR.
149

150. AorticValve Replacement
AVR is recommended for adults with
symptomatic severe AS, even if symptoms are
mild
150

151. 151

152. Surgical Aortic Valve
Replacement
The Society of Thoracic Surgeons (STS)
National Database Committee reported an
overall operative mortality rate of 3.2% in
67,292 patients undergoing isolated AVR and
5.6% in 66,074 patients undergoing AVR and
CABG
152

153. Transcatheter Aortic Valve
Replacement
In patients deemed high risk for surgery, TAVR
was shown to be noninferior and perhaps
superior to SAVR.
153

154. Indications of TAVI
154

155. Indications of TAVI
155

156. Contraindications of TAVI
156

157. 157

159. Indications
for
surgery
159

160. Disease Course
Asymptomatic Patients
Generally, repeat imaging is performed every
6 to 12 months for severe AS,
every 1 to 2 years for moderate AS, and
every 3 to 5 years for mild AS,
unless a change in signs or symptoms prompts
repeat imaging sooner
160

161. Disease Course
Asymptomatic Patients
Generally, repeat imaging is performed every
6 to 12 months for severe AS,
every 1 to 2 years for moderate AS, and
every 3 to 5 years for mild AS,
unless a change in signs or symptoms prompts
repeat imaging sooner
161

162. Disease Course
Asymptomatic Patients
Of patients with mild valve thickening but no
obstruction to outflow (e.g., aortic sclerosis),
16% will have valve obstruction at 1 year of
follow-up, but only 2.5% will develop severe
valve obstruction at an average of 8 years
after the diagnosis of aortic sclerosis.
162

163. Disease Course
Asymptomatic Patients
Of patients with mild valve thickening but no
obstruction to outflow (e.g., aortic sclerosis),
16% will have valve obstruction at 1 year of
follow-up, but only 2.5% will develop severe
valve obstruction at an average of 8 years
after the diagnosis of aortic sclerosis.
163

164. Disease Course
Asymptomatic Patients
Survival free of symptoms is 84% at 2 years
when aortic velocity is less than 3m/sec,
compared with only 21% when velocity is
greater than 4m/sec
164

165. Disease Course
Asymptomatic Patients
exercise testing and serum B-type natriuretic
peptide (BNP) levels have been evaluated as
measures of disease progression and predictors
of symptom onset.
165

166. Disease Course
Symptomatic Patients
Once even mild symptoms are present, survival
is poor unless outflow obstruction is relieved.
average survival without AVR is only 1 to
3 years after symptom onset
166

167. Disease Course
Symptomatic Patients
Among symptomatic patients with severe AS,
the outlook is poorest when the left ventricle
has failed and the cardiac output and
transvalvular gradient are both low.
The risk of sudden death is high with
symptomatic severe AS, so these patients
should be promptly referred for AVR.
167

168. Disease Course
Symptomatic Patients
Among symptomatic patients with severe AS,
the outlook is poorest when the left ventricle
has failed and the cardiac output and
transvalvular gradient are both low.
The risk of sudden death is high with
symptomatic severe AS, so these patients
should be promptly referred for AVR.
168

169. 169