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• Aortic stenosis is the most common valvelesion in
adults with chronic valvular HD
Types:
Valvular As
AQRTIC STENQSIS
Sub-valvular As
Supra valvular As
Etiologies
Congenital bicuspid aortic valve
Rheumatic fever
Degenerative calcified aortic valve disease Active biologic process
AfraTafreeh.cdms
Normal Aortic valve
Rheumatic AS
O0:02:10
Similar to vascular
atherosclerosis
Congenital Bicuspid
Aortic Stenosis
Calcific Degenerative AS
Aortic Stenosis
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Radiation
Mechanical stres
Lipid infiltration
Lipid-derived species
Cytokines
SPLA,
VIC
Lp(a)
Ox-LDL
Ox-PL
AT
S-LO
Leukptrienes
NOS
ATX lysoPC
Lp-PLA,
oupling
LPAR
AA
LDL
lusoPA
COX2
MMPs
VEGF
Prostaglandins
aortic valve
TNE
BMP2
IL-sß
TGFB
IL-6
WNT3a
Arp
AfraTafreeh.com
Inflamimation
Angiotgnsin
→Chymase ACE
+PPi
AMP Adenosine
ALP|
Angiotensin l
P
RANKL,
TNE
LDL
Mineralization
VEGE
Collagen
Fibrosis
Calcification
AD, common in males
Fibro-calcific response
Congenital Bicuspid aortic valve:
Lipids
Caleium
hydroxyapatite
Inflammation
Transforms into osteoblasts
Monocyte
Osteogenice transition
3Mastocyte
T oell
Formation of bone matrix protein
Apoptosis
Valve interstitial cells/ Valvular myofibroblasts in
Blood
vessel
Macrophage
Calcifying
Deposition of calcium hydroxyapatite in the form of
LOGInodules
microvesicles
• Rheumatic fever associated with coexistinq mitral
valve disease along with in AR
• It is mnost common congenital heart valve defect
Aortic Stenosis
2
• Turner syndrome increases the risk
• It associated with AS, Aneurysm, Dissection
Pathophysiology:
• It is left ventricular outflow tract obstruction
Creates a Systolic pressure gradient between LV&
aorta (Trans-aortic valve pressure gradient)
It decreases Cardiac output
Adoptive response → Concentric LV hypertrophy
(Maladaptive response) → lschemia
tLV Systolic
pressure
tLV mnass
LV dysfunction
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Aortic stenosis
LV outflow obstruction
tLVET
TMyocardial
0, consumption
LV diastolic AO pressure
pressure
LDiastolic
time
O0:11:18
• Aortic stenosis 4Omm Hg
Aortic Stenosis
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Clinical presentation
• Long asymptomatic period d/t compensatory
Concentric LV hypertrophy
• Common age: 6th togth decade
Classical triad of AS
Classical triad of AS:
Angina
Dyspnea:
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exercise
Exertional dyspnea
• Initially fatigue, decreased exercise tolerance, finally
leads exertional dyspnea
Angina:
Dyspnea d/t LV diastolicdysfunction (↑ EDP leads
topulmonary congestion) and inability to tCO with
LOGIN OR SUCO
decompensation
Syncope
• AS associated MS → Atrial fibrillation → Acute
O0:16:40
• d/t demand-supply mismatch
relived by rest)
Mimies angina of CAD (Precipitated by excursion
• Coexistent CAD may present
Aortic Stenosis
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Syncope:
• d/t yCO → Cerebral hypoperfusion
Sometimes presyncopal episode like mild dizziness
qiddiness, blackouts may present
Heart failure:
• Features of heart failure (LV or RV) seen in
advanced severe AS
LV failure
Orthopnea
- PND
- Pulmonary
RV failure
Co existent AS+ MS:
- Pulmonary
congestion
oedema AraTafreeh.com
MS lowers the TAV pressure gradient
• This can mask the findings of AS
SccEss
Aortic Stenosis
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G bleeding:
ASsociated with HAYDE Syndrome
Gt bleeding
d/t associated
manifestation:
Angiodysplasia of right
side colon
AS
Infective endocarditis:
valve
Pulse:
Increased risk of IE in young pt with bicuspid aortic
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Examination findings
Small micro thrombi in BAV → Cerebral embolism
& stroke
Acquired WD
LOGN ORSUCCESS
• Early stages - Normal
Usually regular
• Advanced cases → Low volume pulse
O0:26:50
• In case AF → Irregular pulse
• Character - slow rising late peaking pulse (or)
"Pulsus parvus at tardus (or) Anacrotic pulse
Aortic Stenosis
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S45.
Normal arterial pulse waveform
Normal
Blood pressure:
Systole
→Percussion wave
JVP:
Tidal wave
→ diarotic wave
Diastole
Appreciated by simultaneous palpation of carotid
artery and apex, AS shows delay
Narrow pulse pressure
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Systemic hypertension
P
Aortic stenosis
low volume
slow upstroke
sustained peak
slow downstroke
• Thrill/carotid shudder: Palpable over carotid artery
LOGNOR SUC
Lowering of systolic BP (or) systolic decapitation
• A wave is prominent d/t LV hypertrophy
Aortic Stenosis
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Palpation of precordium:
Apex beat:
• Initialy normal in location
• As disease progresses, it displaced laterally d/t LV
concentric hypertrophy
Concentric
hypertrophy
|Apex displaces
downwards
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Systolic thrill:
• Hearing apex (Reflection of pressure overload)
Eccentric hypertrophy
Auscultation:
Apex beat displaced
Mainly at base of heart towards the right of
down & out
sternum and also at suprasternalnotch
• S1 - Normal
Best felt in full expiration & pt leaning forward
• S2 - Abnormal
LOGIN OR SUCCeSS
• In severe as → Prolongation of LV systole
A2 occurs late, sometimes even after P2
Paradoxical split of S2 or Single S2
Aortic Stenosis
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Single S2 d/t:
- A2 coinciding with P2
- A2 is inaudible
• S3:may present in LV failure
• S4: Present d/t vigorous LA contraction against
stiff Noncompliant ventricle
Ejection sound
These are high frequency, clicky systolic sound
• Occurs d/t vibrations associated with opening of
aortic and pulmonary valve
• It can be aortic or pulmonary ejection sound
Aortic ejection sound:raTafreeh.com
• It ishigh frequency, clicking systolic sound and
corresponds to upstroke of carotid
Etiology
- Congenital bicuspid aortic valve
- Ascending aorta aneurysm
Properties
O0:42:19
- It is widely transmitted
- Best heard over apex
- Can be heard over the base (2nd right ICS close to
sternum)
• Intensity dose not vary with in respiration
Aortic Stenosis
Pulmonary ejection sound:
Etiology
- PS
- ldiopathic dilation of pulmonary artery
- Chronic PAH
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Not widely transmitted
• Best heard at Lt 2nd ICS
Intensity decreases with inspiration (This is only
right sided cardiac event which decrease in intensity
with inspiration)
• Note: In calcified rigid aortic valve, aortic ejection
sound is absent
Murmur of AS
Ejection systolic/ Mid systolic murmur
• Starts shortly after S1
ejection
• Increases in intensity, reaches peak at middle of
LOGNOR SUC
O0:44:09
aortic valve closure
Subsequently it decreases in intensity and ends before
That's why it is called Crescendo - decrescendo
murmur (or) Dimond shaped murmur
10
Aortic Stenosis
• AS
2
Differential diagnosis for ESM:
• PS
3
• HOCM
• Large ASD
Character of murmur:
Radiates to carotids
Gallarvardin phenomenon
- As wmurmur radiates to
- It has musical quality
PSM MR,TR,VSD
• Low pitched, rough rasping type om
Loudest at the base of the heart (2nd Rt ICS)
ESM
• Intensity
ESM
Extends to P2
Timing
AS
- It is DDof pansystolic murmur of MR
PS
pencCESS
Correlation between murmur and severity of AS:
Severe AS - Grade 3 or more
- Severe AS - late peaking murmur
-mild to moderate as early peaking murmur
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Aortic Stenosis
• Dynamic auscultation
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- In squatting → 1stroke volume > Augmentation of
murmur
- In standing (or) strain phase of Valsalva →
Attenuation or decrease in intensity of the
murmUr
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Aortic Stenosis