2.  AS causes progressive obstruction to LVOT
resulting in pressure hypertrophy of LV and
S/S/O HF, angina and syncope.
 obstruction most commonly occurs at
valvular level, though it may occur sub
valvular or supravalvular

3.  Calcified Ao valve disease:
› M. C cause of AS in adults
› Related to active process of inflammation
involving RAS, lipid accumulation, resultant
calcification
› Asso. With atherosclerosis, smoking, HTN,
dyslipidemia
› Increased risk of CV death, MI.
› Other condition asso are paget’s disease and
ESRD

5.  Bicuspid Ao Valve:
› Most common is fusion of Rt and LT cusps.
› Concurrent Coarctation, Ao root dilatation,
propensity for Ao dissection.
› Present in 1-2% of population
› Severe stenosis develops by 4th-5th decade
› Unicuspid valve are uncommon and usually
severely stenotic at early age.

6.  Current ACC/AHA guidelines recommend
evaluation of AV valve by echo regularly
› Ao dia > 4cm and bicuspid valve shuold have
yearly follow up
› Ao dia >5 cm or increase by >0.5cm/yr surgical
intervention recommoded
› If valve requires surgery, aorta replacement is
recomomnded if >4.5cm @ time of surgery
 Rheumatic AS:
› Often co exists with AR, and MV lesions
› Rare cause of isolated AS

7.  Congenital condition, may not be apparent at
birth
 Circumferential fibromuscular membrane
involving AMV leaflet (+) in LVOT below AV
 Maladaptive response to abnormal flow
dynamics in LVOT. Though not clear
 Difficult to diagnose when asso, HOCM and
LVH present

8.  Shone’s syndrome:
› Supravalvular MV membrane
› Parachute MV(single PM attached to both MV leaflets)
› Sub aortic stenosis
› Coarctation of aorta

9.  Uncommon
 Caused by lipid deposition in familial
hypercholesterolemia
 Part of congenital Williams syndrome,
caused by mutation in elastin gene
› Hypercalcemia
› Elfin facies
› Devp delay
› Small strature
› Multiple stenoses in AO and periph art

10.  Resistance to systolic ejection occurs and a systolic
pressure gradient develops between the left
ventricle and the aorta.
 This outflow obstruction leads to an increase in left
ventricular (LV) systolic pressure and after load
 As a compensatory mechanism to normalize LV
wall stress, LV wall thickness increases by parallel
replication of sarcomeres, producing concentric
hypertrophy.
 At this stage, the chamber is not dilated and
ventricular function is preserved, although diastolic
compliance is reduced.

11.  LV end-diastolic pressure (LVEDP) rises, which
causes a corresponding increase in pulmonary
capillary arterial pressures and a decrease in
cardiac output due to diastolic dysfunction.
 contractility of the myocardium may also diminish,
which leads to a decrease in cardiac output due to
systolic dysfunction. Ultimately, heart failure
develops.
 Diastolic dysfunction due to:
› impaired LV relaxation and/or decreased LV compliance
› increased afterload,
› LV hypertrophy, or myocardial ischemia.

12.  Atrial contraction plays a particularly important role
in diastolic filling of the left ventricle.
 Development of AF in AS often leads to heart failure
due to an inability to maintain cardiac output.
 Myocardial perfusion compromised by:
› relative decline in myocardial capillary density
› reduced diastolic transmyocardial (coronary) perfusion
gradient due to elevated LV diastolic pressure.
› the subendocardium is susceptible to underperfusion,
which results in MI.

13.  myocardial oxygen requirement increased:
› Increased LV mass
› increased LV systolic pressure
› prolongation of the systolic ejection phase,
especially in the subendocardial region.
› Although coronary blood flow may be normal
when corrected for LV mass, coronary flow
reserve is often reduced.

14.  Angina results from a
› concomitant increased oxygen requirement by
the hypertrophic myocardium
› diminished oxygen delivery secondary to
diminished coronary flow reserve
› decreased diastolic perfusion pressure
› and relative subendocardial myocardial ischemia

15. Risk of SCD <2%
Aymptomatic valvular AS:
Mean AVG increase by 7mm
Hg/yr
AV area decrese by 0.1cm2/yr

16.  Severe symptomatic AS
› SCD can occur in case of hypotension, arrythmia
› Exercise stress testing is absolutely
contraindicated

17.  Asymptomatic latent period of 10-20 years.
 Exertional dyspnea is the most common initial
complaint, exertional chest pain, effort dizziness
or lightheadedness, easy fatigability, and
progressive inability to exercise.
 Classic triad of
› chest pain
› heart failure
› syncope

18.  carotid arterial pulse typically has a delayed and
plateaued peak, decreased amplitude, and gradual
downslope (pulsus parvus et tardus).
 Narrow pulse pressure
 Pulsus alternans can occur in the presence of LV
systolic dysfunction.
 The jugular venous pulse may show prominent a
waves reflecting reduced right ventricular
compliance consequent to hypertrophy of the
interventricular septum.
 A hyperdynamic LV is unusual and suggests
concomitant aortic regurgitation or mitral
regurgitation.
 Palpable systolic thrill 2nd Rt IC space

19.  S1 is usually normal or soft.
 A2, is usually diminished or absent
 Paradoxical splitting of the S2 also occurs,
resulting from late closure of A2 in case of
severe AS
 S3- poor LV systolic function
 S4- reduced LV compliance

20.  The classic crescendo-decrescendo systolic
murmur of aortic stenosis
› begins shortly after the first heart sound
› intensity increases toward midsystole, then
decreases, and the murmur ends just before the
second heart sound.
› rough, low-pitched sound that is best heard at the
second intercostal space in the right upper sternal
border in sitting position at the end of full expiration
› radiates to 1 or both carotid arteries.
 In elderly persons with calcific aortic stenosis,
however, the murmur may be more prominent
at the apex, because of radiation of its high-
frequency components (Gallavardin
phenomenon). Mistaken as a MR.

21.  ECG:
› LVH with strain pattern
› LA enlargement
› AF
› IV conduction defect
 CXR:
› Mostly normal
› Concentric LVH cardiac silhoutee boot shaped
› Cardiomegaly if concomitant AR +

23.  Two-dimensional and Doppler
echocardiography is the imaging modality of
choice to diagnose and determine the
severity of aortic stenosis
 Regular follow with echo
› Asymptomatic severe: yearly
› As pt became symptomatic or develop new
symptoms
› moderate AS: 1-2 years follow up
› Mild AS: 3-5 yrs

24.  PLAX:
› Mechanism and severity of AS
› Degree of LVH
› LA/LV enlargement
› LVOT dia.
› Systolic leaflet doming can be seen in congenital
or rhematic AS
 PSAX:
› Most useful for cause of congenital AS

25.  A5C:
› CWD in LVOT recorded for conitnuity equation
› From suprasternal view As Ao and Ds Ao
diameter can be measured
 TEE:
› Morphology of valve
› Diagnosis of sub aortic membrane to differentiate
b/w HOCM or valvular AS

26.  Doppler echocardiography:
› Standard for TVPG and AVA
› Simplified bernoullis equation
› Continuity principle(physiologic area)
 Cardiac catheterization:
› Pt >50yrs of age, angina, significant CAD risk
factors
› Severe AS low osmolar non ionic contrast
› Gorlin fromula to calculate AVA(true anatomic
area)
› Hakki equation: simplified gorlin firmula

27.  Asymptomatic:
› Primary CAD prevention, BP control, maintain sinus
rhythm
 Symptomatic:
› Rx for HF: diuretics and NTG: used cautiously
› LVD /AF: digitalis/ACEI, avoid Beta blocker
› Severe AS + CAD: surgical Mx optimal
 Vasodialtors relatively C/I:
› Aggravates syncope ; decrease SVR
 Statins:
 Antibiotic prophylaxis:
› Prior to dental surgery only in H/O IE and prosthetic
valves

28.  Percutaneous Aortic Balloon Valvuloplasty:
› Pediatric, congenital, non-calcified AS
› AR can occur as a complication
› AVR necessray after 10 years of PABV
› Not useful for adults
› In all symptomatic pt and asymptomatic pt with
TVG >60mmHg or ST-T changes on ecg

29.  Symptomatic pt with severe AS
 Severe AS + LVEF <50%
 Severe AS or moderate AS undergoing CABG
or other valvular surgeries
 Ross procedure: (homografts)
› In pediatrics or adolescent
› IE of naive or prosthetic valve with pyogenic
complication
› When LVOT is very small

30.  Mechanical valves
› St. Jude, medrotonic hall and carbomedics
› Requires anti coagulant life long
 Bioprosthetic valves
› Porcine heterografts or bovine pericardial
prostheis
› Age >60 yrs
› Low thromboembolism
› No long term anticoagulant

31.  CABG in Mod MS:
› Benefit + if AVA <1.5 cm2
 High risk pt AVR recommended:
› Highly calcified AV valve & rapid rise in pressure
gradient
› Trans aortic flow velocity >4m/s
› LVD d/t AS
› Exercise induced hypotension
› PAH >60mmHg
› Before pregnancy

32.  LVD d/t afterload mismatch Sx corretion
leads to improvement/ normalization of LVEF
 Primary contractile dysfunction: overall poor
prognosis/ unlikely to get benefit from AVR
 High TVG:
› Measure of high afterload mismatch
› TVG >40 mmHg= AVR recommended

33.  Low TVG:
› Severe AS <1.0cm2 and low TVG < 30 mmHg
poor prognosis with out surgical correction
› Improved after surgical treatment if they
demonstrate contractile reserve
 Contractile reserve:
› Ability to increase TV flow >20% from baseline
when challenged with dobutamine

34.  True AS: (dobutamine)
› Increase CO, TVG
› AVA same
 Vasodilator:
› TVG increase
› CO not
› AVA same/ decrease
 Aorti
pseudostenosis:
(dobutamine)
› Increase CO
› TVG not increase
› AVA incr. >0.3 cm2
 Vasodiator:
› Increase CO
› Dec. TVG
› AVA increase

35.  Severe AS; low gradient; preserved LVEF
early surgical intervention recommended
 Subaortic stenosis: surgical removal of
membrane
› Symptomatic
› Asymptomatic: PG >50mmHg or assoicated
more than mod AR.