………………………………………………..
 1.rheumatic heart disease:
Is the most common cause resulting from
adhesions and fusions of the commissures
and cusps.
 2. congenitally abnormal aortic valve:
normal valve may be stenotic with
commissural fusion at birth but usually
not causing serious narrowing of the
aortic orifice during childhood.
 The abnormal architecture induces
turbulent flow which traumatizes the
leaflets and leads to fibrosis , increased
rigidity, calcification of leaflets and
narrowing of the aortic orifice in
adulthood.
3.senile aortic stenosis:
Age related AS degeneration and
calcification of previously normal
valve in elderly , usually smokers,
daibetics, hypertension and
hyperlipidemic.
 4.SLE and severe familial
hypercholesterolemia occasionally cause
aortic stenosis.
 7% of total cases of CHD
 Increased pressure in the LF side of the
heart (LV hypertrophy)
 Assessment… murmur ,thrill ,high BP, high
HR.
 Murmur is loudest
 Loudness is
proportional to
severity
 LVH
 ……………
 Obstructed left ventricular outflow due to
aortic stenosis leads to increased left
ventricular pressure and compensatory
left ventricular hypertrophy.
 Cardiac output at rest is maintained
within normal limits in most patients with
severe AS, it often fails to rise normally
during exertion.
 late in the course of the disease , the
cardiac output and stroke volume decline
(due to LV dysfunction) resulting in
decline of pressure gradient across the
aortic valve and rise in pulmonary arterial
pressure.
 Ischemia in AS:
due to hypertrophy , heart required more
blood for oxygenation that may be not be
possible in sever AS resulting in myocardial
ischemia even in the absence of coronary
artery disease.
 High left ventricular pressure may compress
the coronary blood flow manifesting as
myocardial ischemia angina, and left
ventricular failure.
 This ischemia become more severe on
exercise.
 Severity of AS is determined by the valve
area and the pressure gradient across the
valve(usually by echo).
 Normal aortic valve size is 3-4 cm.
 Severe AS: critical obstruction to left
ventricular outflow is usually characterized
by a peak systolic pressure gradient
exceeding 50mmhg in the presence of a
normal cardiac output and aortic valve area
less than 0.8cm.
 Moderate AS: aortic valve area less than 1.0 -
1.5cm.
 Mild AS: 1.5-2.0 cm.
 Symptoms:
 1.long asymptomatic phase.
 2.symptomatic AS manifests as:
angina
exercise induced syncope.
exertional dysphea and ultimately
heart failure and sudden death.
 these symptoms appear when the aortic
orifice is reduced to one third of its normal
size.
 Syncope attacks are due to markedly
decreased cerebral perfusion that occurs
during exertion due to systemic
vasodilatation in the presence of reduced
cardiac output due to fixed obstruction.
 Angina occurs due to myocardial ischemia
which develops when left ventricular oxygen
demand exceeds supply .
 Decreased coronary blood flow which does
not fulfill the requirement of the
hypertrophied heart particularly after
exercise.
 Decreased coronary blood flow may be due
to compression of coronary arteries by the
hypertrophied myocardium.
 Exertional dyspnea orthopnea and PND are
late symptoms in AS and reflect pulmonary
venous hypertension.
 HEART FAILURE:
heart failure occurs due to both left
ventricular systolic and diastolic dysfunction.
 Gastrointestinal bleeding GI bleeding may
develop in patients with severe AS ,often
associated with vascular malformations with
malformations associated with severe AS
 INSPECTION OF PERCORDIUM:
 Apex beat is not displaced , visible on its
normal position.
 PALPATAION:
 Apex beat is not displaced because
hypertrophy (in contrast to dilatation) does
not produce cardiomegaly.
 Apex beat is heaving in character (forceful)
due to left ventricular hypertrophy(as result
of pressure overload).
 A systolic thrill may be felt in the aortic
area or suprasternal notch and is
transmitted along the carotid arteries.
 Right ventricular failure with
hepatomegaly , and edema precedes left
ventricular septum that encroaches the
right ventricular cavity causing
impairment of right ventricular filling
 HEART SOUNDS:
 S1 is normal .
 A prominent fourth heart sound.
 MURMUR:
 Mid systolic murmur present at aortic area.
 The murmur is usually rough in quality and
best heard in aortic area .
 It radiates to the carotid artery and also the
precordium to the apex.(it usually produces
confusion that patient has two lesions AS and
MR ; however remember that systolic
murmur at apex is murmur of MR that
pansystolic while murmur of AS is mid
systolic ).
 The murmur of AS is reduced in intensity
when standing due to reduced transvalvular
flow.
 Longer the murmur severe is the aortic
stenosis .
 However when the left ventricle fails the
stroke volume falls , the systolic murmur of
AS becomes softer, rarely it disappears
altogether.
 PULSE: carotid pulse is low volume and
slowly rising .
 Simultaneous palpation of the apex and
carotid artery reveals delay in carotid pulse
in severe AS.
 JVP: prominent due to reduced compliance
of right ventricular due to pulmonary
hypertension or hypertrophy of the
ventricular septum.
 CHESTCX RAY:
 May be normal .
 In critical AS the heart is usually normal in
size or slightly enlarged.
 Dilation of ascending aorta on PA view in
commonly seen.
 ECG:
 Left ventricular hypertrophy.
 Left ventricular pressure overload.
 Left atrial enlargement.
 ECHOCARDIOGRAPHY:
 This shows thickened .calcified and immobile
aortic valve cusp.
 Detects left ventricular hypertrophy , its
systolic and diastolic function.
 Demonstrates the pressure across the valve
and the valve area.
 Pressure more than 50mmhg or an aortic
area less than 0.8 cm2 indicates that the
aortic stenosis is severe enough to cause
patients symptoms.
 Medical treatment is not effective for aortic
stenosis.
 Patients who develops any of the three
symptoms( angina, syncope or heart
failure)is candidate for valve replacement.
 Surgery is not indicated for asymptomatic
patients except those with declining left
ventricular function, very severe left
ventricular hypertrophy and very high
pressure or reduced valve area.
 Treatment..
- Beta-blocker or ca channel blocker to
decreased hypertrophy
- Balloon valvoplasty
 Medical treatment is given to those
patients who are inoperable (usually
comorbids).
 Avoid physical activity.
 Carefully follow up of the patient because
the disease is progressive.
 Pressure increase by 4-8mmhg per year
while valve area decrease by 0.2-
0.3cm2m per year.
 In mild AS, repeat echo every 2 years.
 In asymptomatic patient severe AS echo
should be done every 6-12months.
 Angina may be treated with bete-blockers
but cautiously because they may lead to
shock or heart failure.
 ACE inhibitors in small does are indicated
in patients with symptomatic left
ventricular systolic dysfunction who are
not candidate for surgery.
 Valve replacement is indicated early and
in following conditions:
 All symptomatic patients including with
left ventricular dysfunction .
 Asymptomatic patient with decling left
ventricular function.
 Severe left ventricular hypertrophy.
 Severely reduced valve area.
 Patient of severe AS undergoing another
cardiovascular operation.
………………………………

Aortic stenosis

  • 1.
  • 2.
     1.rheumatic heartdisease: Is the most common cause resulting from adhesions and fusions of the commissures and cusps.  2. congenitally abnormal aortic valve: normal valve may be stenotic with commissural fusion at birth but usually not causing serious narrowing of the aortic orifice during childhood.
  • 3.
     The abnormalarchitecture induces turbulent flow which traumatizes the leaflets and leads to fibrosis , increased rigidity, calcification of leaflets and narrowing of the aortic orifice in adulthood.
  • 4.
    3.senile aortic stenosis: Agerelated AS degeneration and calcification of previously normal valve in elderly , usually smokers, daibetics, hypertension and hyperlipidemic.
  • 5.
     4.SLE andsevere familial hypercholesterolemia occasionally cause aortic stenosis.
  • 6.
     7% oftotal cases of CHD  Increased pressure in the LF side of the heart (LV hypertrophy)  Assessment… murmur ,thrill ,high BP, high HR.
  • 8.
     Murmur isloudest  Loudness is proportional to severity  LVH  ……………
  • 9.
     Obstructed leftventricular outflow due to aortic stenosis leads to increased left ventricular pressure and compensatory left ventricular hypertrophy.  Cardiac output at rest is maintained within normal limits in most patients with severe AS, it often fails to rise normally during exertion.
  • 10.
     late inthe course of the disease , the cardiac output and stroke volume decline (due to LV dysfunction) resulting in decline of pressure gradient across the aortic valve and rise in pulmonary arterial pressure.
  • 11.
     Ischemia inAS: due to hypertrophy , heart required more blood for oxygenation that may be not be possible in sever AS resulting in myocardial ischemia even in the absence of coronary artery disease.
  • 12.
     High leftventricular pressure may compress the coronary blood flow manifesting as myocardial ischemia angina, and left ventricular failure.  This ischemia become more severe on exercise.
  • 13.
     Severity ofAS is determined by the valve area and the pressure gradient across the valve(usually by echo).  Normal aortic valve size is 3-4 cm.  Severe AS: critical obstruction to left ventricular outflow is usually characterized by a peak systolic pressure gradient exceeding 50mmhg in the presence of a normal cardiac output and aortic valve area less than 0.8cm.
  • 14.
     Moderate AS:aortic valve area less than 1.0 - 1.5cm.  Mild AS: 1.5-2.0 cm.
  • 15.
     Symptoms:  1.longasymptomatic phase.  2.symptomatic AS manifests as: angina exercise induced syncope. exertional dysphea and ultimately heart failure and sudden death.  these symptoms appear when the aortic orifice is reduced to one third of its normal size.
  • 16.
     Syncope attacksare due to markedly decreased cerebral perfusion that occurs during exertion due to systemic vasodilatation in the presence of reduced cardiac output due to fixed obstruction.
  • 17.
     Angina occursdue to myocardial ischemia which develops when left ventricular oxygen demand exceeds supply .  Decreased coronary blood flow which does not fulfill the requirement of the hypertrophied heart particularly after exercise.  Decreased coronary blood flow may be due to compression of coronary arteries by the hypertrophied myocardium.
  • 18.
     Exertional dyspneaorthopnea and PND are late symptoms in AS and reflect pulmonary venous hypertension.  HEART FAILURE: heart failure occurs due to both left ventricular systolic and diastolic dysfunction.
  • 19.
     Gastrointestinal bleedingGI bleeding may develop in patients with severe AS ,often associated with vascular malformations with malformations associated with severe AS
  • 20.
     INSPECTION OFPERCORDIUM:  Apex beat is not displaced , visible on its normal position.  PALPATAION:  Apex beat is not displaced because hypertrophy (in contrast to dilatation) does not produce cardiomegaly.  Apex beat is heaving in character (forceful) due to left ventricular hypertrophy(as result of pressure overload).
  • 21.
     A systolicthrill may be felt in the aortic area or suprasternal notch and is transmitted along the carotid arteries.  Right ventricular failure with hepatomegaly , and edema precedes left ventricular septum that encroaches the right ventricular cavity causing impairment of right ventricular filling
  • 22.
     HEART SOUNDS: S1 is normal .  A prominent fourth heart sound.
  • 23.
     MURMUR:  Midsystolic murmur present at aortic area.  The murmur is usually rough in quality and best heard in aortic area .  It radiates to the carotid artery and also the precordium to the apex.(it usually produces confusion that patient has two lesions AS and MR ; however remember that systolic murmur at apex is murmur of MR that pansystolic while murmur of AS is mid systolic ).
  • 24.
     The murmurof AS is reduced in intensity when standing due to reduced transvalvular flow.  Longer the murmur severe is the aortic stenosis .  However when the left ventricle fails the stroke volume falls , the systolic murmur of AS becomes softer, rarely it disappears altogether.
  • 25.
     PULSE: carotidpulse is low volume and slowly rising .  Simultaneous palpation of the apex and carotid artery reveals delay in carotid pulse in severe AS.  JVP: prominent due to reduced compliance of right ventricular due to pulmonary hypertension or hypertrophy of the ventricular septum.
  • 26.
     CHESTCX RAY: May be normal .  In critical AS the heart is usually normal in size or slightly enlarged.  Dilation of ascending aorta on PA view in commonly seen.
  • 27.
     ECG:  Leftventricular hypertrophy.  Left ventricular pressure overload.  Left atrial enlargement.
  • 28.
     ECHOCARDIOGRAPHY:  Thisshows thickened .calcified and immobile aortic valve cusp.  Detects left ventricular hypertrophy , its systolic and diastolic function.  Demonstrates the pressure across the valve and the valve area.  Pressure more than 50mmhg or an aortic area less than 0.8 cm2 indicates that the aortic stenosis is severe enough to cause patients symptoms.
  • 29.
     Medical treatmentis not effective for aortic stenosis.  Patients who develops any of the three symptoms( angina, syncope or heart failure)is candidate for valve replacement.  Surgery is not indicated for asymptomatic patients except those with declining left ventricular function, very severe left ventricular hypertrophy and very high pressure or reduced valve area.
  • 30.
     Treatment.. - Beta-blockeror ca channel blocker to decreased hypertrophy - Balloon valvoplasty
  • 31.
     Medical treatmentis given to those patients who are inoperable (usually comorbids).  Avoid physical activity.  Carefully follow up of the patient because the disease is progressive.  Pressure increase by 4-8mmhg per year while valve area decrease by 0.2- 0.3cm2m per year.
  • 32.
     In mildAS, repeat echo every 2 years.  In asymptomatic patient severe AS echo should be done every 6-12months.  Angina may be treated with bete-blockers but cautiously because they may lead to shock or heart failure.  ACE inhibitors in small does are indicated in patients with symptomatic left ventricular systolic dysfunction who are not candidate for surgery.
  • 33.
     Valve replacementis indicated early and in following conditions:  All symptomatic patients including with left ventricular dysfunction .  Asymptomatic patient with decling left ventricular function.  Severe left ventricular hypertrophy.  Severely reduced valve area.  Patient of severe AS undergoing another cardiovascular operation.
  • 34.