This document discusses aortic valve disease, including aortic stenosis and aortic regurgitation. It provides definitions and descriptions of aortic valve stenosis in terms of etiology, pathophysiology, clinical presentation, investigations, and treatment options including surgical aortic valve replacement and percutaneous approaches. For aortic regurgitation, it covers etiology, pathophysiology, symptoms, physical exam findings for assessing severity, investigations, and indications for surgical valve replacement. Key points are made about compensatory changes in the left ventricle and how these relate to severity and timing of intervention.

1. Aortic valve
stenosis
Aortic valve
regurge
Aortic valve disease

3. By
Prof. Hatem Abdel Rahman
MD cardiology
Dr. Mohamd Ashraf Ahmad
MD cardiology
Aortic Stenosis

4. Definition
 Aortic stenosis
refers to obstruction
of flow from the LV
to aorta.
 Anatomically, It
may be:
 1-Valvular:
 2- Subvalvular:
 3-Supravalvular :

5. Aortic valve Stenosis
Etiologies
 Congenital 0-30 yrs
 Bicuspid 30-50 yrs
 Rheumatic 30-60 yrs
 Degenerative >60 yrs

6. Aortic valve Stenosis

8. Pathophysiology
 Valvular aortic stenosis results in chronic left
ventricular pressure overloading.
 Compensatory concentric LVH allows the
ventricle to maintain stroke volume with
increases in diastolic pressure, and patients
remain asymptomatic for many years.

9.  Later on, LVH causes either
 Diastolic dysfunction with the onset of
congestive symptoms
 Myocardial oxygen needs in excess of
supply with the onset of angina.
 Some patients might also experience
exertional syncope, probably reflecting
the inability to increase cardiac output
and maintain blood pressure in
response to vasodilation.

10. Clinical presentation
- Asymptomatic
- The classic symptoms of severe AS:
1- Angina.
2- Syncope.
3- Congestive heart failure.
4-Sudden cardiac death.

11. Aortic Stenosis

12. Natural history of aortic stenosis. At the onset of
symptoms (arrow), there is a rapid progression and
survival is severely limited

13. On examination :
 Delayed slow-rising carotid upstroke (pulsus
parvus et tardus).
 Sustained left ventricular apical impulse.
 Fourth heart sound.
 Harsh systolic murmur of aortic stenosis,
loudest at the base of the heart and radiating
to the carotids, is often but not always
prominent. Low output states, obesity, or
chronic lung disease may mask the findings.
 Other hallmarks of significant aortic valve
stenosis include a single (pulmonic)
component of the second heart sound.

15. Investigations
 ECG often shows changes of left ventricular
hypertrophy.
 The chest X ray occasionally shows heavy
calcification of the valve or ascending aortic
dilation.
 Echocardiography:
Test of choice in the evaluation of patients
with suspected valvular disease.
It allows assessment of the valve anatomy as
well as of chamber size and ventricular
function.
Doppler studies permit estimation of pressure
gradients and estimations of aortic valve area
.

16.  Stress ECG:
 Cardiac catheterization:
It is generally performed as preoperative
coronary angiography in men older than 35
years, women older than 45 years to exclude
coronary artery disease.

19. Treatment
 Medical:
 To date, no medical therapy exists for the treatment
of calcific aortic stenosis.
 Prophylaxis against recurrent rheumatic fever in
rheumatic patients.
 Antibiotic prophylaxis against infective endocarditis
in conditions associated with bacteraemia.
 Surgical:
 Aortic valve replacement
 Percutaneous:

21. TAVR

22. Indications for surgery
1- Symptomatic patients (i.e., those with
angina, syncope, or dyspnea) with severe
aortic stenosis should undergo valve
replacement.
2- Patients with severe AS undergoing
coronary artery bypass grafting
3- Patients with severe AS undergoing
surgery on the aorta or other heart valves .

23. 3- Asymptomatic Patients with severe AS and
left ventricular ejection fractions less than
0.50.
4- Patients with moderate aortic stenosis
undergoing coronary artery bypass grafting or
surgery on the aorta or other heart valves
(Class IIa indication).
5- Aymptomatic patients with severe AS who
exhibit an abnormal response to exercise
(hypotension).

25. Aortic Regurgitation

27. Aortic Regurgitation
 Etiology
 Physical Examination
 Assessing Severity
 Natural History
 Prognosis
 Timing of Surgery

28. Etiology of AR
 Congenital
 Bicuspid valve
 Acquired
 Rheumatic heart
disease
 Dilated aorta (e.g.
hypertension..)
 Degenerative
 Connective tissue
disorders
 E.g. ankylosing
spondylitis, rheumatoid
arthritis, Reiter’s
syndrome, Giant-cell
arteritis )
 Aortopathy
 Cystic medial
necrosis
 Collagen disorders
(e.g. Marfan’s)
 Ehler-Danlos
 Osteogenesis
imperfecta.
 Acute AI: aortic
dissection, infective
endocarditis,
trauma

29. :Pathophysiology of AR
 Acute or subacute significant AR causes
the abrupt introduction of a large volume
of blood into a noncompliant LV, thus
increasing LV end-diastolic and
pulmonary venous pressures and
leading to acute dyspnea or pulmonary
edema.

30.  In chronic AR, compensatory LV changes
occur over time. The excess volume load
causes stretching and elongation of
myocardial fibers, which in turn increase
wall stress.
 When the ventricle can not dilate further,
diastolic pressure increases and results in
dyspnea, another sign of
decompensation.

31. Symptoms of AR
 Dyspnea, orthopnea, PND
 Palpitations.
 Chest pain.
 Nocturnal angina >> exertional angina
 ( diastolic aortic pressure and increased
LVEDP thus  coronary artery diastolic
flow).
 With extreme reductions in diastolic
pressures (e.g. < 40 mmHg) may see
angina

32. Peripheral Signs of Severe AR
 Quincke’s sign:
capillary pulsation
 Corrigan’s sign:
water hammer
pulse
 De Musset’s sign:
systolic head
bobbing
 Mueller’s sign:
systolic pulsation of
uvula
 Durosier’s sign:
femoral retrograde
bruits
 Traube’s sign: pistol
shot femorals
 Hill’s sign: BP
Lower extremity
>BP Upper
extremity by
 > 20 mm Hg - mild
AR
 > 40 mm Hg – mod

33. Cardiac Signs of Severe AR
 Apex:
 Displaced
 Hyper-dynamic
 Palpable S3
 Austin-Flint
murmur

34. Murmur of aortic regurge:
 High pitched,
blowing,
decrescendo
diastolic murmur at
LSB best heard at
end-expiration &
leaning forward
 length correlates
with severity
(chronic AR)
 in acute AR
murmur shortens
as
Aortic DP=LVEDP

35. Assessing Severity of AR
 Assess severity by impact on peripheral signs
and LV
  peripheral signs =  severity
 Dilated LV =  severity
 S3
 Austin –Flint
 Radiological cardiomegaly

36. Investigations
 ECG
 Chest X ray
 Echocardiography
 Stress ECG
 Coronary angiography (preop.)

39. Echo Indications for Valve Replacement
in Asymptomatic AR & MR
Type of
Regurgitatio
n
LVESD
mm
EF
%
FS
Aortic > 55 < 55 <0.27
Mitral > 45 < 60 < 0.32

40. Indication for Valve Replacement in severe
AR:
 ACC/AHA Class I
 Symptomatic patients with preserved LVF
(LVEF >50%)
 Asymptomatic
 Patients with mild to moderate LV dysfunction (EF
25-49%)
 Patients undergoing CABG, aortic or other
valvular surgery
 ACC/AHA Class II a
 Asymptomatic patients with preserved
LVEF but severe LV dilatation (EDD>75
mm or ESD > 55mm)