This document discusses the etiology, pathophysiology, clinical features, investigations, and treatment of aortic regurgitation and aortic stenosis. It provides details on: 1. The various causes of aortic regurgitation including congenital bicuspid valve, connective tissue disorders like Marfan's syndrome, rheumatic heart disease, and infective endocarditis. 2. The typical asymptomatic phase of chronic aortic regurgitation and signs of left ventricular dysfunction like reduced ejection fraction and heart failure symptoms. 3. The characteristic physical exam findings of aortic regurgitation including widened pulse pressure, diastolic murmur, and signs related to abrupt distension and collapse of arteries

1. NORMAL ANATOMY OF CARDIAC
VALVES

2. AORTIC VALVE

3. AORTIC REGURGITATION

4. ETIOLOGY
 Any conditions resulting in incompetent aortic
leaflets(either a primary valve ds or primary aortic root
ds.)
 Congenital
 Bicuspid valve
 Aortopathy
 Cystic medial necrosis
 Collagen disorders (e.g. Marfan’s)
 Ehler-Danlos
 Osteogenesis imperfecta
 Pseudoxanthoma elasticum

5.  Acquired
 Rheumatic heart disease(in 2/3 pt of valvularAR )
 Dilated aorta (e.g. hypertension..)
 Degenerative
 Connective tissue disorders
 E.g. ankylosing spondylitis, rheumatoid arthritis, Reiter’s syndrome, Giant-
cell arteritis )
 Syphilis (chronic aortitis)
 Acute AR---
 : aortic dissection, infective endocarditis, trauma..

8. Natural History of Chronic
Aortic Regurgitation
 Long asymptomatic phase; may be decades long.
 Left ventricular systolic dysfunction ( decline in
EF) NOTE!! LV
dysfunction may occur in the absence of
symptoms
 Symptoms associated with LV dysfunction:
- Exercise intolerance
- Dyspnea on exertion
 Angina (rare)
 Sudden death (rare)

9.  CLINICAL FEATURES---
 1.S/S of impending and overt heart failure,such as
orthopnea,dyspnea,PND…
 2. Chest pain in the form of nocturnal angina is
more common than exertional angina….
 3. Approx. ¾ patients of AR are males,but females
predominate among patients with primary valvular
AR,who have associated MVD….

10.  4. S/S of Infective endocarditis should always be
looked for..(Fever,rapid deterioration of
symptoms,splenomegaly,new murmurs)…
 5. In AcuteAR,Pulmonary oedema and cardiogenic
shock develops rapidly,because of the
noncompliant LV…(LVEDP rises markedly and
quickly)….

11.  6. Chronic AR has a long latent period…
 Palpitations may be the presenting
complaints,which can be due to Sinus
tachycardia/VPCs….
 7. AR is a cause of refractory angina and angina
in absence of CAD….

12.  In GPE,the jarring of the entire body and the
bobbing motion of the head with each systole can
be appreciated…
 The examination should also be directed towards
the detection of conditions predisposing to AR,such
as Marfan’s Syndrome/Ankylosing spondylitis…
 The reason behind various peripheral signs of AR is
abrupt distension and collapse of the arteries…

13.  Quincke’s sign: capillary pulsation
 Corrigan’s sign: water hammer pulse
 Bisferiens pulse (AS/AR > AR)
 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 AR
– > 60 mm Hg – severe AR

14. Widened pulse pressure
 Systolic – diastolic = pulse pressure
 High pitched, blowing, decrescendo diastolic murmur at LSB
 Best heard at end-expiration & leaning forward
 Hands & Knee position
s1 s2 s1
• Apex:
– Enlarged
– Displaced
– Hyper-dynamic
– Palpable S3
– Austin-Flint murmur

15. • Aortic diastolic murmur
– length correlates with severity (chronic AR)
• Assess severity by impact on peripheral
signs and LV
–  peripheral signs =  severity
–  LV =  severity
– S3
– Austin -Flint
– LVH
– radiological cardiomegaly

16.  ECG---
 LVH
 LAD
 LAD with STRAIN pattern in lateral wall
leads…(I,Avl,V5,V6)…
 CXRPAView---
 Down and out displaced apex…
 Dilatation of the aorta may be seen…

17. INVESTIGATIONS
 ECHO:- a rapid high frequency fluttering of
the regurgitant jet is a characteristic finding.
Echo is useful in determination the cause of
AR, by detecting dilatation of the aortic
annulus and root or aortic dissecton.

18.  Definition of severe AR on ECHO---
 Central jet width > 65 % of LV Outflow tract ..
 Regurgitant jet volume > 60 ml/beat ..
 The regurgitant fraction > 50 %....

19. Treatment
 Medical :- diuretics and vasodilators (ACE I , CCB,
hydralazine). Penicillin therapy in syphilis aortitis.
Beta # may be useful to retard the rate of aortic
root enlargement in pts with marfan syndrome and
aortic root dilatation.
 Surgical:- AV replacement……

20. Indication for Valve
Replacement in Aortic
Regurgitation
 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)
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21. Indication for Valve
Replacement in Aortic
Regurgitation
 ACC/AHA Class II b
 Patients with severe LV dysfunction (EF < 25%)
 Asymptomatic patients with normal systolic func-tion
at rest (EF >0.50) and progressi ve LV dilata-tion when
the degree of dilatation is moderatelysevere (EDD 70
to 75 mm, ESD 50 to 55 mm).
 ACC/AHA Class III
 Asymptomatic patients with normal systolicf
unction at rest (EF >0.50) and LV dilatation when
the degree of dilatation is not severe (EDD <70
mm, ESD <50 mm).
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22. AORTIC STENOSIS

26. AS occurs in ¼ of all the
patients with chronic valvular ds
and 80% of symptomatic adults
with AS are males.
 Normal aortic valve area 2.5-3.5 cm2
 Mild stenosis 1.5-2.o cm2
 Moderate stenosis 1.0-1.5 cm2
 Severe stenosis < 1.0 cm2
 Onset of symptoms
~ 0.9 cm2 with CAD
~ 0.7 cm2 without CAD

27. Pathophysiology of Aortic Stenosis
 Left ventricular outflow obstruction
LV systolic pressure > aortic pressure
 Concentric left ventricular hypertrophy
Sustains high LV pressures
Normalizes wall stress (radius x pressure/wall
thickness)
Eventually results in impaired LV diastolic
compliance
 LA hypertrophy and enlargement
 Severe stenosis: Limits ability to increase stroke
volume on demand
Critical aortic stenosis = fixed cardiac output

31.  ETIOLOGY :- young (functional/bicuspid
AV),RHD, older(aortic stenosis/sclerosis)
 CLINICAL FEATURES:- AS is rarely of clinical
importance until the valve orifice has narrowed
to approx. 1cm2. . Even severe AS may exist for
years without any symptoms(becoz of ability of
hypertrophied LV to generate the elevated I/v
pressure required for stroke volume.)

32. • Cardinal Symptoms
– Chest pain (angina)
• Reduced coronary flow reserve
• Increased demand-high afterload
– Syncope/Dizziness (exertional pre-syncope)
• Fixed cardiac output
• Vasodepressor response
– Dyspnea on exertion & rest
– Impaired exercise tolerance
• Other signs of LV failure
– Diastolic & systolic dysfunction

33.  “Diamond” shaped, harsh, systolic crescendo-
decrescendo . Intensity and thrill DOES NOT
predict severity.
 Decreased, delay & prolongation of pulse
amplitude(pulsus parvus et tardus)
 Paradoxical S2 (reversed splitting)
 S4 (with left ventricular hypertrophy)
 S3 (with left ventricular failure)

34. Aortic Stenosis: Physical
Findings
S1 S2 S1 S2
Mild-Moderate Severe

35.  ECG shows–
 LV Strain
 LAD
 LVH….

36. Investigations
 ECHO:- LV hypertrophy and/or multiple
bright thick echoes from valve in case of
calcific valvular degeneration….. It is useful in
for identifying coexisting MS/MR. aneurysmal
enlargement in up to 20% of patients with
bicuspid AV ds.
 Other – chest Xray, cardiac catheterisation,
coronary angiography(r/o CAD in sev AS
considered for operative t/t).

37. Treatment
 Medical:- avoid dehydration and
hypovolemia. Beta #, ACE(I) for LV
remodelling and to dec cardiac workload.
Nitroglycerine for relieving angina. Statins
have a controversial role.
 Surgical :- indicated in – sev AS who are
symptomatic and EF <50%.Those pts with
aneurysmal or expanding aortic root even if
asymptomatic.

38. Aortic Stenosis

39. Operative mortality of AVR
in the elderly
 ~ 4-24%/year
 Risk factors for
operative mortality
 Functional class
 Lack of sinus rhythm
 HTN
 Pre-existing LV
dysfunction
 Aortic regurgitation
 Concomitant surgical
procedures:CABG/MV
surgery
 Previous bypass
 Emergency surgery
 CAD
 Female gender
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40. Prosthetic Heart Valves

41. Prosthetic Valves
 MECHANICAL
 Durable
 Large orifice
 High thromboembolic
potential
 Best in Left Side
 Chronic warfarin
therapy
 BIO-PROSTHETIC
 Not durable
 Smaller
orifice/functional
stenosis
 Low thromboembolic
potential
 Consider in elderly
 Best in tricuspid position
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