AORTIC

REGURGITATION

BY : dr. MEIDIANASER PUTRA

Aortic Regurgitation:
Etiology
Any conditions
resulting in
incompetent aortic
leaflets
Congenital
Bicuspid valve

Aortopathy
Cystic medial necrosis
Collagen disorders (e.g.
Marfans)
Ehler-Danlos
Osteogenesis imperfecta
Pseudoxanthoma
elasticum

Acquired
Rheumatic heart
disease
Dilated aorta (e.g.
hypertension..)
Degenerative
Connective tissue
disorders
E.g. ankylosing
spondylitis,
rheumatoid
arthritis, Reiters
syndrome, Giantcell arteritis )

Syphilis (chronic
aortitis)

Aortic Regurgitation:
Symptoms
Dyspnea, orthopnea, PND
Chest pain.
Nocturnal angina >> exertional angina
( diastolic aortic pressure and
increased LVEDP thus coronary artery
diastolic flow)

Physical Exam Auscultation

A2 often soft/absent, P2 normal
S3 if LV function severely depressed
High frequency decrescendo diastolic
murmur over the 3rd or 4th intercostal
space at left sternal border
Best heard sitting up, leaning forward at end
expiration

Austin Flint murmur: mid-to-late diastolic

apical rumble, possibly due to vibration of
anterior mitral leaflet as it is struck by a
posteriorly directed AR jet.

Peripheral Signs of Severe

Aortic Regurgitation
Quinckes sign:
capillary pulsation
Corrigans sign: water
hammer pulse
Bisferiens pulse (
De Mussets sign:
systolic head bobbing
Muellers sign: systolic
pulsation of uvula
Rosenbachs sign
systolic pulsations of
the liver
Gerhards sign
systolic pulsations of
the spleen

Durosiers sign:
femoral
retrograde bruits
Traubes sign:
pistol shot
femorals
Hills sign:BP
Lower extremity
>BP Upper
extremity by
> 20 mm Hg - mild
AR
> 40 mm Hg mod
AR

Aortic Regurgitation:
Physical Exam
High pitched,
blowing,
decrescendo
diastolic murmur
at LSB
Best heard at endexpiration &
leaning forward
Hands & Knee
position

S1
S1

S2

Acute AR Pathophysiology

Patients often present with

pulmonary edema or cardiogenic
shock.
May present with myocardial
ischemia: As LVEDP approaches
diastolic aortic and coronary
pressures, myocardial perfusion
pressure in the subendocardium is
diminished.
LV dilation and thinning of LV wall
result in increased afterload, and
combined with tachycardia leads to

Chronic AR Pathophysiology

Early Compensated
Enlarged chamber size
afterload
hypertrophy of LV which
preserves compliance
normal filling pressures
LVH LV mass
normal LV vol/mass ratio &
EF
Progressive LV dilation
and systolic HTN wall
stress and vol/mass ratio
wall stress eventually
leads to overt LV
dysfunction.

Decompensated
LV systolic dysfunction
accompanied by
decreased LV diastolic
compliance due to
hypertrophy and
fibrosis
Leads to high filling
pressures and CHF
symptoms
Exertional dyspnea
common; angina can
occur due to reduced
coronary flow reserve

TEKANAN DI RUANG-RUANG
JANTUNG (SISTOLE/DIASTOLE)
Atrim kanan

0/3

mmHg
Ventrikel kanan

25/3

mmHg
Atrium kiri

0/7

mmHg
Ventrikel kiri
mmHg

115/7

Different Stages of AR

djian R, et al. Circulation 2005; 112: 125-134.

Aortic Root Disease

Dilation here is common; especially in
AS; does not lead to AR

Between the
annulus and the
ascending aorta is
a collagenous
segment that
forms the sinuses
of
valsalva.
As little as
2mm of
dilation here
can cause AR

Dilation here is
rare

Aortic Root Disease

Dilation of the
aortic ridge
eliminates the
normal overlap of
the valves

Chest X-Ray
Cardiomegaly
Prominent Left
Ventricle
Ascending
Aortic dilatation
LAE only if
severe LV
dysfunction

Chest X-Ray

Aortic Regurgitation:
Natural History
Asymptomatic %/Y
Normal LV function (~good prognosis)
Progression to symptoms or LV dysfunction
<6

Progression to asymptomatic LV
dysfunction
3.5
75% 5-year survival
Sudden death

<

TX: Medical Surgery BEFORE LV

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)

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).

Medical Management
Rx CHF diuretics, aldactone, dig
avoid vigorous exertion if
symptomatic AI
control diastolic BP (increases
regurg)
avoid BB - prolong diastole,
increase AR

Vasodilators?
Short-term studies on the effects of
vasodilators in acute severe AR have
suggested improvement in hemodynamic and
structural parameters.
The long-term benefit of vasodilator therapy
in chronic severe AR is unclear.
A total of 10 studies of vasodilator therapy in
asymptomatic patients with chronic, severe
AR have yielded conflicting and quite
inconsistent results.
Only two studies have assessed clinical outcomes
such as time to AVR (the remainder have only
reported hemodynamic and/or structural
parameters).

Vasodilators Clinical
Outcomes
Evangelista et al. randomly assigned 95 patients
with chronic, severe AR to nifedipine, enalapril, or
placebo.
Followed patients for ~7 years.
Rates of AVR were not significant across the 3
groups:

12/31 (39%) of control group

16/32 (50%) of enalapril group
13/32 (41%) of nifedipine group
11% of patients dropped out of study, though ontreatment analysis yielded similar rates of progression

No significant changes in SBP, DBP, or HR noted;

furthermore saw no significant changes in LVEF,
LVESD, LVEDVI

gelista A, et al. NEJM 2005; 353: 1342-1349.

Current Guidelines for

Vasodilators
Class I:
Chronic therapy in severe AR with symptoms or LV
dysfunction when not a surgical candidate.

Class IIa:
Short-term therapy to improve hemodynamics in
patients with severe CHF Sx and severe LV
dysfunction before proceeding with AVR.

Class IIb:
Long-term therapy in asymptomatic patients with
severe AR who have LV dilatation but normal systolic
function (previously a class I indication before the
Evangelista article).

w RO, et al. Circulation 2006; 114: e84-e231.

TERIMA KASIH

Echocardiography
Most important diagnostic test for
evaluation of AR as well as for serial
follow-up
Allows for:
Assessment of the anatomy of the aortic
leaflets and the aortic root
Detection of the presence and severity
of AR
Characterization of LV size and function

M-Mode
Echocardiography
The aortic regurgitation jet can cascade
across the anterior mitral leaflet
Creates a high-frequency fluttering of the
anterior mitral leaflet
Increased duration between E and A peaks
Increased distance between the maximal
anterior motion of the mitral valve in early
diastole (E point) and the most posterior
motion of the interventricular septum (e.g.,
increased E-point septal separation [EPSS])

In acute AR, premature closure of the MV

can also be seen by M-mode
Due to rapidly increasing LV pressure

AR by 2D Echo
2D Echo will give you a detailed
evaluation of the aortic valve and root
Detailed evaluation of LV size and
function
Many important causes of AR easily seen
on 2D imaging
Even when AR is severe, sometimes 2D
imaging is surprisingly normal
Indirect signs of AR:
Diastolic curving of anterior mitral leaflet with
concavity towards ventricular septum due to

Dilated
aortic root
due to
aortoannul
ar ectasia

Bicuspid
aortic valve
with
characteristi
c elliptical
opening

djian R, et al. Circulation 2005; 112: 125-134.

Large,
mobile
vegetati
on

Acute
AR due
to
aortic
dissecti
on

Echo Indications for Valve

Replacement
in Asymptomatic AR & MR
Type of
LVESD mm
Regurgitation

EF

FS
%

Aortic

> 55

< 55

<0.27

Mitral

> 45

< 60

< 0.32

Color Flow Doppler

Color flow jet composed of 3 distinct
segments:
Proximal flow convergence zone = area of flow
acceleration into the orifice
Vena contracta = narrowest and highest
velocity region of the jet at or just downstream
from the orifice
The jet itself occurs distal to the orifice in the
LV cavity

Measurement of the jet area or

penetration into the LV cavity is not
accurate in assessing AR severity, though:

Color Flow Doppler

Color flow Doppler is the most common
technique to visualize AR
Sensitivity > 95%
False negatives can occur in tachycardia with
mild AR
Frame rate allows only a few diastolic frames
to be displayed
Can be overcome by using CW -- has a higher
sampling rate

Specificity ~100%
Detects even trivial AR
1% of subjects under age 40

 Eccentric AR jet
Width measured at
origin of jet
adjacent to leaflets
Jet width/LVOT
width is <25%
Case of mild AR

Jet width/LVOT
width > 65%
Case of severe AR

djian R, et al. Circulation 2005; 112: 125-134.

e patient aortic valve endocarditis as cause of AR)

AR jet directed toward anterior mitral leaflet