MITRAL STENOSIS

Diastol :
FISH
MOUTH
shape

Symetrical fussion ot commisure,

the anterior leaflet not it right
position

LUTENBACHER SYNDROME
Rheumatic Fever (20 yr)
ASD + MS
Congenital
End stagerigid cant open or
Inhomogenous
Rheumatic mitral Valve :
shutcombined MS,MR
refractory period,
1. Fibrous thickening and calcification
reentry
2. Fussion ot commissures
Chronic LA enlgmn streach cond. Fibre AF
3. Thickening & shortening chordae tendinea rapid : shortened diastolic time filling CO
Dominan
LA press
MR Normal : negligible pressure difference LA/LV early diastole
MS : OBSTRUCTION Abnormal Pressure gradien between LA & LV LA press (necessery for
blood to flow) transmitted to pulmonary vein and capiler hidrostatik press transudation fluid to
lung interstitium and alveolidyspnoe,CHF symtom
PH : Passive or reactive (30-60mmHg)
Passive : 60%, ok Backward transmission to pulmonal vein
Reactive : 40% vasocontriction, Remodeling PA medial hypertrophy, intimal fibrosis
protecting capillary(ok resistensi , flow ,hidrostatic pressure) RV press
RV Failure
Severe case Collateral to bronchial Vein RupturHemoptysis
Impaired filling LV SV and CO
Stagnation blood flow(dilated LA)
Tromboemb
antikoagula
AF
oli
n
INCREASE FLOW (takikardi) INCREASE LA PRESSERE ? increase LA pressure : increase flow.
MVA : 4-6 cm2,< 2 haemodinamic significans
AF rapid
exercise
Fever
Increase
LA
CONGE
Anemia
flow
pressure
STI
Pregnanc
Increase

DYSPNO
y
HR
E
CO
Tiroid

AF rapid
Decrease
Emosi
diastolic
Sex
Filling time

SYMTOM
co,

AF rapid

congesty
DYSPNEA
Ruptur
(ORTNER SYNDROME)
bronch.vein,

Penekanan n.laryngeus
recuren ok dilatasi atr.kiri,
dilatasi a.pulmonalis

PALPITATION

odem paru, infarc

paru
HAEMOPTYSIS

EMBOLIC

HOARSENESS
HEMOSIDEROSIS

repeated hemoptisis

CHEST PAIN

??, emboli koroner

Perjalanan MS :
- Reccurent
- Chronic autoimune proses
- Super imposed calcified valve

RHF
NYHA IV Untreat all death in 10 years

PHYSICAL EXAMINTATION
FASIES MITRALISlow co, sistemic
vasoconstriction.
Pinkish-purple patches on cheeks.

Wide closing ot
leaflet,pressure
Normal tidk terpisah lebar?
imobile
P2 ,
S2.narow

split single S2
(PH)

RV ENLARG
RV lift, PR, TR

PH --> palpable P2 (2nd left ICS), Loud

DIASTOLIC THRILL
apex, left lateral recumbent

S1 :

AF, irreguler
pulse

P2, PR,
RV lift (left parasternal), S2 narrow split,

OS

: sudden tension ot
c.tendinea
and stenotic leaflet, sudenly
stop,
apexdiafragma stetoskop
S2-OS intervalseverity;
makin cepatLA press
Bedakan dengan P2

Jugular venous
pressure
Prominen v wave

MID DIASTOLIC MURMUR

setelah OS
Turbulent flow across the stenotic
valve
Pre systolic accentuation, bell
GRAHAM
PR (PH) :
stetoskop, STEELL
apex, MURMUR
axilla
decresendo
Durationseverity
Diastolic murmur LSB.
PAN SISTOL MURMUR TR (dialtasi RV,
PH): ICS IV LSB
S3 RV,

CXR-LAE
: : posisi PA
-RVH : retrosternal filling

Severitas MS : PH, interval P2-OS, durasi

murmur

-Kongesti : Upperlobe vascularity , Kerley B lines

-Hemosiderin deposition
-Pulmonal ,menonjol
-LV normal

ECG AF; LAE : p mitral, bifasik di V1; RV Hypertrophy : r/s>1 V1 , s

persisten, RAD

ECHO : - thickened leaflet

- Fussion Commisure
- LAE
- MVA : mild >2, mod 1,1-1,5,
sev<1
- Trombus
- Velocity
- Wilkin score
- Aortic valve ?

Sampai usia 40 thn

10 tahun stlh onset
terakhir
Seumur hidup : high
risk, (prostetic
valave?), severity

high risk pat prostetic valave,

high risk prosedure, prev
endocarditis, CHD

Table 774 Medical Treatment of Mitral Stenosis

Antibiotic prophylaxis

Aritmia (AF) : B blocker, Diltiazem

verapamil, DIGOXIN, cardioversi hanya
bila hemodinamik tidak stabil
ANTIKOAGULAN : Warfarin. (NOC : no
eviden base) ms + af / ms +
LAE/ms+trombus
KONGESTI : diuretic
CHF : ACE-I
PH : Venodilator , long acting nitrat.
Komorbit : RHD, IE

Recurrent rheumatic fever

Infective endocarditis
Restrict activities (moderate/severe mitral stenosis)
Severe exercise
Competitive sports
Arrhythmias
Prevent or control
Atrial fibrillation/flutter
Control ventricular rate

Anticoagulation: start with IV heparin and warfarin; when INR is 2 to 3 discontinue heparin
Restore sinus rhythm
Cardiac medications
Warfarin anticoagulation: INR at 2 to 3
Atrial fibrillation/supraventricular arrhythmias

Pada MS + AF, MS dgn SR bila

pada echo : trombus, SEC, LAE
(D>50mm)

Systemic emboli
LA thrombus
Pulmonary emboli
LV Systolic dysfunction
Elevated pulmonary venous pressure: diureticsa
"Heart failure"
Pulmonary congestion: diureticsa
Pulmonary edema: diuretics,a venodilators if necessarya

LV systolic dysfunction: digitalis, ACE inhibitors

Elevated systemic venous pressure and fluid retention: digitalis, diuretics, ACE inhibitors;
B blockers (second generation) after patients are stabilized and there is LV systolic
dysfunction.
ACE, angiotensin-converting enzyme; INR, international normalized ratio; LA, left atrial; LV, left ventricular.
a
Use judiciously; patients with severe mitral stenosis need an elevated LA pressure to maintain adequate LV filling and
cardiac output.

MITRAL REGURGITATION

ETIOLOGI
Rheumatic Disease :
pemendekan korda, fussion ot
commissures, retractile fibrosis of
leflets and chordae
Degenerative Mitral
Regurgitation
- Calcification eldery,
accelerated by HT, aortic
stenosis, DM
- Connective tissue Marfan
Infective Endocarditis
Interposition between leaflets , Ruptur
Chordae
5 % surgery
Ischemic and functional mitral
regurgitation
LV dysfunction and dilatation, asymmetrical,
transient dysfunction ot papillary muscles.

Weight-loss drug (FENFLURAMIN, PHENTERMIN ) Thickened cardiac valve MR

PATHOPHYSIOLOGY
Direct consequences of MR
1. LA pressure
2. LA volume
3. Forward CO
4. LV volume related stress regurgitant
volume

MR lebih baik : SVR , PVR (LAP) , sedkt

takikardi
Severity of MR
1. Mitral orifice during
regurgitation
2. LV, LA Systolic press
gradient
3. SVR, PVR
4. LA complience, LV
MRV = mitral regurgitant volume, MROA = mitral regurgitant orifice area, C =
constant, TS = time or duration of systole, LVP = LV mean systolic pressure,
and LAP = left atrial mean systolic pressure.

Preload frankstarling EF
Afterload a portion lv output direct to low pressure LA
Acute (tall v wave) odem paru, afterload , EF ,
shortening
Kronis LA dilatasi, LV dilatasi (eccentric hypertrophy) ,
low output syndrome, AF, afterload N End systolic
volume, afterload, preload
Volume overload Frankstarling mechanism EF
SV (nonfailling heart) Forward CO near normal level.
LV dysfunction HF.
Low normal EF impaired myocardial function
Moderately reduce EF (40-50%) severe, irreversible
impairement contractility poorly after surgery
EF < 35% advanced myocardial dysfunction
Inotropic, diuretic, vasodilator reduce LV size reduce
regurgitant orifice size v wave intensity and duration
of systolic murmur.

Coronary flow rate ,

Low incidence of myocardial
ischemia
Determinan MVO2 :
- LV wall tension
- HR
- Contractility
Pada MR hanya shortening yang
tidak mempengaruhi
MVO2
END SYSTOLIC PRESSUREVOLUME
Evaluation LV function , useful
index
pre operatif evaluation
> 40 mm impaired LV
systolic function after surgery.
Neurohormonal : NE , TNF a

CLINICAL MANIFESTATIONS (MR)

SYMPTOMS
Preserved EF Symptom

(+)
ACUTE : Odem paru
CHRONIC : Low output syndrome : Fatique, weakness PH

CHF : DOE, PND, OP

Severe chronic : RHF : edema perifer
Pulmonal Hypertension
Carotid pulse is sharp, brisk

Diminished
S1

AF, hemoptisis
S2 wide split
Shortening LV ejection timePH : P2 >
A2

Early diastolic
murmurincrease
mitral flow

S3 : Increase volume retuning

HOLOSYSTOLIC MURMUR (Pansystolic Murmur)
to LV. Not HF left lateral
apeks menjalar ke axila
decubitus
spesifik untuk rematik (Anterior leaflet).
Cardiac palpation : Lateral displaced,
Sudden standing : diminished the murmur,
Hyperdinamic
squatting : augments it.
Apical THRILL
Valsava manuver
tidak dipengaruhi inspirasi (beda dgn murmur TR
Predominan MR : S3, Rapid LV
mengeras dengan inspirasi)
filling wave, LV impulse, Soft S1
Pada ISKEMIK (POSTERIOR) regurgitasi bisa ke
Predominn MS : S1, OS, Short
anterior katup, posterior aorta, at the base ot
soft systolic murmur, Short A2heart, murmur bisa terdengar seperti murmur AS
OS interval
(left sternal border). Bedanya : murmur AS bisa
berubah2 tiap beat, tergantung durasi sistol, murmur
MR bertambah keras dengan clench the fist (SVR ).

ECG

Principle : LAE,
LVH : 1/3 psn dgn severe MR,
RVH : 15%
AF
Predominan MR : Kardiomegali, paru relatif normal
Predominan MS : mild kardiomegali, paru kongesti.

CX

LV Enlarg, LAE, giant LA is

rare
Acute / CHF interstitial
edema (Kerley B lines)
Calcification ot anulus
posterior third ot cardiac

1. Hemodinamik ( large V wave)

2. Severity MR ( MR regurgitant volume, regurgitant fraction) FICK methode
3. LV Function
4. Coronary anatomy (angiography ) age 40-50

CARDIA
C

MANAGEMENT
TH : CO, Regurgitan, pulmonary congestion
Pharmacologic Therapy uncertain Vasodilators, diuretic, inotropic (digoxin),
spironolakton
Acute MR Vasodilator (nifedipin, nitroprusside,ACEI)
In Chronic MR Vasodilator are less useful only for HT or LV systolic dysfunction who
not candidat for surgery
AF Digoxin/B blocker, Oral anticoagulan
ACEI in MR conflicting result, blockade RAAS fail to improve LVEF and remodeling
in canine model (fibrosis (-))
B Blocker improved LV function in dog need for large clinical trial
Prevention of IE (no longer recomended), prophylaxis rheumatic fever.
ACUTE MR
ALO + Shock pd pasn MCI ok ruptur m.
Papillaris
IE , Trauma
hyperdinamic function + HF
IABP, inotropic, vasodilators
MVr better than MVR :
- Loss of annular chordal
papillary muscle continue
- Risk of thromboembolism
- Risk of hemorrhage
- IE
MVR : survival was not clearly better
then the natural history ot disease

PERCUTANEUS INTERVENTION
EVEREST I & II (Endovascular Valve
Edge-to-edge repair study) The
prosedure reduce MR less efective than
MVr
FUNCTIONAL MR
Aggressive medical management for LV systolic
dysfunction
Severe MR not usually improved by
revascularization alone
persistence residual MR mortality risk
Severe MR corrected at bypass

AORTIC
Etiology
1. Kongenital
valve)
,

severe
turbulen
leaflet

fibrosis,
2. Calcific
disease
AS (normal
AS
in
- Faktor
-

(lipid,
(katup
tear
stress
SEAS ,
statin

3. Rheumatic
fusion
fibrosis
-

stenotic
katup

STENOSIS
(bicuspid
superimposed
calcification
obstruction

flowinjury
ot
inflamasi,
kalsifikasi.
Aortic
valve
SENILE
(degenerative)
or bicuspid)
Common cause
adult
resiko
=
FR
atherosclerosis
DM, HT, smoker)
Inflamasi katup
aorta : wear and
shear
stress),
oksidatif
ASTRONOMER
tdk
mempengaruhi
mortalitas
Aortic Stenosis.
Adhesion
and
ot commissure,
inflamation,
Regurgitant and
Melibatkan
mitral (95%)

AS

Afterload

AS : chronic:course
asymtomatik
Kompensasi
LV hypertrophy
LV
AS AFTERLOAD
dysfunction
Afterload
: wall stress usaha untuk

membuka
katup aorta=
Wall
stress N
CHF
P x r / 2h

complience
isovolumetric
contraction systolic
LV

kompensasi dengan LV hypertrophy

dysfunction
(meningkatkan
h)

LV stiff diastolic dysfunction LVEDP

LAE S4 PCWP kongesti paruCHF

AF

Afterload mismatch
inadequate wall
thickening

Afterload usaha
lebih meningkatkan
pressure dari volume

Kontraksi atrium sangat dibutuhkan untuk

mengisi ventrikel yang kaku (25%) bila terjadi
AF mortalitas
Normal AVA : 3-4cm2

Pressure gradien

Gender difference : + concentric,

eccentric
SVR Contribute total LV afterload,
Hypertension increase total LV load.
AVA increase with exercise (0,2 cm2)
Severe AS : FIXED COabnormal blood
pressure respon to exercise.
LVH systolic pressure Prolongation of
ejection MVO2
PH mild (+)
PA, RV, RA press edema, water

CLINICAL MANIFESTATIONS

AS : slow progressive
20 year 20%
mildsevere
Age 50-70
1. ANGINA
AS + Symptom :
2. SYNCOPE
lethal
3. CHF ( DOE, OP, PND, Odema)

Trias :

SYNCOPE
Cerebral blood flow
- Fixed CO on exertion
- Peripheral vasodilatation
Other :
AF, PH , sudden death
GI bleeding angiodysplasia (right colon),
shear stress induced platelet
aggregationvon willebrand factor
Heyde Syndrome

ANGINA :
1. O2 demand LV mass, LV wall
1.1.
stress , LV systolic pressure ,
Prolongation ejection
2. O2 supplay Diastolic pressure,
compression of intra-myocardial
Coronary arteries

Table 752 Physical Examination of Patients with Varying Severity of Aortic Valve Stenosis

Arterial pulse
Jugular
pulse

Mild

Moderate

Severe +
Function

Normal

Slowly rising

Parvus et tardus

Parvus et tardus

Small volume

Normal

Normal

Normal

venous Normal

Normal

LV Severe
+
Dysfunction

LV Severe
Failurea

Heart

Carotid thrill

Cardiac impulse

Normal

Heaving

Heaving,
sustained Heaving
palpable a wave

Heaving or reduced

Precordial thrill

Usually ++

S4

S3

ESS/ EC

Peak of ESM

Early
systole

Midsystole

Late systole

Late to midsystole, Midsystole, soft or

soft
absent

S2

Normal

Normal
single

Auscultation

or Single or paradoxical

Single

Single

ESM, ejection systolic murmur; ESS, ejection systolic sound; LV, left ventricular; S 2, second heart sound; S3, third heart
sound (diastolic gallop); S4, fourth heart sound (presystolic gallop). aThere may be signs of mitral and tricuspid
regurgitation and of pulmonary hypertension.

PARVUS AND TARDUS : rise slowly, longer time

to EJECTION
reach peak,SYSTOLIC
peak is reduce
MURMUR (ESM)
Lokasi
:
Base
of
the
heart
(ULSB &tindih
URSB)P2
Single S2 (A2 inaudible), A2 tumpang
Physical
S2
Radiated
:
carotids
and
apex
(gallavardin
Severe AS : prolongation ejection, LBBB,LV dysf
examination
phenomenon)
=murmur MR
CXR
: Normal cardiac size,splitting
Rounding LV border
paradoxical
spliting
- Late peaking, grade 2-4/6, CHF : mid systole
and apex. Dilated ascending aorta (post
Systolic murmur
- High pitch
decresendo
diastolic
+
stenotic dilatation), Calcium in aortic valve 40ECG
: LVH (strain),
LAE,murmur
LAD/RAD,
murmurConduction
AR :AVA,
50thn (lateral view),
delay
(LBBB, RBBB,
AV block) Ao
CATH
ECHO
:LV size,
angiography
morfologi

katuo
FR sama,
(bikuspid),
- Varies
from
beat
to beat
CHF
: Cardiac
size,
dialtation,
pulmonary
valve
calcification
extending
to
conducting
S4Coanda
gallop,
Heart
Systolic
failure,
thrill
: URSB, AS,
insiden
kalsifikasi,
CAD,
AVA,Hemodinamik
Peak
gradient,
Jet
Fick
Velocity,
effect
LV,LA
supravalvular
TDS
in right
arm
Carotid palpation

Table 754 Aortic Valve Disease: Indications for Coronary Arteriography

Patients 35 years
Patients <35 years
Left ventricular dysfunction
Symptoms or signs suggesting CAD
Two or more risk factors for premature CAD (excluding gender)

MANAGEMENT

Table 7513 Medical Treatment of Patients with Aortic Valve Stenosis

I. Antibiotic prophylaxis
A. Infective endocarditis (See Chap. 85)
B. Recurrent rheumatic carditis (See Chap. 74)
II. Restriction of activities
A. Severe exercise
B. Competitive sports
III. Arrhythmias
A. Prevent and/or control
B. Restore sinus rhythm, if possible
IV. Cardiac medications (only if essential)
A. Avoid negative inotropic and proarrhythmic agents if possible
B. Diureticsuse cautiously
C. Arteriolar and venodilatorsuse cautiously
V. Followup of asymptomatic patients
A. Mild aortic stenosis: every 25 years
B. Moderate aortic stenosis: every 612 months
C. Develop symptoms: immediate

Table 7514 Severe Aortic Valve Stenosis: Indications for Surgery

Aortic
Stenosis.
Frontal
radiograph
demonstrates isolated enlargement of the
ascending aorta (white arrow)post stenosis
dilatation. The left ventricle is enlarged (yellow
arrow) and the heart is mildly enlarged overall.
The descending aorta is not enlarged (green

No therapy can improve outcome

Mild to mod AS: do not need any spesific
therapy
mildnormal life, mod avoid mod to severe
act
AF reverted rapidly
urgencyCardioversion
Severe+symptom Surgery (AVR or TAVI)
PELLIKA study
Surgery : AVR, TAVI, CBV (catheter balloon

I. All symptomatic patients

A. LV function normal: as soon as possible
B. LV dysfunction: urgent
C. Heart failure: emergent
II. Asymptomatic patients
A. Patients undergoing surgery for CAD, aorta, other valves
B. Associated significantly obstructed CAD
C. LV dysfunction
D. Progressive decline of LVEF
E. Marked or excessive LVH:
1. 1112 mm in smaller people, e.g., women
2. 13-14 mm in larger people, e.g., men
F. Patients aged 6065 years
2

G. "Very" severe AS 0.7 cm ; 0.4 cm /m

H. Others:
1. Abnormal response to exercise
a. Hypotension/no or minimal increase of blood pressure
b. Ischemia
c. LV dysfunction
d. Arrhythmias
2. Arrhythmias
a. Ventricular/atrial tachyarrhythmias
b. A-V block >1 AVB

Diuretics accumulation ot
fluidhati2 hipovolumia
ACEI symptomatic LV dysfunction not
candidat for surgery
caution(hypotension)
Bblocker depressed myocardial
function K.I
Treat Hypertention
HF symptom : digoxin, diuretics,
ACEI or ARB no suit / waiting for
surgery
urgent for surgery

Asymptomatic severe patn

controversy
no data to support early AVR
requires weighing benefit against
Balloon Valvuloplasty important role
in pediatric. Adult limited role :
bridging to AVR or TAVI

PARTNER TRIAL (TAVI)

- TAVI non inferior for all-cause mortality
at 1year
- Cerecrovascular event, vascular
complication
- Bleeding and AF
TAVI for high risk AVR

Table 7518 Suggested Indications for Catheter Balloon Valvuloplasty (CBV) in Patients with Severe Calcific Aortic
Valve Stenosisa
I. "Bridge" procedure to eventual AVR
A. Cardiogenic shock
B. Moderate to severe heart failure
C. Emergent/urgent need for noncardiac therapeutic procedures (e.g., operation)
II. Patient with limited life span
A. Noncardiac reasons (e.g., carcinoma)
B. Cardiac reason(s) other than aortic stenosis
III. Others
A. Patient at extremely high risk for AVR
B. AVR not desirable for noncardiac reasons or cardiac causes other than aortic stenosis
C. Patient refuses surgery
IV. Rare
A. "Therapeutic test": patients with small stroke volume and small valve gradient, with valve stenosis suspected to be
severe but severity in doubt even after provocative diagnostic tests

AORTIC REGURGITATION
ETIOLOGY

PATHOPHYSIOLOGY
AR regurgitant volume LV dilatasi FRANK-STARLING MECHANISM
AR (seperti MR) Acute vs Kronis.

Acute : LV normal size and complience LV

diastolic pressureLAP & pulmonary press
pulmonary edema.
MRagainst
low press
RA
kompensasi
via
Kronis
: LV compensatory
eccentric
hypertrophy
LV
frankstarling
complience

ARagainst
SVR, Afterload
pada
ARpress
lbh N
volume
, LV diastolic
pressure N
LA
kompensasi
frank starling + hipertropi
regurgitan
volumevia

(dilatasi+hipertropi)
frank starling stroke volume ,
diastolic press (widened pulse pressure)
AS afterload
ok Press
, AR afterload
ok SV (25l/m)
Compensatory
High
Complience
pump large
volume( r) pada AR hipertropi + dilatasi.
asymtomatic
Remodelling LV , afterload mismatch Systolic
AR : - LV
dilatasi,
LVsupplay
hipertrofi,
Systolic
dysfunction

COCHF
Diatolic
press
-O2

increase LV
hypertension
size
Angina
Preload mismatch preload reserve has been
reach
(pe preload tdk me SV ok afterload juga ikut
meningkat)
Afterload mismatch hipertrofi tidak mampu
menurunkan afterload ok dilatasi

Exercise :
- SVR diastolic press regurgitant
volume
-HR
juga
diastolic
time regurgitant volume
SVR
berpengaruh

CLINICAL MANIFESTATIONS
Symptoms : DOE, fatique, Uncomfortable sensation of a forceful heartbeat lying down
Angina, Nocturnal Angina ok saat tidur HR waktu diastolik regurgitan
volume SV
perfusi koroner angina, diaphoresis.
Head pounding emosional stress, exertion, takikardi

Stigmata

Compressed proximalsystolic,
compressed distal diastolic
Diastolic press, korotkoff sounds persist to
0mmHg (diastolic press rerely < 30 mmHg)
CHF SVR Diastolic pressure widened
pulse pressure
Pressing a glass slide on the lip, light trough
fingertips

Early diastolic mrmur

Diastolic thrill (3rd left
(decresendo) ICS 3 a 4
ICS)
sittng forward
Blowing systolic murmur
SV

TO and FRO
murmur

Precordium hyperdinamic
Apical impulse displace
lateraly

Austin Flint Murmur OK arus

regurgitant mendorong mitral
anterior
turbulen (DD: MSOS(+)

S1 soft mitral leflt close to each other

Prematur mitral closure prolong PR
S3 gallop
LV
dysfungtion
indikasi

S2 single,ok P2 tertutupi
murmur
S2 narrow, paradox, absen
Mild

Moderate

Severe

Severe + Left
Ventricular Systolic
Dysfunction

Severe + Heart Failure +

Left Ventricular Systolic
Dysfunction

Normal

Corrigan + to ++

Corrigan +++

Corrigan ++

Corrigan +

Systolic

Normal

Increased + to ++

Increased +++

Increased ++

Normal/+

Diastolic

Normal

Decreased + to ++

Decreased +++ to ++++

Decreased ++ to +++

Decreased +

Arterial pulse

Pulse
pressure

Often normal Increased + to ++

Increased +++ to ++++

Increased ++ to +++

Increased +

Cardiac
impulse

Often normal Hyperdynamic

Very hyperdynamic
visible chest may rock

Hyperdynamic

May be hypodynamic

Systolic

Diastolic

S4

S1

Normal

Often soft

Soft

Soft

Soft

S2

Normal

Normal or sing

Often single

Often single

Often single

S3

++ to +++

+++

+++

ESM

+ to ++

+ to ++

AoDM

++

+++ to ++++

++ to +++

+ to ++

thrill

Austin Flint
murmur

CXR Cardiomegali (LV enlargement), enlarge of entire aorta

LV enlarge in inferior and leftward

Syphilitic Aortitis linear cakcification ascensing
aorta
Aneurysma and dilatation of aortic root aortic root
disease

ECG :
-

LAD
LV diastolic Volume overload (Q AVL, V3-V6,
Small wave V1)
LV Strain (ST-T change)
T tall precordial early stage

TREATMENT
NO SPHESIFIC THERAPY
ASYMTOMATIC : - Mild to mod Follow echo 12-24 months
Echo : LV function, size.
- Severe, normal EF 6 month (Long acting nifedipin ? )

- Treat Hypertension increase regurgitant Vasodilator (nifedipin) ,

ACEI

- Prefent Bradiaritmia and AF (B-blocker hati-hati) treat vigorously

- Do not need AB prophylaxis for IE (see guidelines)

SYMTOMATIC SURGERY

Vasodilator Regurgitant volume

PADUA TRIAL Nifedipin in asymtomatic severe AR
(vs digoxin)
Benefit
BARCELONA TRIAL Not benefit
Subject not severe AR
ACE I : no benefit

Table 7528 Medical Treatment of Patients with Aortic Regurgitation

I. Antibiotic prophylaxis
A. Infective endocarditis
B. Recurrent rheumatic carditis
II. Restriction of activities (moderate/severe AR)
A. Severe exercise
B. Competitive sports
III. Arrhythmias
A. Prevent and/or control
B. Restore sinus rhythm, if possible
IV. Cardiac medications
A. Asymptomatic, normal LV function
1. Mild AR:

None

2. Moderate AR: ?

Nifedipine long-acting if no KI (?)

3. Severe AR:

Nifedipine long-acting

B. Severe AR symptomatic (while waiting for surgery)

1. Normal LV function:

Nifedipine long-acting

2. LV dysfunction:

Digitalis
ACE inhibitors
Hydralazine nitrates, if needed
Diuretics, if needed
Dobutamine, if needed

C. Severe AR + heart failure:

Digitalis, diuretics, ACE inhibitors
Hydralazine + nitrates
IV nitroprusside, if IV therapy needed
Dobutamine, if needed
V. Followup of asymptomatic patient
A. Mild AR:

Every 25 years

B. Moderate AR:

Every 12 years

C. Severe AR:

Every 612 months

D. Develop symptoms:

Early or immediate