2.5.1.

DEMAM REMATIK

Yerizal Karani
 Definisi
• Demam rematik (DR) adalah penyakit
autoimun dengan peradangan menyeluruh
yang timbul setelah infeksi bakteri
Streptokokus grup A
• Penyakit Jantung Rematik (PJR) merupakan
komplikasi non nonsupurstif dari faringitis
streptokokus grup A yang disebabkan oleh
respon imun tertunda
 Epidemiologi
• WHO (2000) : 12 juta DR dan PJR didunia, 3
juta dg gagal jantung kongestif
• Di Indonesia, data PJN Harapan Kita prevelensi
DR 3,9%, rentang usia 6-17 th atau sekitar 8,5
kasus dari 1000 pasien
• Di negara berkembang : 1 per 100.000 anak
usia sekolah di Kostarika, 72,2 per 100.000 di
Polynesia, 100 per 100.000 di Sudan hingga
150 per 100.000 di Cina
 Patogenesis
• Terdapat bukti antara infeksi Strepcc B hemolitikus grup A
dg DR akut
• DR adalah respon autoimun
• Limfosit T-sel berperan dalam Karditis rematik
• Sel T teraktivasi oleh bakteri melepaskan sitokin
• Terjadi interaksi antara pejamu dan patogen dg pengikatan
ligan permukaan bakteri pada reseptor spesifik sel pejamu
• Respon tubuh : produksi antibodi, opsonisasi dan
fagositosis
• Reaksi yang terjadi tergantung : kerentanan tubuh, virulensi
dan lingkungan
Diagnosis
 Diagnosis DR
• Terdapat : 2 manifestasi mayor atau
1 mayor dan 2 minor
ditambah bukti adanya infeksi streptocc grup
A sebelumnya
 Gambaran klinis karditis
PERIKARDITIS MIOKARDITIS ENDOKARDITIS

-Pericardial friction rub -Gagal jantung kongestif -Murmur holosistolik apex

-Bisa pada episode primer -Kardiomegali (MR)
atau pada rekuren -Murmur middiastolik apex
(Carey Coombs)
-Murmur diastolik dibasal
-Adanya murmur baru yg
signifikan pd pasien
riwayat PJR
 Tatalaksana Medis
UMUM.
• Perawatan di RS
• Posisi Fowler – tempat tidur kursi
• Pasien dg Karditis dirawat 4 minggu
• Swab tenggorokan, ECG, Ro torak dan Echo
• Kultur darah --- endokarditis
Terapi Antimikrobial
• Eradikasi infeksi streptocc :
Benzathin benzylpenisilin, 600.000 – 1.200.000 U im
Phenoxymethyl penisilin oral, 250-500mg 2-3 kali
Amoksisilin 25-50 mg/kg/hari 3 kali
Sefalosporin generasi pertama
Eritromisin

• Supresi proses inflamasi :

Aspirin 100mg/kg/hari 4-5kali
Prednison 2mg/kg/hari 3-4kali, ssd 2-3 minggu dosis
dikurangi 20-25% tiap minggu
Tatalaksana gagal jantung
• Biasanya ada respon dengan istirahat total
dan steroid
• Bisa ditambah diuretik, ACE-inhibitor dan
digoksin bila kondisi berat
• Restriksi diet sodium
Terapi Pembedahan
• Pembedahan dilakukan utk penyakit katup
rematik kronik
• Indikasi bedah bila simtom berat dan fungsi
kardiak lemah secara signifikan
 Pengegahan DR
• Pencegahan primer : terapi antibiotik adekuat
utk mencegah serangan awal DR akut pada
pasien ISPA Streptocc grup A
• Pencegahan sekunder : terapi antibiotik utk
melawan kekambuhan dari infeksi streptcc
faringeal
 Lama pencegahan
KATEGORI PASIEN DURASI
DR tanpa karditis Sedikitnya sampai 5 tahun sesudah
serangan terakhir atau hingga usia 18 th

DR dengan karditis tanpa bukti adanya Sedikitnya sampai 10 tahun setelah

penyakit jantung residual/kelainan katup serangan terakhir atau hingga usia 25 th,
dipilih jangka waktu yang terlama

DR akut dengan karditis dan penyakit Sedikitnya 10 tahun sejak episode terakhir
jantung residual/ kelainan katup persisten atau hingga usia 40 th , dan kadang-
kadang seumur hidup

Setelah operasi katup jantung Seumur hidup

Valvular Heart Disease
Aortic Regurgitation

Yerizal Karani MD
Cardiology Division
Faculty of Medicine Andalas University
 Aortic Regurgitation
• Etiology
• Physical Examination
• Assessing Severity
• Natural History
• Prognosis
• Timing of Surgery

© Continuing Medical Implementation

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 Aortic Regurgitation:
Etiology
• Any conditions resulting in • Acquired
incompetent aortic leaflets – Rheumatic heart disease
• Congenital – Dilated aorta (e.g.
– Bicuspid valve hypertension..)
– Degenerative
• Aortopathy
– Connective tissue disorders
– Cystic medial necrosis • E.g. ankylosing spondylitis,
– Collagen disorders (e.g. rheumatoid arthritis, Reiter’s
Marfan’s) syndrome, Giant-cell arteritis
– Ehler-Danlos )
– Osteogenesis imperfecta – Syphilis (chronic aortitis)
– Pseudoxanthoma elasticum • Acute AI: aortic dissection,
infective endocarditis,
trauma
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 Aortic Regurgitation:
Symptoms
• Dyspnea, orthopnea, PND
• 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) may see angina

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 Peripheral Signs of Severe
Aortic Regurgitation
• Quincke’s sign: capillary
pulsation
• Corrigan’s sign: water
hammer pulse
• Bisferiens pulse (AS/AR >
AR)
• 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 AR
– > 60 mm Hg – severe AR

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 Aortic Regurgitation:
Physical Exam

• Widened pulse pressure

– Systolic – diastolic = pulse
pressure
• High pitched, blowing,
decrescendo diastolic
murmur at LSB
• Best heard at end-
S1 S2 S1
expiration & leaning
forward
• Hands & Knee position

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 Central Signs of Severe
Aortic Regurgitation
• Apex: • Aortic diastolic
– Enlarged murmur
– Displaced – length correlates with
severity (chronic AR)
– Hyper-dynamic
– in acute AR murmur
– Palpable S3 shortens as
– Austin-Flint murmur Aortic DP=LVEDP
– in acute AR - mitral pre-
closure

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 Assessing Severity
of AR
• Assess severity by impact on peripheral signs
and LV
–  peripheral signs =  severity
–  LV =  severity
– S3
– Austin -Flint
– LVH
– radiological cardiomegaly

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 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 < 0.2
• Abnormal LV function
– Progression to cardiac symptoms 25
• Symptomatic (Poor prognosis)
– Mortality > 10

TX: Medical  Surgery BEFORE LV dysfunction

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Bonow RO, et al, JACC. 1998;32:1486.
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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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Valvular Heart Disease
Aortic Stenosis

Yerizal Karani

© Continuing Medical Implementation

…...bridging the care gap
 Aortic Stenosis
• Etiology
• Physical Examination
• Assessing Severity
• Natural History
• Prognosis
• Timing of Surgery

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 Aortic Stenosis - Etiology
• Young patient think • Rarely
congenital – Unicuspid valve
– Sub-aortic stenosis
– Bicuspid • Discrete
• 2% population • Diffuse (Tunnel)

• 3:1 male:female • Middle aged patient(4&5th

distribution decades) think bicuspid or
rheumatic disease
• Co-existing • Old patient think
coarctation 6% of degenerative (6,7,8th
patients decades)

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 Common Clinical Scenarios
• Younger people • Older people
– Functional murmur vs – Aortic sclerosis vs aortic
MVP vs bicuspid AV stenosis

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 Aortic Stenosis: Etiology
• Congenital bicuspid valve is the most common
abnormality
• Rheumatic heart disease and degeneration with
calcification are found as well

Normal Bicuspid Ao V “Normal” geriatric

calcific valve
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Bicuspid Aortic Valve

© Continuing Medical Implementation

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 An 83 year old man with
exertional dyspnea

• Previously well
• Gradual onset Class
2/4 dyspnea
• Occasional
lightheadedness with
exertion
• O/E: 2/6 ejection
murmur

© Continuing Medical Implementation

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 Aortic Stenosis: Symptoms
• 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

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 Common Murmurs and
Timing (click on murmur to play)

Systolic Murmurs
• Aortic stenosis
• Mitral insufficiency
• Mitral valve prolapse
• Tricuspid insufficiency
Diastolic Murmurs
• Aortic insufficiency
• Mitral stenosis
S1 Implementation
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Aortic Stenosis: Physical Findings

S1 S2 S1 S2
Mild-Moderate Severe

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 Aortic Stenosis: Physical Findings
• Intensity DOES NOT predict severity
• Presence of thrill DOES NOT predict severity
• “Diamond” shaped, harsh, systolic crescendo-
decrescendo
• Decreased, delay & prolongation of pulse amplitude
• Paradoxical S2
• S4 (with left ventricular hypertrophy)
• S3 (with left ventricular failure)

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An 83 year old man with
exertional dyspnea

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Left ventricular hypertrophy (LVH)

There are many different criteria for LVH.

Sokolow + Lyon (Am Heart J, 1949;37:161)
S V1+ R V5 or V6 > 35 mm
Cornell criteria (Circulation, 1987;3: 565-72)
SV3 + R avl > 28 mm in men
SV3 + R avl > 20 mm in women
Framingham criteria (Circulation,1990; 81:815-820)
R avl > 11mm, R V4-6 > 25mm
S V1-3 > 25 mm, S V1 or V2 +
R V5 or V6 > 35 mm, R I + S III > 25 mm
Romhilt + Estes (Am Heart J, 1986:75:752-58)
Point score system
Left atrial abnormality (dilatation or hypertrophy)
M shaped P wave in lead II
prominent terminal negative component to P wave in lead V1
(shown here)
Etiology of Aortic Stenosis

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 Severity of Stenosis
• Normal aortic valve area 2.5-3.5 cm2
• Mild stenosis 1.5-2.5 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

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 Echocardiogram

• Etiology
• Valve gradient and area
• LVH
• Systolic LV function
• Diastolic LV function
• LA size
• Concomitant regional wall
motion abnormalities
• Coarctation associated
with bicuspid AV

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 MANAGEMENT
• Medical
– Diuretik, ACE Inhibitor / ARB
– Calcium Channel Blocker (diltiazem/verapamil)
– Beta blocker
• Non Surgical intervention
– BAV (Balloon Aortic Valvuloplasty)
– TAVI (Transcatheter Aortic Valve Inplantation)

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• Operative :
– Symptomatic AS
– Severe stenosis (AVA<1cm)
– LV dysfunction (EF<50%)

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 Aortic Stenosis: Prognosis

Symptom/Sign Live expectancy

Angina 5 years
Syncope 2-3 years
Congestive Heart Failure 1-2 years

Therapy: Valve replacement for severe aortic

stenosis
Operative mortality (elderly) ~ 4-24%/Morbidity ~ 3-11%
Event rate ©inContinuing
asymptomatic severe AS ~ 1%/year
Medical Implementation
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Natural History of Aortic Stenosis

• Heart failure reduces

life expectancy to less
than 2 years
• Angina and syncope
reduce life expectancy
between 2 and 5 years
• Rate of progression 
@ 0.1 cm2/year

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Caged-Ball Valve

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Disc Valve

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Bio-prosthetic Valve

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

© Continuing Medical Implementation

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Valvular Heart Disease
Mitral Regurgitation

Yerizal Karani MD
Cardiology Division
Faculty of Medicine Andalas University
 Mitral Regurgitation
• Etiology
• Symptoms
• Physical Exam
• Severity
• Natural history
• Timing of Surgery

© Continuing Medical Implementation ®

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 Mitral Regurgitation:
Etiology
• Valvular-leaflets • Annulus
– Myxomatous MV – Calcification, IE (abcess)
Disease • Papillary Muscles
– Rheumatic
– CAD (Ischemia,
– Endocarditis Infarction, Rupture)
– Congenital-clefts – HCM
• Chordae – Infiltrative disorders
– Fused/inflammatory • LV dilatation &
– Torn/trauma functional regurgitation
– Degenerative
• Trauma
– IE

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 MR Etiology:Surgical series
• MVP(20-70%)
• Ischemia (13-40%)
• RHD (3-40%)
• Infectious endocarditis(10-12%)

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 MR Pathophysiology
• Chronic LV volume overload -» compensatory
LVE initially maintaining cardiac output
• Decompensation (increased LV wall tension) -
»CHF
• LVE – » annulus dilation – » increased MR
• Backflow – » LAE, Afib, Pulmonary HTN

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 MR Symptoms
• Similar to MS
• Dyspnea, Orthopnea, PND
• Fatigue
• Pulmonary HTN, right sided failure
• Hemoptysis
• Systemic embolization in A Fib

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 Recognizing Chronic
Mitral Regurgitation
• Pulse: • Murmer-Fixed MR:
– brisk, low volume – pansystolic
• Apex: – loudest apex to axilla
– no post extra-systolic
– hyperdynamic
accentuation
– laterally displaced
– palpable S3 +/- thrill
• Murmer-Dynamic MR(MVP)
– mid systolic
– late parasternal lift 2 to LA
filling – +/- click
• S 1 soft or normal –  upright

• S 2 wide split (early A2) • S 3 / flow rumble if severe

unless LBBB

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 Recognizing Acute Severe
Mitral Regurgitation
• Acute severe dyspnea, CHF • RV lift
& hypotension • TTE/TEE for diagnosis
• LV size normal – Chordal or papilllary
• LV may/may not be muscle rupture/tear
hyperdynamic – Infarction with papillary
• Loud S1 muscle ischaemia or tear
• Systolic murmur may/may – Infectious endocarditis
not be pan-systolic with leaflet perforation
• Inflow/rumble or disruption or chordal
• S3 present-may be only tear
abnormality – Flail MV segment

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 Comparing AS and MR

Systolic Murmurs
• Aortic stenosis
• Mitral insufficiency
• Mitral valve prolapse
• Tricuspid insufficiency
Diastolic Murmurs
• Aortic insufficiency
• Mitral stenosis
S1 Implementation
© Continuing Medical S2 ® S1
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 Assessing Severity of Chronic
Mitral Regurgitation
Measure the Impact on the LV:
• Apical displacement and size
• Palpable S3
• Longer/louder MR murmer (chronic MR)
• S3 intensity/ length of diastolic flow rumble
• Wider split S2 (earlier A2) unless HPT narrows
the split

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 Recognizing Mitral
Regurgitation
• ECG: • CXR:
– LA enlargement –  LV
– Afib –  LA
– LVH (50% pts. With –  pulmonary
severe MR) vascularity
– RVH (15%) – CHF
– Combined – Ca++ MV/MAC
hypertrophy (5%)

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© Continuing Medical Implementation ®
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 Mitral Valve Surgery
• Only effective treatment is valve
repair/replacement
• Optimal timing determined:
– Presence/absence of symptoms
– Functional state of ventricle
– Feasability of valve repair
– Presence of Afib/PHTN
– Preference/expectations of patient

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 Mitral Regurgitation
ACC/AHA recommendations
Surgery Recommended in patients who are
• Symptomatic
• Asymptomatic with
– Any LV dysfunction
– Atrial fibrillation
– Pulmonary hypertension
– Reparable valves
– Recurrent VT

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Valvular Heart Disease
Mitral Stenosis

Yerizal Karani MD
Cardiology Division
Faculty of Medicine Andalas University
 Mitral Stenosis
• Etiology
• Symptoms
• Physical Exam
• Severity
• Natural history
• Timing of Surgery

© Continuing Medical Implementation

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 Mitral Stenosis: Etiology
• Primarily a result of rheumatic fever
(~ 99% of MV’s @ surgery show rheumatic damage )
• Scarring & fusion of valve apparatus
• Rarely congenital
• Pure or predominant MS occurs in approximately
40% of all patients with rheumatic heart disease
• Two-thirds of all patients with MS are female.

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 Mitral Stenosis:
Pathophysiology

• Normal valve area: 4-6 cm2

• Mild mitral stenosis:
– MVA 1.5-2.5 cm2
– Minimal symptoms
• Mod mitral stenosis
– MVA 1.0-1.5 cm2 usually does not produce symptoms
at rest
• Severe mitral stenosis
– MVA < 1.0 cm2

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 Mitral Stenosis:
Pathophysiology
Right Heart Failure:  Pulmonary HTN
Hepatic Congestion Pulmonary Congestion
JVD LA Enlargement
Tricuspid Regurgitation Atrial Fib
RA Enlargement LA Thrombi
 LA Pressure

RV Pressure Overload
RVH
RV Failure LV Filling

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 Mitral Stenosis: Symptoms
• Fatigue
• Afib
• Palpitations • Systemic embolism
• Cough • Pulmonary infection
• Hemoptysis
• SOB
• Right sided failure
• Left sided failure – Hepatic Congestion
– Edema
– Orthopnea
• Worsened by conditions that
– PND  cardiac output.
• Palpitation – Exertion,fever, anemia,
tachycardia, Afib, intercourse,
pregnancy, thyrotoxicosis

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 Recognizing Mitral
Stenosis
Palpation:
• Small volume pulse Auscultation:
• Tapping apex-palpable S1 • Loud S1- as loud as S2 in aortic
• +/- palpable opening snap area
(OS) • A2 to OS interval inversely
• RV lift proportional to severity
• Palpable S2 • Diastolic rumble: length
proportional to severity
ECG: • In severe MS with low flow- S1,
• LAE, AFIB, RVH, RAD OS & rumble may be inaudible

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 Mitral Stenosis: Physical Exam

S1 S2 OS S1

• First heart sound (S1) is accentuated and snapping

• Opening snap (OS) after aortic valve closure
• Low pitch diastolic rumble at the apex
• Pre-systolic accentuation (esp. if in sinus rhythm)

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 Common Murmurs and
Timing (click on murmur to play)

Systolic Murmurs
• Aortic stenosis
• Mitral insufficiency
• Mitral valve prolapse
• Tricuspid insufficiency
Diastolic Murmurs
• Aortic insufficiency
• Mitral stenosis
S1 Implementation
© Continuing Medical S2 S1
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 Auscultation-
Timing of A2 to OS Interval

• Width of A2-OS
Say Timing Severity Other
inversely correlates seconds of MS HS’s
with severity Prrr  0.06 Severe

• The more severe the Pada .07-.08 Mod-

severe
MS the higher the LAP Pata .08-.09 Mod
the earlirthe LV Papa  0.10 Mild PK
pressure falls below 0.1-0.110
Tu-  .12 A2-S3
LAP and the MV opens huh 0.12-0.18

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 Mitral Stenosis: Natural History
• Progressive, lifelong disease,
• Usually slow & stable in the early years.
• Progressive acceleration in the later years
• 20-40 year latency from rheumatic fever to
symptom onset.
• Additional 10 years before disabling symptoms

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 Mitral Stenosis: Complications
• Atrial dysrrhythmias
• Systemic embolization (10-25%)
– Risk of embolization is related to, age, presence of atrial
fibrillation, previous embolic events
• Congestive heart failure
• Pulmonary infarcts (result of severe CHF)
• Hemoptysis
– Massive: 20 to ruptured bronchial veins (pulm HTN)
– Streaking/pink froth: pulmonary edema, or infection
• Endocarditis
• Pulmonary infections

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 Mitral Stenosis: EKG
• LAE
• RVH
• Premature contractions
• Atrial flutter and/or fibrillation
–  freq. in pts with mod-severe MS for several years
– A fib develops in  30% to 40% of pts w/symptoms

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A 75 year old woman with loud first heart sound
and mid-diastolic murmer

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 Mitral Stenosis: Role of
Echocardiography
• Diagnosis of Mitral Stenosis
• Assessment of hemodynamic severity
– mean gradient, mitral valve area, pulmonary artery
pressure
• Assessment of right ventricular size and function.
• Assessment of valve morphology to determine
suitability for percutaneous mitral balloon valvuloplasty
• Diagnosis and assessment of concomitant valvular lesions
• Reevaluation of patients with known MS with changing
symptoms or signs.
• F/U of asymptomatic patients with mod-severe MS
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 Mitral Stenosis:Therapy
• Medical
– Diuretics for LHF/RHF
– Digitalis/Beta blockers/CCB: Rate control in A Fib
– Anticoagulation: In A Fib
– Endocarditis prophylaxis
• Balloon valvuloplasty
– Effective long term improvement

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 Mitral Stenosis:Therapy
• Surgical
– Mitral commissurotomy
– Mitral Valve Replacement
• Mechanical
• Bioprosthetic

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Recommendations for Mitral Valve Repair
for Mitral Stenosis

• ACC/AHA Class I
– Patients with NYHA functional Class III-IV symptoms, moderate or
severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology
favorable for repair if percutaneous mitral balloon valvotomy is
not available
– Patients with NYHA functional Class III-IV symptoms, moderate or
severe MS (mitral valve area <1.5 cm 2 ),*and valve morphology
favorable for repair if a left atrial thrombus is present despite
anticoagulation
– Patients with NYHA functional Class III-IV symptoms, moderate or
severe MS (mitral valve area <1.5 cm 2 ),* and a non-pliable or
calcified valve with the decision to proceed with either repair or
replacement made at the time of the operation.

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