Peny.

Jantung REUMATIK dan

Peny. Jantung TIROID
Dr. Zainal Safri, SpPD, SpJP
Dr. Dede Moeswir, SpPD

Pendahuluan
Demam Rematik
proses radang akut tenggorokan yang

didahului oleh infeksi kuman streptokokus

beta hemolitikus grup A
penyakit multi-organ, hanya kecacatan
pada jantung yang permanen

mayoritas

penyakit jantung yang diperoleh

pada anak-anak, yang berdampak besar
terhadap morbiditas dan mortalitas.

Penyakit Jantung Rematik

Penyakit Jantung Rematik kronik
merupakan residual sequele dari
demam rematik akut, dan diperkirakan
282.000 penderita demam rematik akan
menderita
PJR setiap tahunnya

Meski banyak penderita PJR yang tidak

dapat mengingat/mengetahui riwayat
demam rematik sebelumnya

Epidemiologi
1994:

2005:

12 juta penderita penyakit jantung

rematik 4
15 hingga 19 juta penderita,
2.4 juta berusia 5-14 tahun
79% diantaranya dari negara berkembang

Indonesia:
0,3-0,8 diantara 1000 anak
sekolah Indonesia menderita demam
rematik 2

DEMAM REUMATIK :
- >> 5 15 THN.
- DAN JARANG < 5 THN.

MANIFESTASI KLINIS :
- ARTRITIS (70%)
- KARDITIS (50%)
- KHOREA (15%)
- NODULUS SUBKUTAN & ERITEM
MARGINATUM (5%)
3

DIAGNOSIS PJR

RIW. DEMAM REUMATIK

KRITERIA JONES
(2 MAYOR ATAU 1 MAYOR + 2 MINOR)

TAB. 1. KRITERIA JONES

KRITERIA MAYOR
KRITERIA MINOR
-KARDITIS
-DEMAM
-POLIARTRITIS
-ARTHALGI
-KHOREA
-INT. P-R
MEMANJANG
-NOD. SUBKUTAN
-ERIT. MARGINATUM REAKTAN FASE
AKUT
DITAMBAH BUKTI INF. STREPTOKOKUS :
-BIAKAN FARING (+) STREPT.
-ASTO
5

Diagosis karditis :
. Perubahan sifat bising jantung organik
. Ukuran jantung bertambah
. Bising gesek perikardial/efusi perikardial
. Tanda gagal jantung kongestif
Nodul subkutan : nodul kecil, seukuran kacang,
lokasi pada tendo ekstensor tangan, kaki, siku, tepi
patela, kulit kepala.
Khorea : gangguan sistim syaraf pusat yang ditandai
gerakan tiba-tiba, tanpa tujuan, tidak teratur,
kelemahan otot, emosi tak stabil.
Eritem marginatum : ruam merah bersifat
sementara, berpindah-pindah, tidak gatal, tidak
indurasi, memucat pada tekanan.
Test antibodi streptokokus : standarisasi paling
luas digunakan Pasien DR titer > 200 unit/ ml.

FOTO THORAX UKURAN JANTUNG

EKG PEMANJANGAN INT. P R

EKOKARDIOGRAFI DOPPLER :
- RUANGAN JANTUNG
- FUNGSI VENTRIKEL
- DERAJAT REGURGITASI KATUP
6

PENATALAKSANAAN :
1. ISTIRAHAT
2. ERADIKASI KUMAN
3. ANTI RADANG
4. SUPORTIF
5. PROFILAKSIS SEKUNDER
6. PENYULUHAN
7. OPERASI
7

TERAPI
1 Salisilat
2. Penisilin (Tx AHA):
Anak anak: Benzathin penicilline 600.000-900.000 U
Dewasa: Benzathin penicilline 1,2 juta U
Ataau : oral Penicilline 4 x 250 mg/ hari (10 hari)
atau kombinasi IM daan oral (10 hari)
Bila alergi peniciline eritromisin 4 x 250 mg (10 hari)
3. Kortikosteroid
4. Bed rest
5. TKTP
6. Penenang untuk chorea

PROFILAKSIS TERHADAP
KEKAMBUHAN
Jauhi penderita URI
2. Penisilin
Pada non RHD: min 3-5 tahun
Pada RHD, resiko tinggi: selama mungkin
3. Sulfonamides
4. Pengobatan sedini mungkin URI
1.

ANTIBIOTIKA PADA DEMAM RHEUMA

AKUT
Penisilin diberikan selama perjalanan
penyakit untuk eradikasi streptokokus.
Injeksi Benzathin Penisilin G 1,2 juta unit
sekali. Pilihan obat per oral adalah penisilin
G 200.000-250.000 unit 4 kali shari
Bagi penderita yang alergi terhadap
penisilin dapat diberi eritromisin 250 mg 4
kali sehari
Lama pengobatan 10 hari.

Report of a WHO Expert Consultation Geneva 10 October 1 November 2001

World Health Organization. Geneva 2004

Prevensi Primer

Report of a WHO Expert Consultation Geneva 10 October 1 November 2001

World Health Organization. Geneva 2004

Profilaksis Sekunder

Report of a WHO Expert Consultation Geneva 10 October 1 November 2001

World Health Organization. Geneva 2004

Durasi Profilaksis

Report of a WHO Expert Consultation Geneva 10 October 1 November 2001

World Health Organization. Geneva 2004

Peny. Jantung Thyroid

ACTION OF THYROID HORMONE

Two active hormones are secreted by the
thyroid: thyroxine (T4) and triiodothyronine
(T3).
Most studies support the hypothesis that T3
is the final mediator and T4 is a
prohormone,

Thyroid hormone's effect

Thyroid hormone (TH) can have a (+) or (-) effect on

regulating gene transcription.

Positive effects : myosin heavy-chain alpha, Ca2+-ATPase,

Na+, K+-ATPase, beta1-adrenergic receptor, glucose
transporter, cardiac troponin, and atrial natriuretic protein.

Negative effects regulate genes, e.g., myosin heavy-chain

beta and the glucose transporter Glut-1.

Thyroid Extranuclear Actions

T3 increases both glucose and Ca uptake by

the heart.

Extranuclear effects include THs direct

effect on Ca current and cytosolic Ca
changes induced by inotropic factors.

RELATIONSHIP BETWEEN THE THYROID AND

THE SYMPATHETIC NERVOUS SYSTEM

The effects of TH on the heart are indirect and secondary to

changes in activity of the sympathetic nervous system.
The cardiovascular effects of hyperthyroidism, i.e.,
tachycardia, systolic hypertension, increased cardiac output,
and myocardial contractility, can be abolished or reduced by
blocking the activity of the sympathetic nervous system.
TH is increasing the activity of the sympathoadrenal system
or by enhancing the response of cardiac tissue to normal
sympathetic stimulation.

RELATIONSHIP BETWEEN THE THYROID AND

THE SYMPATHETIC NERVOUS SYSTEM

TH's effect in three areas has been explored: adrenergic

output, adrenergic receptors, and adrenergic transduction
mechanisms.

Administration of TH causes an increase in both the number

of receptors and their affinity for their ligand, while
hypothyroidism induces the opposite effect.

TH also increases mRNA levels for the beta1-adrenergic

receptor.

RELATIONSHIP BETWEEN THE THYROID AND

THE SYMPATHETIC NERVOUS SYSTEM

Changes in receptor number and affinity then lead to

changes in sensitivity of the myocardium to beta
adrenoceptor agonists. For example, stimulation of
adenylate cyclase activity by isoproterenol is increased in
hyperthyroidism and reduced in hypothyroidism.
Changes are also seen in the force of contraction.
These effects were also observed in vivo in dogs, in
which propranolol-induced reductions in heart rate and
myocardial contractility were greater in hyperthyroid than
euthyroid animals.

Effect of Thyroid Hormone on the Heart

T4 enhances the rate of contraction of cardiac
muscle, even in the presence of adrenergic
blockade.
The major actions of T4 on the left ventricle are
(1) a direct (+) inotropic effect and (2) an
increase in the size of the ventricular cavity
without a change in end-diastolic pressure or
length of the sarcomere in diastole.

Effect of Thyroid Hormone on the Heart

The direct effect of thyroid hormone on the
heart is primarily mediated via a change in
protein synthesis.
Specifically, synthesis of myosin heavy
chains is changed from the beta to the alpha
form.

Effect of Thyroid Hormone on the Heart

TH increases expression of Na-Ca-ATPase, which augments

trans-sarcolemmal Ca influx in cultured ventricular cells.
TH modifies the electrical activity of the heart by several
mechanisms.
It increases recruitment of slower inactivating Na channels.
It modifies the expression and/or composition and thereby the
activity of one or more K channels and several Ca channels.
These effects probably result from altered gene transcription
because of TH.

Effect of Thyroid Hormone on the Heart

The tachycardia in hyperthyroidism appears to be

due to an increased rate of diastolic depolarization
and a decreased duration of the action potential in
the SA node cells.

The propensity for the development of AF may be

due to the shortened refractory period of atrial
cells.

Hyperthyroidism
Hyperthyroidism is a relatively common disease that occurs more often in

women than men, with a peak incidence in the third and fourth decades.
Signs and symptoms : fatigue, hyperactivity, insomnia, heat intolerance,
palpitations, dyspnea, increased appetite with weight loss, nocturia,
diarrhea, oligomenorrhea, muscle weakness, tremor, emotional lability,
increased heart rate, systolic hypertension, hyperthermia, warm moist skin.
Hyperthyroidism is the clinical state resulting from excess production of T4,
T3 or both.
The most common cause is a diffuse toxic goiter
The second most common form of hyperthyroidism is nodular toxic goiter
Serum T4 levels are increased and serum TSH is suppressed.

CARDIOVASCULAR MANIFESTATIONS

Cardiovascular signs and symptoms are therefore

important clinical features of hyperthyroidism.
Palpitations, dyspnea, tachycardia, and systolic
hypertension are common findings.
Diastolic hypertension can also occur. Typically noted
are a hyperactive precordium with a loud first heart
sound, a third heart sound; occasionally, a systolic
ejection click is heard.

CARDIOVASCULAR MANIFESTATIONS

Coronary blood flow are increased, systolic

ejection and preejection period are abbreviated,
pulse pressure is widened, systemic vascular
resistance is reduced.

CARDIOVASCULAR MANIFESTATIONS

The changes in cardiac function are secondary to the

increased metabolic demands of peripheral tissue.
TH exerts a direct cardiac stimulant action independent of
its effect on general tissue metabolism.
Normalization of the myocardial contractile may not occur
until several months after normalization of thyroid function.
The overall pathological consequences associated with
thyrotoxicosis result from an interaction between the effect
of TH on the heart and its effect on the peripheral
circulation.

CARDIOVASCULAR MANIFESTATIONS

Cardiovascular effects of hyperthyroidism.

CARDIOVASCULAR MANIFESTATIONS

C-XR and ECG changes are common, but nonspecific in

hyperthyroidism.
On chest x-ray the left ventricle, aorta, and pulmonary
artery are prominent, and generalized cardiac enlargement
can be noted.
In Px sinus rhythm, the magnitude of the tachycardia in
general parallels the severity of the disease.
Sinus tachycardia is present in 40 % of patients with
hyperthyroidism and occurs most frequently.
Ten to 15 percent of patients with hyperthyroidism have
persistent AF.

CARDIOVASCULAR MANIFESTATIONS
Intraatrial conduction disturbances, manifested
by prolongation or notching of the P wave and
prolongation of the PR interval in patients with
hyperthyroidism.
Second - or third-degree heart block may result.
The cause of the AV conduction disturbance is
not clear.

CARDIOVASCULAR MANIFESTATIONS

Intraventricular conduction disturbances, commonly

RBBB, occur in 15 % of patients with hyperthyroidism
without associated heart disease of other etiology.

Paroxysmal SVTand flutter are rare in hyperthyroidism.

Occult thyrotoxicosis may underlie either chronic or

paroxysmal isolated AF

CARDIOVASCULAR MANIFESTATIONS
Angina and CHF occur in patients with hyperthyroidism.
Five lines of evidence have suggested:
(1) CHF has been produced in animals by administering T4.
(2) CHF in children with thyrotoxicosis and no underlying cardiac
disease.
(3) Angina reported in a hyperthyroid Px with normal coronary arteries,
presumably secondary to thyroid-induced coronary artery spasm.
(4) The abnormal left ventricular function observed in hyperthyroid Px
is not reversed by beta blockade but is reversed by treating the
hyperthyroidism.
(5) The cardiomyopathy in patients with thyrotoxicosis may be
irreversible.

DIAGNOSIS OF HYPERTHYROIDISM
Hyperthyroidism in most patients is clinically
manifested as described above.
The diagnosis is confirmed with a low TSH level,
which reflects an elevated level of TH in the blood.
In elderly patients with apathetic hyperthyroidism,
cardiovascular manifestations predominate,
specifically, AF and/or CHF.

TREATMENT OF CARDIOVASCULAR
MANIFESTATIONS OF
HYPERTHYROIDISM
Beta blockers can be administered, with caution in

patients with CHF.

The heart failure with tachycardia, beta blockade may be
beneficial. Beta-blocking drugs also slow the ventricular
rate in AF.
The agents for correcting the fundamental defect are
thionamides.
Iodine inhibits the release of TH from the thyrotoxic gland.
It is therefore useful for rapid amelioration of the
hyperthyroid state in patients with thyroid heart disease.