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: 12 juta penderita penyakit jantung rematik
4

2005: 15 hingga 19 juta penderita,



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

2.4 juta berusia 5-14 tahun
79% diantaranya dari negara berkembang

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)
4
TAB. 1. KRITERIA JONES
KRITERIA MAYOR KRITERIA MINOR
-KARDITIS
-POLIARTRITIS
-KHOREA
-NOD. SUBKUTAN
-ERIT. MARGINATUM
-DEMAM
-ARTHALGI
-INT. P-R
MEMANJANG
- 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
1. 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
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.