I.

INTRODUCTION
1.1 Thyroid Heart Disease
Thyroid gland is part of endocrine system that have many effect in metabolic
process for all tissue, especially in heart. Thyroid gland disorder can cause smiliar
symptom to primary heart disease. Thyroid heart disease is one of heart disease with
some manifestation that occured because of increasing or decreasing free tyrosin
hormon in sirculation.1
Hypertiroid can be caused by several causes, including grave disease, toxic
multinodular struma, toxic adenoma, hashimoto Thyroiditis, Thyroiditis post partum,
viral, drugs like amiodaron, hypofisis adenoma, etc. hypertrioidsm can occur ein
endemic area or sufficient iodium, so people who have hypertiroidsm need better
treatment.1,2
Many case of hyperthyroidism can be found in Indonesia, and occure more in
women than men with ratio 1: 5, and also many case occured in midle age. Thyroid
disease often occure during pregnancy. Sex hormon in women is more susceptible to
Thyroid gland disfungction. There is strong familial (genetic) predisposition in about
15% of graves patients who have close relatives of the same disorder and
approximately 50% of families of patients with graves disease have thyroid
autoantibodies circulating in the blood. This disease can occur at any age, with a peak
incidence in the age group of 20-40 years. Hyperthyroidism does not only occur in
middle age, but also in children and adolescents can occur, even though the incidence
and prevalence in Indonesia is uncertain. Some foreign resources say the incidence of
childhood is estimated at 1 / 100,000 children per year. Starting from 0.1 / 100,000
children per year for children aged 0-4 years, up to 3 / 100,000 children per year in
adolescence.3
Hyperthyroidism causes abnormalities in many organs, one of them is
cardiovascular system. Several studies and research have suggested that atrial
fibrillation occure 33 out of 47% of patients over the age of 60 years. As well as less
than 1% of cases of new atrial fibrillation due to hyperthyroidism. A study conducted
by Nakazawa reported 11,345 patients with hyperthyroidism , there are 288 cases
with atrial fibrillation, 6 cases experienced systemic embolism, 4 of whom had heart
failure. 5 of them were more than 50 years old. Hyperthyroidism can cause heart
failure, atrial fibrillation, mitral regurgitation and tricuspid regurgitation.4

A. Clinical Manifestation
Hyperthyroidism can cause various clinical manifestations, depending on the
etiology of hyperthyroidism, which affects the function of the heart, blood pressure,
body metabolism, excretion through the kidneys, gastrointestinal system ,muscles,
fat, and hematopoietic system. Clinical manifestations that occur due to
hyperthyroidism affect more to function of the heart, where the heart is driven to
work faster, resulting in heart muscle contracting faster due to ionotropic effects that
directly exaggerate the thyroid hormone excessively so as to increase the long chain
expansion ratio α: β, with the heart muscle contracting faster, also resultng decreased
cardiac output and increases blood pressure, the cardiac ictus clearly visible,
cardiomegaly, systolic murmur with pulse. Cardiac arrhythmias occured almost
without exception, including supraventricular that happened especially in young
patients. Between 2% to 20% of hyperthyroidsm patient appear with atrial
fibrillation, and 15% of patients with atrial fibrillation are unexplained. Atrial
fibrillation decreases the efficiency of heart response to increase circulation needs and
can cause heart failure.5

B. Hormon Effect To Cardiovascular System

The direct effect of thyroid hormones is generally due to the effect of T3 that
binds to receptors in the nucleus of cells which regulates the expression of genes that
responsive to thyroid hormones, in other words that changes in heart function are
mediated by regulation of heart-specific T3 gen.6
 Table I. Direct Influence of Thyroid Hormone on The Cardiovascular System
Direct Effect Indirrect Effect
Regulation of specific heart genes Adrenergic activity increases
Regulation of thyroid hormone receptor Increase work of the heart
expression
Increase heart contractility Heart hypertrophy
Decreased peripheral vascular resistance Cardiac Output Increase

There are two types of T3 receptor genes, alpha and beta, with at least two
mRNAs for each gene, namely alpha-1 and alpha-2, and beta-1 and beta-2. T3 also
works on extranuclear by increasing protein synthesis. The following is an
explanation of the direct effect of thyroid hormone on the cardiovascular system.6,7
1. T3 regulate Heart Spesific Genes
Administration of T3 in animals increases cardiac muscle contractility through
stimulation of the synthesis of fast myosin heavy chain and inhibits the
appearance of slow beta isoform. In human heart ventricle, mostly consists of
myosin heavy chain, so T3 ¬ does not affect changes in myosin. Increasing
contractility in human mostly because of increased reticulo sarcoplasma
expression CA2+ATPase, altough most are also by beta isoform.8
2. T3 regulate receptor expression that sentitive to thyroid hormones
T3 causes an increase in the sarcoplasmic reticulum Ca2 + ATPase and a
decrease in regulatory protein Ca2 + ATPase work. T3 also regulates ATPase-
dependent Na-K, malate enzymes, atrial natriuretic factors, Ca channels, and
beta-adrenergic receptors.8
3. Thyroid Hormon Increase Cardiac Muscle Contractility
Thyroid hormones will stimulate the work of the heart by affecting ventricular
function, through increased cardiac contractile protein synthesis or increased
function of the Ca-ATPase sarcoplasmic reticulum so that hyperthyroid patients
will have hypertrophic heart.8
4. Thyroid hormones cause decreased peripheral vascular resistance T3 may affect
the flow of sodium and potassium in smooth muscle cells causing a decrease in
smooth muscle contractility and arteriolar tone of the arteries.8

C. Indirect Effect Thyroid Hormon to Cardiovascular System

The state of hypermetabolism and increased body heat production due to the
influence of thyroid hormones will indirectly affect the cardiovascular system in the
presence of compensation, including:
1. Thyroid hormone increase sympathoadrenal system activity
Hyperthyroid patients have clinical symptoms that are similar to hyperadrenergic
states, whereas hypothyroidism describes a condition in which sympathetic tone
is decreased. In hyperthyroidism there is an increase in the beta-receptor level or
affinity, inotropic responses to isoprotrenol and norepinephrine.8 Many studies
have concluded that thyroid hormones interact with catecholamines where in
hyperthyroid patients there is an increased sensitivity to catecholamine work and
hypothyroidism decreases sensitivity to catecholamines.4,6,9
2. Cardiac Work Increases
Increased stroke volume and heart rate increase cardiac output.
3. Cardiac muscle hypertrophy due to increased heart work
Thyroid hormones do not directly cause the union of amino acids and there is no
measurable effect on contractile protein synthesis of the heart muscle. So, what
causes hypertrophy is an increase in the work of the heart itself.6
4. Decreased peripheral vascular resistance and increased blood volume.
Thyroid hormones cause decreased peripheral vascular resistance. Some
researchers say that thyroid hormones increase metabolic activity and oxygen
consumption that leading to low systemic vascular resistance and reduces blood
diastolic pressure resulting in increased cardiac output.6
D. HyperThyroid Effect to Cardiac Structure and Function
Analysis data of hyperthyroid patient showed that hyperthyroid patients who
experienced cardiac abnormalities were found 14 patients from 136 hyperthyroid
patients whose data was collected. According to the literature, hyperthyroidism is
caused by excessive production of T4 and T3, where T4 and T3 increase the work of
the sympathetic nerves and increases cardiac muscle contractility so cardiac output,
blood pressure and pulse increase. Beside hyperthroid effect to the heart, it also cause
weight loss. hyperfagi, excessive sweating due to hypermetabolism, etc., so that
physical and laboratory examinations of TSH, FT4, T4 and T3 are diagnosed for
hyperthyroidism, and this state of hyperthyroidism is given anti-thyroid drug therapy
so that hyperthyroidism does not cause cardiac abnormalities, because for hypertiroid
to makes cardiac abnormalities ,some factor is needed such time suffering from
hypertiroid, physical diagnosis, laboratorium, and treatment.6,10
Cardiac abnormalities obtained from hyperthyroid patients show that the most
common valve abnormalities are mitral regurgitation, tricuspid regurgitation, aortic
regurgitation, and mitral valve prolapse. The results of this study are consistent with
the results of a study conducted by Kumei Kage in Japan which states that the
incidence and prevalence of mitral regurgitation, tricuspid regurgitation, mitral
regurgitation are accompanied by tricuspid regurgitation, and mitral valve prolapse is
higher in the Graves Disease (GD) group of patients.6

E. Effect of Hyperthyroidism Etiology That Causes Heart Disease

The high production of T4, T3 comes from thyroid hormone stimulation
antibody (TSH-Ab) or thyroid stimulating immunoglobulin (TSI) which interacts
with the TSH receptor in the thyroid follicular epithelial membrane, which results in
an increase in the body's sympathetic nerve activity, that increases sympathetic nerves
in heart, so that electrical impulses from the heart's SA node increase causing
increased cardiac contraction resulting in reduced ventricular ejection fraction,
increased blood pressure and pulse, and makes heart valves to work quickly and
cause chordae tandinea rupture and makes cardiac valve don’t close tightly and valve
regurgitation or prolaps occured.11,12,13
Cardiomyopathy can occur within a few months to several years, as well as
thickening of the cardiac muscle or cardiac hypertrophy due to rapid and increased
cardiac contractions, so that cardiomyopathy and heart failure can occur.14,15

F. Heart Disease Caused by Hypertiroidsm

Heart diseases can be caused by hyperthyroidism. And this is the following
types of heart disease that caused by hypertiroidsm:
1. Mitral regurgitation
Mitral regurgitation is a condition in which blood flow returns from the left
ventricle to the left atrium at systolic phase due to incomplete closure of the
mitral valve. Mitral regurgitation is divided into acute and chronic mitral
regurgitation.15
2. Tricuspid Regurgitation (Tricuspid Regurgitation / TR)
Tricuspid regurgitation is the return of blood flow from the right ventricle to
the right atrium due to the closure of the tricuspid valve. 15
3. Cardiomyopathy
This heart disease is quite special, because it directly affects the heart muscle
or myocardium which is not caused by pericardium disease, hypertension,
coronary disease, congenital abnormalities, or valve abnormalities.15
4. Heart Failure
Heart failure is a clinical syndrome characterized by shortness of breath and
fatigue (at rest or during activity) caused by structural abnormalities or heart
function.15
5. Mitral Valve Prolaps
MVP can occur in primary conditions without any connection with other
diseases and can be familial or non familial. But MVP can also be secondary
to other diseases, such as Ehlers-Danlos syndrome, osteogenesis imperfacta,
pseudoxanthoma elasticum, periarteritis nodosa, myotonic dystrophy, von
 Wildebrand's disease, hyperthyroidism, and congenital malformations. MVP
symptomps are fatigue, palpitations, postural orthostasis, ,other anxiety and
neuropsychiatric symptoms.15
6. Atrial Fibrilation
Atrial fibrillation is an arrhythmia characterized by atrial depolarization
without effective atrial contraction. Thyrotoxicosis manifestations can be
considered in patients with long onset of atrial fibrillation. The prevalence of
atrial fibrillation in hyperthyroidism is 13.8%. Atrial fibrillation symptoms are
determined by multifactors including heart condition, very fast and irregular
ventricular velocity, and atrial contraction absent. 15
7. Sinus Tachycardia
Tachycardia in adults is set 100 times / minute. Sinus tachycardia is a
physiological reaction or pathophysiology of stress, such as fever,
hypotension, thyrotoxicosis, anemia, anxiety, exersion, hypovolemia,
pulmonary embolism, myocardial ischemia, congestive heart failure or
shock.15

G. Laboratory Test
To find out thyroid hormone levels in the body, laboratory tests are performed
by measuring serum TSH levels, serum T4 and T3. For measurement of serum TSH
performed due to thyroid dysfunction that usually arises from primary disorders of
the thyroid gland, this measurement of serum TSH is done more to determine the
thyroid dysfunction that appears. The sensitivity of the hypothalamus-pituitary-
thyroid axis ensures that the occurrence of primary hypothyroidism and
thyrotoxicosis due to primary thyroid disorders or external thyroid hormones can be
detected.4
Serum T4 and T3 serum and T4 and T3 measurements were measured by
various automated testing techniques. Serum total thyroid hormone concentration is
widely available and accurate to predict patients with clear thyroid dysfunction. The
free T4 concentration itself is used to diagnose thyroid dysfunction, where the
number of conditions from true / primary hyperthyroidism or hypothyroidism must be
distinguished. In some cases, true / primary hyperthyroidism is not included in
normal serum TSH levels, on the contrary, there is also the possibility of a condition
in the free thyroxine serum that can become subnormal to individual euthyroid.
Reference value for free T4 index test (FT4I) is euthyroid = 3.7-6.5, hyperthyroidism
= 7,8-20,2, hypothyroidism = 0.1-2.6.12.12

H. Radiology Examination
Radiological features are generally normal, sometimes there is an ascending
or descending aorta enlargement, bulging of the pulmonary segment and in severe
cases an enlarged heart can be found.
 Electrocardiography (ECG)
On the ECG , rhythm disturbances or conduct disturbances can be found quite
often. Usually with sinus tachycardia, atrial fibrillation is found in 10-20% of cases.
In severe cases can be seen enlargement of the left ventricle, sometimes encountered
widening and elongation of the P wave and prolongation of the PR interval,
promising T waves, increased voltage, changes in ST-T wave and QT interval
shortening.15,16
 Echocardiographic examination
Heat examination can use several instruments , and one of them is
echocardiography. In echocardiography equipped with the Dopler with the principle
of sound wave transmission by erythrocytes, so that it can be measured speed
(velocity) and blood flow in the heart and blood vessels. 15,16

I. Theraphy
The principle of theraphy of hyperthyroidism is based on the first cause, with
the aim is to quickly reducing the state of hypermetabolism and thyroid hormone
levels in circulation based on age, gender, cardiovascular system status,
hyperthyroidism level, and history of the disease.10
 The purpose of managing hyperthyroidism is to improve the function of the
heart because of existing cardiovascular disease and to treat the causes of
hyperthyroidsm.
We can find functional disorders in patients with hypertiroid disease
according to the New York Heart Association (NYHA) I to IV classification.
Functional disorders that arise or heart failure are due to the inability of the heart to
meet the needs of the body's hypermetabolic, coupled with the work of thyroid
hormones which directly spur continuously so that it can cause arrhythmias. Frequent
complaints such as palpitations, weakness, shortness of breath, which leads to signs
of left heart failure. Treatment is carried out covering medical and non-medical.12
 Non Medical Therapy
Bed Rest and heart diet with the aim to reduce the burden of the heart with a soft
diet, low in salt and calories, and reduce all forms of stress both physical and
psychological that can aggravate the work of the heart.
 Medical Therapy
A. Beta blockers group, is intended to reduce the work of the heart and fight the
work of thyroid hormones which are inotropic and negative chronotropic. The
beta blocker will rest the heart and give a longer diastolic filling time so it will
overcome the heart failure. Propanolol is also important to overcome the
peripheral effects of thyroid hormones which are stimulators of beta-
adrenergic receptors. Beta blockers are also suppressive to the nervous system
so they can reduce palpitations, anxiety, and hyperkinesis. Beta blockers do
not affect the increase in oxygen consumption. Dosage is 40-160 mg / day if
there is no decompensation of the cord.13
B. Diuretics, can be given to reduce the burden of heart volume and overcome
pulmonary oedem.13
C. Digitalis is still controversial, because of its negative chronotropic but positive
inotropic properties. Negative chronotropic work is expected to overcome the
existing tachycardia, but positive inotropic work can increase the work of the
heart in hyperthyroid heart disease, thyroid hormone is actually also positive
 chronotropic. Dosage more than normal is needed to control heart rate during
atrial arrhythmia.13
D. Anticoagulants is recommended for AF, especially if stays 3 days or more,
continued for 4 weeks after returning to sinus rhythm and euthyroid
conditions. 13
The main therapy for hyperthyroidism to reduce the amount of thyroid
hormone produced by the thyroid gland directly using antithyroid drugs, besides that
it can be supported by radioactive iodine therapy and subtotal thyroidectomy
surgery.14
 Antithyroid drugs
The most commonly used antithyroid drugs are profiliouracil (PTU) and
metimazol, as well as beta-blockers namely propanolol. But sometimes stable iodine
can be used, especially for surgical preparation. Both PTU and metimazol have
almost the same effect, only PTU has the work of inhibiting peripheral changes in T4
to T3, so that PTU is faster to show symptomatic therapy, most patients can be
controlled by hyperthyroidism with PTU 100-150 mg every 6-8 hours. From another
literature, the appropriate dosage for patients with hyperthyroid heart disease is PTU
250 mg and propanolol 20 mg three times a day.11 Or a dose of propanolol 40-160
mg / day and a dose of propylthiouracil 400-600 mg / day and a dose of metimazol
60-80 mg / day. A three times daily dose of PTU is reduced to 200 mg after about 2
weeks (tapering off), then gradually reduced to 100 mg after about 8 weeks.
Furthermore, maintenance doses can be given 50 mg three times a day or
approximately for 1-1.5 years. In PTU administration, the dosage must be monitored
with plasma T4 and T3 levels since the patient showed a different response. The time
needed for plasma T4 and T3 to return to normal varies around 6-10 weeks. Giving
propranolol can be stopped if therapy with PTU has shown good results.
Chronotropic and negative inotropic effects are quick to yield compared to PTU. How
it works is by reducing the synthesis of T4 and T3 syntheses so that recurrence can
occur, unless spontaneous remission occurs, for example in the Grave disease for a
while which must be monitored with plasma T4 and T3 levels. In severe
hyperthyroidism or thyroid crisis, both PTU and metimazol are not very useful
because their work is slow, but their use is still recommended to reduce peripheral T4
conversion to T3. Propanolol is given in large doses, for example 40 mg every 4
hours. Iodine can also be given as a concentrated solution of potassium iodide, 5
drops every 4 hours. It is estimated that iodide works by reducing the release of the
initial form of thyroid hormone from the gland, but to avoid the side effects of iodide
iodide-based effects (although very rare but very dangerous), PTU or metimazol
should also be given in the administration. PTU side effects are usually absent or
slight, in the form of skin rash. While the effects of hypothyroidism can be controlled
by monitoring plasma T4 and T3 levels. 11,12,14

J. Prognosis
In general, progression of hyperthyroidism is characterized by remission and
exacerbations for long periods of time unless the gland is damaged by surgery or
radioactive iodine. Although some patients can remain euthyroid for a long time after
therapy, many eventually get into hypothyroidism condition. So lifetime follow-up is
an indication for all patients with hyperthyroidism.12
II. Case Report
1.1 . Identity
Name : Mr. M
Age : 35 Years Old
Address : Central Aceh
Status : Married
Religion : Islam
Job : Self Employed
Education : Senior High School
MR : 1-17-40-13

1.2 Anamnesis
a. Main Complaint : shortness of breath since ±2 days
b. Current History :
A 35-year-old man, referral from Datuberu District Hospital, Central
Aceh, with a diagnosis of thyroid heart disease and hyperthyroidism. The patient
has undergone treatment at Datuberu District Hospital, Central Aceh, for ± 1 day.
The patient was treated by a colleague of internal medicine, while being treated,
the patient did not experience improvement.
The patient presented to the RSUDZA Emergency Department with
complaints of shortness of breath. Complaints have been felt since 2 days before
entering the hospital. This symptom was initially complained after the patient
returned home to gardening. Shortness of breath is not affected by weather and
dust. He also complain that he often get tired quickly, but can still move. Sleeping
using 2-3 pillows is denied. Waking up in the middle of the night while sleeping
because of tightness denied. Patient also complain of chest palpitations, so patient
often feel anxious and have trouble sleeping. Chest pain and coughing are denied.
Fever is not presented
Previously patient also complained that there was mass in the neck.
Complaints have been felt since 6 months and felt bigger. He routinely seek
treatment for the complaint. He often get sweat even in a cold place, feeling hot
while in the house. Patients also often complain that he feels hard to sleep due to
anxiety and palpitations. Appetite also increases, but body weight is felt to
decrease. There were no complaints of urination and large water.

C. Past Medical History

hypertension, diabetes mellitus, and bronchial asthma were denied

D. Family Medical History

No family member has a smiliar disease

E. History of drug use

The patient took the thyrozol for 6 months

F. Socio-economic history
Patient is an entrepreneur, lives with his wife and children. He is a also smoker

1.3 Physical Examination

Patient is sensorium compos mentis, blood pressure 110/70 mmHg, pulse
frequency 96 times / minute, irregular rhythm, adequate volume, breathing
frequency 26 times / minute and temperature 370 c(axilla).
From physical examination we found, joffroy sign (+ / +), mobius sign (+
/ +), stelwag sign (+ / +), von grafe sign (+ / +), rossenbach sign (+ / +), anemic
conjunctiva palpebra (- / -), scleral jaundice (- / -). Examination thyroid gland are,
symmetrical enlargement found, unclear boundary, supple, there is no tender pain
, there is no signs of inflammation were found, mass moved while swallowing, no
bruit was present. For heart examination we found ictus cordis palpable on 1
finger to lateral from 5th intercostal, thriil (-), heaving, lifiting, tapping (-), left
heart border 5 IC 1 lateral lateral Mid Clavicula Sinistra Line, 3/6 systolic
murmur in mitral valve (-), cardiac thrill (-)
1.4 Laboratory Finding
Laboraturium 31/5/2018 Satuan
Hb 14,0 gr/dl
Leukocytes 6,0 103mm3
Platelet 150 103mm3
Hematocrit 42 %
MCV 71 fL
MCH 24 pg
MCHC 34 %
RDW 19,0 %
Eosinofil
Basofil 0 %
Rod Neutrophil 1 %
Segment Neutrophil 0 %
Limphocytes 65 %
Monocytes 25 %
9 %
Tiroid
Free T4 56,63
TSHs <0,005
Glucose 134 mg/dl
Ureum 40 mg/dl
Creatinin 0,36 mg/dl
Natrium 148 mmol/L
Kalium 4,24 mmol/L
Chlorida 108 mmol/L
Urinalisa
Makroskopis
- Colour Yellow
 - Purity Cloudy
- Density 1,015
- pH 6,5
- Leukocytes Negatif
- Protein Negatif
- Glucose Negatif
- Keton Negatif
- Nitrit Negatif
- Urobilinogen Negatif
- Bilirubin Negatif
- Blood Negatif
Mikroskopis
- Leukocytes 3-4 LBP
- Eritrosit 1-2 LBP
- Epitel 1-2 LBP

Picture 1. Thorax X- Ray PA

 Picture 2. ECG
Rhytm : Fibrilation ST Segment :
HR : 90 bpm Elevasion ST : (-)
Axis : normoaxis Depression ST : (-)
P Wave : Not Identified T Wave : Inverted (-)
PR Interval : not identified U wave : (-)
QRS Complex : 0,08 second LVH :(-)
Pathology Q : (-) RVH : (-)
Impression : AF NVR

Picture 3. Echocardiography
o Echocardiography Conclusion : MR severe, TR severe, LV dilatation, EF
64%
1.5 Diagnosis
When Patient presented to Zainoel Abidin Hospital emergency department,
based on history and physical examination, patients were diagnosed with Grave
disease and atrial fibrillation. After conducting investigations from laboratory thyroid
function, ECG, chest radiographs, and echocardiography, the patient were diagnosed
with Grave disease and thyroid heart disease.

1.6. Therapy
Therapy given to patients was tirozol 1x10 mg, propanolol 2x10 mg, ramipril
1x5 mg, clopidrogel 1x75 mg, and ISDN 2 x 5 mg for 7 days.
III. Discussion
The patient presented to the RSUDZA ED with complaints of shortness of
breath. Complaints have been felt since 2 days before entering the hospital. Shortness
of breath was initially complained after the patient returned home from farm.
Shortness of breath is not affected by weather and dust. Patients also complain that
they often get tired quickly, but can still move. Sleeping using 2-3 pillows is denied.
Waking up in the middle of the night while sleeping because of tightness denied.
Patients also complained of chest palpitations, so patients often feel anxious and have
trouble sleeping. In accordance with the theory, the clinical manifestations that occu
isr due to hyperthyroidism affect work function of the heart, where the heart is forced
to work faster and resulting heart muscle contracting faster due to the excessive
ionotropic effects of thyroid hormone that exits excessively thus increasing the long
chain expansion ratio α: β, with the heart muscle contracting faster also results in the
resulting cardiac output decreasing and increasing blood pressure, clear cardiac
output, cardiomegaly, cytolic noise and pulse. Hyperthyroidism can cause heart
disease such as mitral valve prolapse that often occurs in Graves or Hashimoto's
disease, compared to the normal population. Cardiac arrhythmias occured almost
without exception, including supraventricular that happened especially in young
patients. Between 2% and 20% of patients with hyperthyroidism with atrial
fibrillation, and 15% of patients with atrial fibrillation are unexplained.
From physical examination we found found : joffroy sign (+ / +), mobius sign
(+ / +), sign sign (+ / +), von grafe sign (+ / +), rossenbach sign (+ / +), conjunctiva
pale palpebra (- / -), scleral jaundice (- / -). According to the theory, hyperthyroidism
can cause eyeball disorders because of lymphocyte infiltration in extraocular muscles
with an inflammatory reaction
For heart examination we found ictus cordis palpable on 1 finger to lateral
from 5th intercostal, thriil (-), heaving, lifiting, tapping (-), left heart border 5 IC 1
lateral lateral Mid Clavicula Sinistra Line, 3/6 systolic murmur in mitral valve (-),
cardiac thrill (-). According to the theory, the effect of hyperthyroidism on the
cardiovascular system causes cardiac muscle hypertrophy.
 From ECG examination we found atrial fibrillation. According to theory, for
hypertiroidsm patient, ECG often show rhythm disturbances or conduct disturbances.
Atrial fibrillation is found in 10-20% of cases. In severe cases , it can shown
enlargement of the left ventricle, sometimes encountered widening and elongation of
the P wave and prolongation of the PR interval, promising T waves, increased
voltage, changes in ST-T wave and QT interval shortening.
From Chest X-ray we found cardiomegaly. According to theory, the
radiological feature is generally normal, sometimes there is an ascending or
descending aorta enlargement, the pulmonary segment protruding and in severe cases
also an enlarged heart.
From Echocardiographic examination we found severe mitral regurgitation,
severe tricuspid regurgitation, dilated left ventricle. According to theory, heart disease
can be caused by hyperthyroidism. And below are the types of heart disease that can
be caused from hyperThyroidsm
 Mitral Regurgitation
Mitral regurgitation is a condition in which blood flow returns from the left
ventricle to the left atrium at the time of the systolic heart due to incomplete closure
of the mitral valve.
 Tricuspid Regurgitation
Tricuspid regurgitation is the return of blood flow from the right ventricle to
the right atrium because the tricuspid valve does not close completely
 Cardiomiopathy
This heart disease is special ,because it’s directly affects the heart muscle or
myocardium which is caused not by the result of pericardium, hypertension, coronary
disease, congenital abnormalities, or valve abnormalities.
 Heart Failure
Heart failure is a clinical syndrome characterized by shortness of breath and
fatigue (at rest or during activity) caused by structural abnormalities or cardiac
function.
  Atrial Fibrilation
Atrial fibrillation is an arrhythmia characterized by atrial depolarization
without effective atrial contraction. Thyrotoxicosis manifestations can be considered
in patients with long onset of atrial fibrillation. The prevalence of atrial fibrillation in
hyperthyroidism is 13.8%. Symptoms of atrial fibrillation are determined by
multifactors including heart condition, very rapid and irregular ventricular velocity,
and atrial loss of contraction.
 Sinus Tachycardia
Tachycardia in adults is set 100 times / minute. Sinus tachycardia is a
physiological reaction or pathophysiology of stress, such as fever, hypotension,
thyrotoxicosis, anemia, anxiety, exersion, hypovolemia, pulmonary embolism,
myocardial ischemia, congestive heart failure or shock.
Therapy for this patient was tirozol 1x10 mg, propanolol 2x10 mg, ramipril
1x5 mg, clopidrogel 1x75 mg, ISDN 2x5 mg for 7 days. According to the theory, the
principle of managing hyperthyroidism is based on the causal, with the aim to quickly
reducing the state of hypermetabolism and thyroid hormone levels in circulation.
 Beta blockers group, intended to reduce the work of the heart and fight the
work of thyroid hormones which are negative inotropic and chronotropic.
 Diuretics, can be given to reduce the burden of heart volume and overcome
the lung dam.
 Digitalis is still controversial, because of its negative chronotropic nature but
positive inotropic. Negative chronotropic work is expected to overcome the
existing tachycardia, but positive inotropic work can increase the work of the
heart because of in hyperthyroid heart disease, thyroid hormone is actually
also positive chronotropic. Doses more than normal is needed to control heart
rate during atrial arrhythmia.
 Anticoagulants is recommended for AF, especially if it persist 3 days or more,
continued given for 4 weeks after returning to sinus rhythm and euthyroid
conditions.
 The main therapy for hyperthyroidism is to reduce the amount of hormones
produced by thyroid disease with antithyroid drugs , and also can be supported by
using radioactive iodine therapy and subtotal thyroidectomy surgery.
 Antithyroid Drugs
Antithyroid drugs that commonly used are profilitiourasil (PTU) and
metimazol, as well as beta-blockers like propanolol.
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Dalam Jilid II. Dalam: Sudoyo AW, Setiyohadi B, Alwi I, editor.Edisi 5.
Jakarta:Departemen Ilmu Penyakit Dalam FKUI. 2009. Hal: 1669-1671.
2. Sherwood, L. Organ Endokrin Perifer dalam Fisiologi Manusia Dari Sel ke Sistem.
Edisi 3. EGC, Jakarta. 2001. Hal:644-651
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