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CASE REPORT

Nurhikmawati

INTRODUCTION
It has long been recognized that thyroid disease
states exert profound effects on the heart and
circulatory system
The close physiological relationship is affirmed by
predictable changes in cardiovascular function
across the entire range of thyroid disease states

INTRODUCTION
Thyrotoxicosis associated with a 50% decline in
systemic vascular resistance
arterial resistance and venous tone venous
return of blood to the heart
mean circulatory filling pressure
oxygen consumption in the periphery and
metabolic demands blood supply and pumping
action of the heart
atrial natriuretic peptide : total protein
synthesis (cardiac hypertrophy)

PATIENT IDENTITY
Name
: Nn. P
Medical Record : 394801
Age
: 22 years old
Address
: Makassar
Admitted to hospital : july 18th 2011

HISTORY TAKING
Chief complaint : Shortness of breath
History taking :
Its been felt since 1 day before admitted to the
hospital, and worsening 3 hours before
admission. Started with chest pain, not radiated,
and no cold sweat
Epigastric pain (+), nausea (+), vomitting (+),
about 3 times
Urination and defecation : normal

MEDICAL HISTORY
History of Hyperthyroid (+), since 2 years
ago, regularly on treatment. (Thyrax,
maintate)
History of heart disease (-)

PHYSICAL EXAMINATION
Vital Sign :

Blood pressure
: 140/90 mmHg
Pulse
: 140x/min
Inspiratory rate : 36x/min
Body temperature
: 36.5oC

Head : Anaemia (-), cyanosis(-)


Neck : JVP R-1 cmH20
Chest : vesicular, Rh-/- Wh -/Heart : S1/S2 regular, murmur (-)
Abdominal : flat, liver/spleen impalpable
Ekstremities : edema -/-

LABORATORY FINDING

Hb
: 14.5 gr/dl
Leukosit : 5.71 x 103 /L
Trombosit : 273.000/ L
Hematokrit
: 41.8 %

Na
: 136
K
: 3.1
Cl
: 104
Albumin : 3.6
FT4
: >7.77
TsHs
: 0.009

GDS
: 101 mg/dl
Ureum
: 18 mg/dl
Kreatinin : 0.4 mg/dl
SGOT : 170 u/L
SGPT
: 400 u/L
Chol. Total : 100 mg/dl
Chol HDL : 32 mg/dl
Chol. LDL : 52 mg/dl
TG
: 82 mg/dl

ADDITIONAL EXAMINATION

ECG :
- Sinus Tachycardia, HR : 150x/menit
- normoaxis

ADDITIONAL EXAMINATION

Echocardiography :

Working Diagnosis
Thyroid Heart Disease

MANAGEMENT

O2 3-4 liter/minute
IVFD NaCl 0.9% 10 dpm
Bisoprolol 2,5 mg 1 0 0
Valisanbe 2 mg 0 0 1
Monitor Rate

Planning

Laboratorium examination : SGOT/SGPT, Ur/Cr, elektrolit

Consult to Endocrine and metabolic department

FOLLOW UP

S : Shortness of breath (+), feels difficult to breath, Chest


pain (+), feels like stabbed, radiated to her back
Vital Sign :
Blood pressure
: 130/80 mmHg
Pulse
: 110x/min
Inspiratory rate : 36x/min
Body temperature
: 36.5oC
Head : Anaemia (-), cyanosis(-)
Neck : JVP R-1 cmH20
Chest : vesicular, Rh-/- Wh -/Heart : S1/S2 regular, murmur (-)
Abdominal : flat, liver/spleen impalpable
Ekstremities : edema -/-

FOLLOW UP
LABORATORIUM
19/7/2011
Hb
: 13.6 gr/dl
Leukosit : 5.19 x 103 /L
Trombosit : 269.000/ L
Hematokrit
: 39.2 %
LED
: 53 mm/83 mm
PT
: 10.8 control 12.1
aPTT
: 26.7 control 25.3
Fibrinogen : 512 control 272
INR
: 0.94
D-dimer : 0.75 ng/ml

FOLLOW UP
LABORATORIUM
20/7/2011
Hb
: 13.0 gr/dl
Leukosit : 5.9 x 103 /L
Trombosit : 293.000/ L
Hematokrit
: 40.6 %
LED
: 49/ 61

PT
: 9.9 control 11.8
aPTT
: 25.2 control 24.2
Fibrinogen : 505 control 276
D-dimer : 0.28
INR
: 0.87

FOLLOW UP
LABORATORIUM
20/7/2011 (akademis)
CK : 203.1
CK MB: 28.5
Trop.T : negative

FOLLOW UP
LABORATORIUM
21/7/2011
Hb
: 13.7 gr/dl
Leukosit : 8.08 x 103 /L
Trombosit : 323.000/ L
Hematokrit
: 39.2 %

Fibrinogen : 311 control 200


D-dimer : 0.28
INR
: 0.87

CK : 19
CK MB: 21

FOLLOW UP
LABORATORIUM
25/7/2011 (akademis)
SGOT : 18.9
SGPT : 68.1
LDH : 156.9
CK : 100
CK MB: 29.9
Trop.T : negative

ADDITIONAL EXAMINATION

CT scan thoraks with contrast :


Bronchopneumonia bilateral
Cardiomegaly
Theres no sign of Aorta dissection

Working Diagnosis
Thyroid Heart Disease
Susp. Myocarditis

MANAGEMENT

O2 3-4 liter/minute
IVFD NaCl 0.9% 10 dpm
Methyprednisolone 125 mg/12 hours/IV
Ozid 1 vial/24hours/IV
Propanolol 10 mg 3x2 tab
Lugol 3x10 gtt
Hepamerz 3x1 sachet
Xanax 0 - 1
Ronem 500 mg/12 hours/IV
Meloxicam 7,5 mg 1- 0 1
Ramipril 5 mg 0 0 1

DISCUSSION

INTRODUCTION
As early as 1806 , a persistent inflammatory
process following such an infection (eg,
diphtheria) of the myocardium led to progressive
cardiac damage and dysfunction
In 1837, the term myocarditis was first introduced
as inflammation or degeneration of the heart by
postmortem
Endomyocardial biopsy in 1980 allows the
sampling of human myocardial tissue during life
and antemortem diagnosis of myocarditis.

INTRODUCTION
Studies suggest that myocarditis is a major cause
of sudden(20%), unexpected death in adults less
than 40 years of age
Prospective and retrospective studies have
identified myocardial inflammation in 1 to 9
percent of routine postmortem examinations.

CAUSATION

A large variety of infections, systemic diseases,


drugs, and toxins have been associated with the
development of this disease
Viruses, bacteria, protozoa, and even worms have
been implicated as infectious agents.

Pathophysiology
Several mechanisms of myocardial
damage
(1) Direct injury of myocytes by the
infectious agent
(2) Myocyte injury caused by a toxin such
as that
from Corynebacterium diphtheriae
(3) Myocyte injury as a result of infectioninduced immune reaction or
autoimmunity.

Pathophysiology
Triphasic disease process
Phase I: Viral Infection and Replication
Phase 2: Autoimmunity and injury
Phase 3: Dilated Cardiomyopathy

Phase I: Viral Infection and


Replication
Coxsackievirus B3 causes an infectious phase,
which lasts 7-10 days, and is characterized by
active viral replication
During this phase initial myocyte injury takes
place, causing the release of antigenic
intracellular components such as myosin into the
bloodstream

Phase 2: Autoimmunity and


injury
The local release of cytokines, such as
interleukin-1, interleukin-2, interleukin-6,
tumor necrosis factor (TNF), and nitric
oxide may play a role in determining the Tcell reaction and the subsequent degree of
autoimmune perpetuation
These cytokines may also cause reversible
depression of myocardial contractility
without causing cell death.

Phase 2: Autoimmunity and


injury
Immune-mediated by CD8 lymphocytes and
autoantibodies against various myocyte
components
Antigenic mimicry, the cross reactivity of
antibodies to both virus and myocardial proteins
Myocyte injury may be a direct result of CD8
lymphocyte infiltration

Phase 3: Dilated
Cardiomyopathy
Viruses may also directly cause myocyte
apoptosis.
During the autoimmune phase, cytokine activate
the matrix metalloproteinases, such as
gelatinase, collagenases, and elastases.
In later stages of immune activation, cytokines
play a leading role in adverse remodeling and
progressive heart failure.
Cardiomyopathy developed despite the absence
of viral
proliferation but was correlated with elevated
levels of
cytokines such as TNF.

Clinical Findings
Symptoms and Signs
- Patients(59%) frequently present days to weeks
after an acute febrile illness, particularly a flu-like
syndrome
- Myocarditis is most commonly asymptomatic,
with no evidence of left ventricular dysfunction
- fever, malaise, fatigue, arthralgias, myalgias,
and skin rash.
-Cardiac symptoms may result from systolic or
diastolic left ventricular dysfunction or from
tachyarrhythmias or bradyarrhythmias (dyspnea,
fatigue, decreased exercise tolerance,
palpitations )

Clinical Findings
Symptoms and Signs
- Chest discomfort(35%) is a common
symptom
and is typically pericardial in nature
- Myocarditis may present as sudden
death, as a
result of malignant ventricular
arrhythmias or
complete heart block
-Systemic and pulmonary thromboemboli
have
also been noted.

Clinical Findings
Physical Examination
-Tachycardia, hypotension, fever and tachycardia
may be disproportionate to the degree of fever
-Bradycardia is seen rarely, and a narrow pulse
pressure is occasionally detected
-Murmurs of mitral or tricuspid regurgitation are
common , S3 and S4 gallops may also be heard.
-Distended neck veins, pulmonary rales, wheezes,
gallops, and peripheral edema may be detected

Diagnosis of Myocarditis

Suspicious for myocarditis = 2 positive categories


Compatible with myocarditis = 3 positive categories
High probability of being myocarditis = all 4
categories positive

Category I: Clinical Symptoms


Clinical heart failure
Fever
Viral prodrome
Fatigue
Dyspnea on exertion
Chest pain
Palpitations
Presyncope or syncope

Category II: Evidence of Cardiac


Structural/Functional Perturbation in the Absence of
Regional Coronary Ischemia
Echocardiography evidence
Regional wall motion abnormalities
Cardiac dilation
Regional cardiac hypertrophy
Troponin release High sensitivity (>0.1 ng/ml)
Positive indium-111 antimyosin scintigraphy and

Normal coronary angiography or


Absence of reversible ischemia by coronary
distribution on perfusion scan

Category III: Cardiac Magnetic Resonance Imaging


Increased myocardial T2 signal on inversion
recovery sequence
Delayed contrast enhancement following
gadolinium-DTPA infusion

Category IV: Myocardial BiopsyPathological or


Molecular Analysis
Pathology findings compatible with Dallas criteria

Presence of viral genome by polymerase chain


reaction or in situ hybridization

Diagnostic Studies
Electrocardiography
The most common abnormality is sinus
tachycardia.
may show ventricular arrhythmias or heart
block, or it may mimic the findings in acute
myocardial infarction or pericarditis.
Relations between these clinical and laboratory
findings

Diagnostic Studies
Chest radiograph
-Mild to moderate cardiomegaly from
dilatation of the left or right ventricular
cavity
-The cardiac silhouette may also be
globular when a pericardial effusion is
present
- Venous congestion and pulmonary
edema may be seen in more severe cases

Diagnostic Studies
Echocardiography
myocardial contractility , chamber
sizes ,
valvular function
Left ventricular systolic dysfunction,
regional wall motion abnormalities ,
global hypokinesis
LV may be normal in size or minimally
enlarged
Mitral or tricuspid regurgitation
Mural thrombi in 15% of cases

Diagnostic Studies
- helpful in demonstrating abnormalities of
diastolic filling that mimic restrictive
cardiomyopathy and indistinguishing
ventricular dilatation from pericardial
effusion
- monitor the course of the illness and to
evaluate therapy

Diagnostic Studies
Myocardial imaging
-Gallium-67 imaging
-> active inflammation of the
myocardium
and pericardium
-Indium-111 monoclonal antimyosin
antibody imaging
-> detecting myocyte injury in patients
-Contrast media-enhanced MRI
->detecting myocardial inflammation

Diagnostic Studies

Cardiac catheterization
- elevated left ventricular end-diastolic pressure,
a depressed cardiac output, and increased
ventricular volumes
- Coronary angiogram typically demonstrates
normal coronary arteries.

Diagnostic Studies
Endomyocardial biopsy
- gold standard for the diagnosis of
myocarditis
-Dallas criteria
(an inflammatory infiltrate of the
myocardium +injury to the adjacent
myocytes)
-borderline myocarditis is made when the
infiltrate is not accompanied by myocyte
injury

Others test

Elevated erythrocyte sedimentation rate (ESR) , mild to


moderate leukocytosis
CK-MB , Cardiac troponin-I
Other laboratory analyses that may be useful include a
Mono-spot test, Epstein-Barr virus titers, hepatitis serology,
and urine and serum for cytomegalovirus (CMV).

Triphasic disease process.

Management of myocarditis
Management is dictated by clinical signs
and symptoms.
MANY proposed therapies, most have only
a theoretical basis. Some have been
tested in animal models
Conventional heart failure therapy is
currently the only accepted therapy for
myocarditis including ACE inhibitors,
angiotensin receptor blocking agents,
diuretics, -blockers or amiodarone.

Diet and Lifestyle


Restrict salt intake to 2-3g of sodium per
day
Exercise especially during the acute phase
of Coxsackie virus B3 murine myocarditis
enhances viral replication rate, enhances
immune mechanisms and increases
inflammatory lesions and necrosis.
Resumption of physical activity can take
place within 2 months of the acute
disease.

THANK YOU