[ PDF ] download ... gelatinase, collagenase or
elastase, and they also support the activity of fibroblasts
→ cause fibrosis associated with the dilated
cardiomyopathy
In later phases of the of immune system activation, cytokines
play the key role in the cardiac remodeling and
progressive heart failure
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Myocarditis
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Myocarditis
CLINICAL MANIFESTATIONS AND COURSE
After a prior infectious disease → persistent feeling of
fatigue, tachycardia, dyspnoe and pallor, symptoms are
worsened by physical exertion
Heart damage symptoms include: hepatomegaly, blood
stasis, weakened heart sounds and cardiac gallop,
accidentally discovered extra-systoles
Auscultation findings: a silent systolic murmur resulting
from the valve insufficiency associated with cardiac
dilatation, sometimes pericardial friction murmur
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Myocarditis
DIAGNOSIS
Often severe
Suspicion of myocarditis is caused by unexplainable heart
failure with the history of an ongoing or preceded virus
disease with fever
The course of disease may vary from inconspicuous
manifestations of tachycardia with fever diseases up to severe
and fulminant course accompanied by the circulatory system
breakdown and shock
In children and adolescents with fulminant course,
information about a preceded physical or psychical exertion
with the onset of infarction (sport event, bad cold or
excessive physical work) can be often found
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Myocarditis
Clinical picture and clinical examination
Patient is tired and pale, out of sorts, even apathetic
Abdominal pain, loss of appetite, vomiting
Noticeable dyspnea even at mild physical exertion
Muscle pain or hypotonia
Severe myocarditis → muffled sounds or cardiac gallop
Tachycardia also during sleep, and often irregular
Systolic murmur present in simultaneous mitral regurgitation
Crepitus may be present on the lung bases
Enlarged and sensitive liver, eyelid edema or perimalleolar swelling
Colder skin on the periphery, poorly palpable peripheral pulsation, sometimes
even thready
Fulminant course: shock condition, heart failure, cardiac rhythm
disorders, consciousness disorders and vomiting, often fatal in newborns
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Myocarditis
Laboratory dg
Laboratory examinations: nonspecific signs of inflammation, ↑
increased CK, CK MB, TnT, LDH, AST, ALT
Detection of etiological agents is difficult (a highly positive finding →
direct evidence of the virus in myocardial tissues or pericardial fluid,
a medium-positive finding → evidence of virus in nasopharynx or in
stool with a 4-fold increase in the specific antibodies titer, or evidence
of the virus with the current specific antibodies titer 1:32, another
possibility → to detect infective agent by analyzing material obtained
from the endomyocardial biopsy
Serological examinations: serology of viruses
Immunology examination: standard immunology examination → small
practical meaning, activation of body cell response, or subpopulation of
T-lymphocytes are evaluated → its contribution is prognostic
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Myocarditis
ECG examination
Cardiac rhythm defects – SVES, KES, SA, AV blocks,
complete AV blocks (bordelaises, rubella and RS virus)
ECG changes during the course of the disease, and it is
important to monitor its dynamics
Varying depolarization disorders; the typical feature is a
low voltage of the ECG curve in all leads, flattening, or
inverted T waves, noticeably small or missing Q wave in the
left precordium, depression of ST segments and widening of
QRS complexes
In the chronic phase → manifestation of left ventricle
hypertrophy with ischemic changes
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Myocarditis
Echocardiography
Heart function disorder
LV wall thickness may change in repeated examinations,
depending on when the disease was detected
Tissue edema manifested by the wall thickening is typical
for the acute phase
Later phases → LV dilatation with the impaired function
→ LV wall is thinning
Secondary mitral regurgitation
Thrombi on the walls can be sometime
is detected in the LV
Pericardial effusion (not necessarily)
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Myocarditis
Chest RTG
Cardiac shade enlargement,
increasing heart insufficiency
Heart failure signs in more
severe course of myocarditis
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Myocarditis
Myocardial biopsy
It is not routinely used to diagnose the acute
myocarditis (high risk and poor efficiency
of the examination)
It is indicated in some patients with subacute or chronic
form, to distinguish between myocarditis and dilated
cardiomyopathy before making decision to start the
immunosuppressive treatment
Standard microscopic diagnosis according to the so called
Dallas criteria defines active myocarditis according to
simultaneously present inflammatory infiltrate and necrosis
foci ...
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Pericarditis
DIAGNOSTIKA
ECG - Initial elevation of the ST wave and positive T
wave, later T wave becomes isoelectric and in further
course inverted, low voltage of QRS complex
RTG examination - cardiac shade enlarged in both
directions
Echocardiography – the examination method of
choice to detect effusion in the pericardium, with
compression of the right atrium and/or right ventricle in
case of massive effusion → indirect warning sign of the
heart tamponade
Laboratory examination – bacterial etiology: standard
examinations (CRP and blood count), hemoculture, serum
for virological examination, immunology examination →
autoimmune diseases, additional dg – e.g., in case of
malignant diseases in the mediastinum, suspected tumor
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Pericarditis
Therapy
Symptomatic (confinement to bed and
antiinflammatory drugs)
More significant effusion → drainage
of the pericardium
Purulent pericarditis→ requires
surgical drainage of the pericardium
and ATB
Drainage of the pericardium → when a
pericardial effusion is massive, in case
of impending cardiac tamponade
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CONSTRICTIVE
PERICARDITIS I.
Very rare in children
Most frequently → TBC inflammation of the
pericardium, often the cause is not detected
Hemodynamics: the most rapid filling occurs in
the early diastole, filling in the late diastole is
restricted by the rigid and non flexible
pericardium
Clinical picture: effort dyspnea, general
malaise, fatigue, edemas, chest pain, syncope
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CONSTRICTIVE
PERICARDITIS II
Diagnosis: decisive → disparity between rather
prominent circulatory failure, meager physical finding on
heart, and x-ray showing small heart,
ECG: changes in P waves, lowered voltage of the QRS
complex, flattened, even inverted T waves
Echocardiographic examination: thickened pericardium,
impaired filling of both ventricles (atypical movement of
septum in diastole), dilated inferior vena cava, enlarged
atria
Definitive diagnostics by Doppler examinations, breathing-
related blood flow fluctuation can help in distinguishing
between constrictive pericarditis and restrictive
cardiomyopathy
Therapy: in progression of the disease, pericardiotomy
is necessary
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Postpericardiotomy
syndrome I
Definition: non-specific response of the pericardium,
epicardium and pleura, manifested by general
inflammatory signs and increased formation of
pericardial and pleural effusion
It occurs within a few days or weeks after the heart
surgery
Etiology: not clear
The autoimmune origin is indicated by a non-constant
relation between the occurrence of the syndrome,
evidence of antibodies against heart muscle and
circulating immune complexes
Simultaneous or activated virus infection in the
traumatised area (virus etiology is supported also by
more frequent occurrence of this disease during the
spring and autumn virosis season)
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Postpericardiotomy
syndrome II
Clinical manifestations: fatigue, chest pain, abdominal
pain, sometimes vomiting, the key manifestation →
formation of pericardial and often pleural effusions
Objective signs: are similar to those of pericarditis
including the risk of heart tamponade, pleural effusions →
palpation shortening and weak breathing at auscultation
Diagnosis: echocardiographic examination
Differential diagnosis: hemopericardium,
chylopericardium, chylothorax and hemodynamic cause of
effusion
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Postpericardiotomy
syndrome III
Laboratory examination: ↑ CRP and FW, sometimes examination
of humoral and cell immunity and screening examination of
system inflammatory diseases are necessary, examination of
antibodies against ECHO virus, Coxsackie A and B, herpetic virus,
adenovirus, EB virus, CMV, influenza and mycoplasma
Therapy: severe effusions → drainage is required, less severe
effusions → the NSA first choice drug, e.g. ibuprofen and
diuretics, sometimes corticosteroids, more rarely
immunosuppressive drugs in recurrent relapses
Course: usually benign course, late postpericardiotomy syndrome
→ threat to patients discharged to homecare when cardiac
tamponade is not detected ...
UPJŠ LF v Košiciach | discipline: Paediatrics, Neonatology | ...: Array | published on: 14. 6. 2018