Myocarditis

Maulana Wasis Waskito

Definisi

 Merupakan inflamasi yang terjadi pada

miokardium yang dapat disebabkan
oleh infeksi atau non-infeksi.
Menurut (WHO)/International Society
and Federation of Cardiology (ISFC) :
merupakan sebuah inflamasi pada otot
jantung
yang
dapat
didiagnosis
melalui kriteria histologi, immunologi,
dan immunohistochemical.

Etiologi

Gejala Klinis
Miokarditis memiliki gejala yang luas,
diantaranya :
Dyspneu
Nyeri dada
Demam
Mialgia
Kelelahan
Palpitasi
Syncop

Diagnosis

ECG
ECG secara luas memiliki sensitifitas
yang rendah dalam screening
miokarditis.
Pada beberapa pasien miokarditis
ditemukan gambaran ECG dari gel. T
yang non spesifik dan elevasi
segmen ST.

MRI

EMB (EndoMyocardial
Biopsy)
EMB sampai saat ini masih dijadikan
sebagai gold standard dalam
mendiagnosis miokarditis.
The Dallas criteria :
Akut miokarditis : infiltrasi limfosit
dengan nekrosis pada miosit.
Borderline miokarditis : inflamasi tanpa
nekrosis miosit.

 Immunohistochemistry :
Infiltrasi mononuclear difus (limfosit T
dan makrofag) >14 cells/mm2

EMB

Histopathological, Immunohistological, and Molecular Biological Findings in Hearts of

Patients With Myocarditis

Histology and immunohistology of (A, B) acute myocarditis and (C, D) chronic myocarditis. In acute myocarditis, numerous necrotic
myocytes (A, arrows) are associated with mononuclear cell infiltrates including CD3 T cells (B), whereas in chronic myocarditis,
inflammatory cells such as CD68 macrophages (D) are mainly present in areas with fibrosis (C, blue staining). (E, F) Radioactive in
situ hybridization reveals PVB19 nucleic acid in endothelial cells of an arteriole in a patient with chronic myocarditis (E), whereas
enterovirus ribonucleic acid is detected in several myocytes (F).

Figure 1. Lymphocytic and Histiocytic Infiltrate and T Lymphocytes in Heart-Tissue Sections from
Patients
with
Acute
Myocarditis.
Panel A shows acute myocarditis with widespread lymphocytic and histiocytic infiltrate (arrow) and associated
myocyte damage (arrowhead) (hematoxylin and eosin). Panel B shows CD3 immunostaining of T lymphocytes in a
patient with acute myocarditis. Images provided courtesy of Dr. Dylan Miller.

Patogenesis

Time Course of Viral

Myocarditis

Time course of viral myocarditis in 3 phases (derived from murine models). The acute phase of myocarditis takes
only a few days, whereas the subacute and chronic phase covers a few weeks to several months. Modified from

Pathophysiology of Viral
Myocarditis

Pathophysiology of viral myocarditis: after viral entry, virus replication leads to acute injury
of the myocytes (acute myocarditis) and to activation of the hosts immune system
(subacute myocarditis). IFN interferon; IL interleukin; TNF tumor necrosis factor. JA

Figure 2 (facing page). Pathogenesis of Myocarditis. The current understanding of the cellular and molecular pathogenesis of postviral and autoimmune myocarditis is
based solely on animal models. In these models, the progression from acute injury to chronic dilated cardiomyopathy may be simplified into a threestage process. Acute injury
leads to cardiac damage, exposure of intracellular antigens such as cardiac myosin, and activation of the innate immune system. Over weeks, specific immunity that is
mediated by T lymphocytes and antibodies directed against pathogens and similar endogenous heart epitopes cause robust inflammation. In most patients, the pathogen is
cleared and the immune reaction is down-regulated with few sequelae. However, in other patients, the virus is not cleared and causes persistent myocyte damage, and heartspecific inflammation may persist because of mistaken recognition of endogenous heart antigens as pathogenic entities. APC denotes antigen-presenting cell.

Figure 2 Infection of cardiac endothelial cells or cardiac myocytes by virus causes direct cellular damage and
subsequently an innate and adaptive immune response, all of which contribute to cardiomyopathy. Cardiomyopathy
from viral injury and the subsequent immune reaction can include diastolic as well as systolic dysfunction.

Terapi

Proposed Diagnostic and Therapeutic Algorithm

for Suspected Myocarditis

Proposed diagnostic and therapeutic algorithm for patients with suspected acute myocarditis considering biomarkers, cardiac
magnetic resonance imaging (cMRI), and endomyocardial biopsy (EMB). Bi-VAD biventricular assist device; Circ. circulatory;
ECMO extracorporeal membrane oxygenation; LV left ventricular; LVAD left ventricular assist device.

Prognosis

 Prognosis sangat bergantung pada

etiologi, gejala klinis, hemodinamik
dan hasil EMB.
Pasien dengan akut miokarditis
memiliki prognosis baik tanpa
menimbulkan sequele.
Pasien dengan sarcoidosis/giant cell
myocarditis, prognosis bergantung dari
penatalaksanaan awal (imunosupresi)

Terima Kasih