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 Kawai (22).

Pathophysiology of Viral MyocarditisPathophysiology of viral myocarditis: after viral entry, virus replication leads to acute injury of the myocytes (acute myocarditis) and to activation of the host’s 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 heart-specific 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