Virusätiologie der inflammatorischen Kardiomyopathie

Zusammenfassung

Ätiologisch und pathogenetisch wichtige Hinweise für die Viruspathogenese der inflammatorischen Kardiomyopathie lassen sich aus In-situ-Hybridisierungsstudien, aber auch aus Untersuchungen mittels Polymerase-Kettenreaktion (PCR) unter Einbezug histologischer und immunhistologischer Parameter ableiten. Neben Enteroviren (EV), insbesondere Coxsackieviren der Gruppe B (CVB) mit gesicherter Ätiopathogenese, wurden in den vergangenen Jahren auch Adenoviren (ADV), verschiedene Herpesviren und zunehmend Parvovirus B19 (PVB19) als potenziell kardiotrope Erreger im menschlichen Herzen identifiziert. Die Diagnose einer inflammatorischen Kardiomyopathie gelingt zweifelsfrei nur aus der Endomyokardbiopsie, wobei aus kardiopathologischer Sicht in Zusammenarbeit der Klinik eine pathogenetisch bedeutsame inflammatorische Infektion von einer harmlosen myokardialen Viruspersistenz ohne Entzündung zu unterscheiden ist.

Summary

Molecular biological methods such as in situ hybridization and the polymerase chain reaction (PCR) have confirmed the pathogenetic role of enteroviruses and primarily coxsackieviruses of group B (CVB) in the induction and maintenance of inflammatory cardiomyopathy. More recently, additional viruses such as adenoviruses (ADV), various herpes viruses and increasingly parvovirus B19 (PVB19) have been identified as potential cardiotropic agents in the human heart. The different cell tropism of cardiotropic viruses implicates distinct pathogenetic principles. Whereas cardiac myocytes are target cells for infection with enteroviruses and adenoviruses with consecutive virus-induced cytolysis, PVB19-associated inflammatory cardiomyopathy is characterized by infection of intracardiac endothelial cells of small arterioles and veins, which may be associated with endothelial dysfunction, impairment of myocardial microcirculation, penetration of inflammatory cells and secondary myocyte necrosis.

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