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Enterovirale Myokarditis und dilatative Kardiomyopathie

Enterovirus myocarditis and dilated cardiomyopathy

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Zusammenfassung

□ In-situ-Hybridisierungsstudien und PCR-Untersuchungen haben gezeigt, daß Enteroviren, speziell Coxsackieviren der Gruppe B, nicht nur bei akuter Myokarditis, sondern auch bei chronischer Myokarditis nachweisbar sind als Beleg für die mögliche Persistenz von Enteroviren im menschlichen Herzmuskel. Zudem gelingt der molekularbiologische Nachweis einer persistierenden enteroviralen Infektion des Herzmuskels auch bei einem Teil der Patienten mit dilatativer Kardiomyopathie als Hinweis für den möglichen ätiologischen Zusammenhang von Myokarditis und dilatativer Kardiomyopathie. Durch die Diagnostik einer persistierenden Virusinfektion des Herzmuskels besteht die Möglichkeit zur Unterscheidung der chronischen Myokarditis bzw. dilatativen Kardiomyopathie, die durch Viruspersistenz charakterisiert ist, von der postviralen, autoimmunologisch bedingten Verlaufsform der Erkrankung. Dies rechtfertigt ein Umdenken im Hinblick auf die erforderlichen therapeutischen Konsequenzen. Inwieweit eine antivirale Therapie mit Interferonen ein therapeutisches Konzept bei gesicherter Viruspersistenz darstellt, muß durch kontrollierte prospektive Studien entschieden werden. Eine immunsuppressive Behandlung ist nur nach Ausschluß einer persistierenden Infektion gerechtfertigt. Experimentelle Arbeiten legen nahe, daß veränderte virale Replikationsstrategien die Unfähigkeit von Effektoren der lokalen Immunität, persistent infizierte myokardiale Zellen zu eliminieren, sowie die Infektion von Immunzellen für die Pathogenese entzündlicher Kardiomyopathien von wesentlicher Bedeutung sind.

Summary

□ In situ hybridization and PCR studies have demonstrated that enteroviruses of the human picornavividae, and in particular coxsackieviruses of group B (CVB), are detectable in endomyocardial biopsies of patients with acute and chronic myocarditis, indicating the possibility of enterovirus persistence in the human heart. As well, such infections are observed in patients with end-stage dilated cardiomyopathy, suggesting an etiologic link between myocarditis and dilated cardiomyopathy. The molecular diagnosis of persistent heart muscle infection allows to differentiate myocarditis and dilated cardiomyopathy, sustained by virus persistence, from postviral immune-mediated cardiac disease. Apart from providing an etiologic diagnosis, there are therapeutic implications from in situ demonstration of myocardial enterovirus infection. As to whether antiviral therapy with interferon is capable of providing protection against enterovirus myocarditis must be determined by controlled prospective clinical studies. Immunosuppressive therapy of myocarditis appears to be justified only after exclusion of persistent heart muscle infection. Experimental studies indicate that altered viral replication strategies, the incompetence of effector mediators of local immunity to eliminate persistently infected myocardial cells as well as infection of cellular constituents of the immune system itself, are major pathogenic determinants for development and maintenance of chronic myocarditis and cardiomyopathy.

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Kandolf, R. Enterovirale Myokarditis und dilatative Kardiomyopathie. Med Klin 93, 215–222 (1998). https://doi.org/10.1007/BF03044796

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