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(Circulation. 2006;114:1581-1590.)
© 2006 American Heart Association, Inc.

Heart Failure

Presentation, Patterns of Myocardial Damage, and Clinical Course of Viral Myocarditis

Heiko Mahrholdt, MD; Anja Wagner, MD; Claudia C. Deluigi, MD; Eva Kispert, RN; Stefan Hager, MD; Gabriel Meinhardt, MD; Holger Vogelsberg, MD; Peter Fritz, MD; Juergen Dippon, PhD; C. -Thomas Bock, PhD; Karin Klingel, MD; Reinhard Kandolf, MD; Udo Sechtem, MD

From the Division of Cardiology (H.M., C.C.D., E.K., S.H., G.M., H.V., U.S.) and Department of Pathology (P.F.), Robert Bosch Medical Center, Stuttgart, Germany; Department of Mathematics, University of Stuttgart, Stuttgart, Germany (J.D.); Department of Molecular Pathology, University of Tuebingen, Tuebingen, Germany (C.B., K.K., R.K.); and Duke Cardiovascular MR Center, Durham, NC (A.W.).

Correspondence to Heiko Mahrholdt, MD, Robert Bosch Medical Center, Auerbachstrasse 110, 70376 Stuttgart, Germany. E-mail Heiko.Mahrholdt{at}rbk.de

Received December 6, 2005; revision received July 10, 2006; accepted August 7, 2006.

Background— Enteroviruses and adenoviruses have been considered the most common causes of viral myocarditis, but parvovirus B19 (PVB19) and human herpesvirus 6 (HHV6) are increasingly found in endomyocardial biopsy samples.

Methods and Results— Consequently, our aim was to evaluate the prevalence and clinical presentation of cardiac PVB19 and/or HHV6 infection in a cohort of myocarditis patients and to follow its clinical course. In addition, we sought to demonstrate patterns of myocardial damage and to determine predictors for chronic heart failure. Our study design consisted of a cardiovascular magnetic resonance protocol as well as endomyocardial biopsies in the myocardial region affected as indicated by cardiovascular magnetic resonance. One hundred twenty-eight patients were enrolled by clinical criteria. In the group of myocarditis patients (n=87), PVB19 (n=49), HHV6 (n=16), and combined PVB19/HHV6 infections (n=15) were detected most frequently. The remaining patients were diagnosed with healing myocarditis (n=15) or did not have myocarditis (n=26). Patients with PVB19 presented in a manner similar to that of myocardial infarction; most had typical subepicardial late gadolinium enhancement in the lateral wall and recovered within months. Conversely, patients with HHV6 and especially with HHV6/PVB19 myocarditis presented with new onset of heart failure, had septal late gadolinium enhancement, and frequently progressed toward chronic heart failure.

Conclusions— Our data indicate that PVB19 and HHV6 are the most important causes for viral myocarditis in Germany and that the clinical presentation is related to the type of virus. Furthermore, clinical presentation, type of virus, and pattern of myocardial damage are related to the clinical course.

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