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(Circulation. 2003;108:945.)
© 2003 American Heart Association, Inc.

Clinical Investigation and Reports

Parvovirus B19 Infection Mimicking Acute Myocardial Infarction

Uwe Kühl, MD, PhD; Matthias Pauschinger, MD; Thomas Bock, MD; Karin Klingel, MD; C. Peter Lothar Schwimmbeck, MD; Bettina Seeberg; Lars Krautwurm; Wolfgang Poller, MD; Heinz-Peter Schultheiss, MD; Reinhard Kandolf, MD, PhD

From the Medical Clinic II (U.K., M.P., C.P.L.S., B.S., L.K., W.P., H.-P.S.), Department of Cardiology, University Hospital Benjamin Franklin, Berlin, Germany; Institute for Pathology (T.B., K.K., R.K.), University Hospital of Tübingen, Tübingen, Germany.

Correspondence to Uwe Kühl, PhD, Department of Internal Medicine, Cardiology and Pneumonology, Benjamin Franklin Hospital, Free University of Berlin, Hindenburgdamm 30, D-12200 Berlin, Germany. E-mail dcmkuehl{at}zedat.fu-berlin.de

Received February 19, 2003; revision received June 2, 2003; accepted June 3, 2003.

Background— Enteroviruses (EVs) and adenoviruses (ADVs) have been considered common causes of myocarditis and dilated cardiomyopathy. In the present study, we report on the association of parvovirus B19 (PVB19) genomes in the clinical setting of acute myocarditis.

Methods and Results— This study included 24 consecutive patients admitted to our hospital within 24 hours after onset of chest pain. Acute myocardial infarction had been excluded in all patients by coronary angiography. Endomyocardial biopsies were analyzed by nested polymerase chain reaction/reverse transcriptase-polymerase chain reaction for EV, ADV, PVB19, human cytomegalovirus, Epstein-Barr virus, Chlamydia pneumoniae, influenza virus A and B, and Borrelia burgdorferi genomes, respectively, followed by direct sequencing of the amplification products. All patients presented with acute onset of angina pectoris and ST-segment elevations or T-wave inversion mimicking acute myocardial infarction. Mean baseline peak creatinine kinase and creatine kinase-isoenzyme fraction were 342±241 U/L and 32±20 U/L, respectively. Mean troponin T was increased to 7.5±15.0 ng/mL and C-reactive protein to 91±98 mg/mL. Eighteen patients had global or regional wall motion abnormalities (ejection fraction 62.5±15.5%). Histological analysis excluded the presence of active or borderline myocarditis in all but one patient. PVB19, EV, and ADV genomes were detected in the myocardium of 12, 3, and 2 patients, respectively (71%). Follow-up biopsies of virus-positive patients (11 of 17) demonstrated persistence of PVB19 genomes in 6 of 6 patients, EV genomes in 2 of 3 patients, and ADV genomes in 1 of 2 patients, respectively.

Conclusions— Virus genomes can be demonstrated in 71% of patients with normal coronary anatomy, clinically mimicking acute myocardial infarction. In addition to EVs and ADVs, PVB19 was the most frequent pathogen.

Key Words: myocarditis • viruses • pericarditis • biopsy • polymerase chain reaction

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