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(Circulation. 2004;110:2938-2945.)
© 2004 American Heart Association, Inc.

Vascular Medicine

Endothelium-Dependent Flow-Mediated Vasodilation of Systemic Arteries Is Impaired in Patients With Myocardial Virus Persistence

Katja B. Vallbracht, MD; Peter L. Schwimmbeck, MD; Uwe Kühl, MD, PhD; Bettina Seeberg, MD; Heinz-Peter Schultheiss, MD

From Charité Medical University, Berlin, Germany.

Correspondence to Dr Med Katja B. Vallbracht, Charité Medical University Berlin, Campus Benjamin Franklin, Department of Cardiology, Hindenburgdamm 30, 12200 Berlin, Germany. E-mail vallbrac{at}zedat.fu-berlin.de

Received October 31, 2003; de novo received January 31, 2004; revision received April 29, 2004; accepted April 30, 2004.

Background— Myocardial virus persistence is frequently observed in patients with cardiomyopathy. Endothelial dysfunction in patients with cardiomyopathy is associated with inflammatory immunoresponses in myocardial biopsies. The aim of this study was to investigate the impact of myocardial virus persistence on endothelial function.

Methods and Results— In 124 patients with suspected cardiomyopathy, myocardial biopsies were examined for virus persistence (by polymerase chain reaction) and inflammation (by immunohistology). Endothelial function of the radial artery was examined by high-resolution ultrasound. Diameter changes in response to reactive hyperemia (flow-mediated dilation [FMD]) compared with glycerol trinitrate (GTN-MD) were measured. Mean age of the patients (55 men, 69 women) was 45±13 years; ejection fraction was 57±17%. In 73 patients, adenovirus, enterovirus, parvovirus, or HHV6 virus (V) was detected; in 51, no virus was detected. FMD was significantly impaired in patients with myocardial virus persistence compared with control subjects (Co): FMD-V, 3.38±2.67%; FMD-Co, 7.34±3.44 (P<0.001). In 86 patients, myocardial inflammation was confirmed (Inf). Of those, 57 had virus, and 29 did not. FMD was significantly impaired in patients with virus compared with controls: FMD-Inf-V, 3.24±2.66%; FMD-Inf-Co, 6.07±3.00 (P<0.001). In 38 patients, immunohistology of the myocardial biopsies was normal (Co); of those, 16 had virus, and 22 did not. FMD was impaired in patients with virus compared with control subjects: FMD-Co-V, 3.88±2.72%; FMD-Co-Co, 9.00±3.32% (P<0.001). Endothelium-independent vasodilation (GTN-MD) was not significantly affected.

Conclusions— Myocardial virus persistence is associated with endothelial dysfunction. Endothelial dysfunction in patients with myocardial virus persistence can occur independently of endothelial activation or myocardial inflammation but is more pronounced in patients with concurrent inflammation.

Key Words: cardiomyopathy • endothelium • inflammation • viruses • vasodilation

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