Endothelium-dependent flow-mediated vasodilation of systemic arteries is impaired in patients with myocardial virus persistence.
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.


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.
Vallbracht
Katja B
KB
Department of Cardiology, Charité Medical University, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. vallbrac@zedat.fu-berlin.de
Schwimmbeck
Peter L
PL
Kühl
Uwe
U
Seeberg
Bettina
B
Schultheiss
Heinz-Peter
HP
D000258:Adenovirus Infections, Human / Q000097:blood / Q000503:physiopathology* / Q000821:virology; D000260:Adenoviruses, Human / Q000302:isolation & purification; D001158:Arteries / Q000503:physiopathology*; D001706:Biopsy; D002097:C-Reactive Protein / Q000032:analysis; D009202:Cardiomyopathies / Q000503:physiopathology; D003384:Coxsackievirus Infections / Q000097:blood / Q000503:physiopathology* / Q000821:virology; D004279:DNA, Viral / Q000302:isolation & purification; D004730:Endothelium, Vascular / Q000503:physiopathology*; D004770:Enterovirus / Q000302:isolation & purification; D004769:Enterovirus Infections / Q000097:blood / Q000503:physiopathology* / Q000821:virology; D006321:Heart / Q000821:virology*; D006439:Hemodynamics; D018056:Hemorheology; D004854:Herpesvirus 4, Human / Q000302:isolation & purification; D015654:Herpesvirus 6, Human / Q000302:isolation & purification; D006801:Humans; D009205:Myocarditis / Q000097:blood / Q000503:physiopathology / Q000821:virology*; D009206:Myocardium / Q000473:pathology; D010322:Parvoviridae Infections / Q000097:blood / Q000503:physiopathology* / Q000821:virology; D016732:Parvovirus B19, Human / Q000302:isolation & purification; D019349:Roseolovirus Infections / Q000097:blood / Q000503:physiopathology* / Q000821:virology; D014664:Vasodilation / Q000502:physiology*
D004279:DNA, Viral; D002097:C-Reactive Protein