摘要
Background -Myocardial virus persistence is frequently observed in patients w ith cardiomyopathy. Endothelial dysfunction in patients with cardiomyopathy is a ssociated with inflammatory immunoresponses in myocardial biopsies. The aim of t his study was to investigate the impact of myocardial virus persistence on endot helial function. Methods and Results -In 124 patients with suspected cardiomyop athy, myocardial biopsies were examined for virus persistence(by polymerase chai n reaction) and inflammation(by immunohistology). Endothelial function of the ra dial artery was examined by high-resolution ultrasound. Diameter changes in res ponse to reactive hyperemia (flow-mediated dilation[FMD]) compared with glycero l 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, en terovirus, parvovirus, or HHV6 virus(V) was detected; in 51, no virus was detect ed. 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 v irus 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 norma l(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 sig nificantly affected. Conclusions -Myocardial virus persistence is associated wi th endothelial dysfunction. Endothelial dysfunction in patients with myocardial virus persistence can occur independently of endothelial activation or myocardia l inflammation but is more pronounced in patients with concurrent inflammation.
Background -Myocardial virus persistence is frequently observed in patients w ith cardiomyopathy. Endothelial dysfunction in patients with cardiomyopathy is a ssociated with inflammatory immunoresponses in myocardial biopsies. The aim of t his study was to investigate the impact of myocardial virus persistence on endot helial function. Methods and Results -In 124 patients with suspected cardiomyop athy, myocardial biopsies were examined for virus persistence(by polymerase chai n reaction) and inflammation(by immunohistology). Endothelial function of the ra dial artery was examined by high-resolution ultrasound. Diameter changes in res ponse to reactive hyperemia (flow-mediated dilation[FMD]) compared with glycero l 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, en terovirus, parvovirus, or HHV6 virus(V) was detected; in 51, no virus was detect ed. 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 v irus 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 norma l(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 sig nificantly affected. Conclusions -Myocardial virus persistence is associated wi th endothelial dysfunction. Endothelial dysfunction in patients with myocardial virus persistence can occur independently of endothelial activation or myocardia l inflammation but is more pronounced in patients with concurrent inflammation.
