Khairy Paul, Rinfret Stephane, Tardif Jean-Claude, Marchand Richard, Shapiro Stan, Brophy James, Dupuis Jocelyn
Department of Medicine, Montreal Heart Institute, University of Montreal, Quebec, Canada.
Circulation. 2003 Apr 22;107(15):1966-71. doi: 10.1161/01.CIR.0000064895.89033.97. Epub 2003 Apr 7.
Although several studies have reported correlations between infections and coronary artery disease, associations with endothelial dysfunction, its precursor, have not been established. This study assessed whether infection with Chlamydia pneumoniae (CP), cytomegalovirus (CMV), Epstein-Barr virus (EBV), or Helicobacter pylori (HP) is associated with decreased endothelial function.
Sixty-five male subjects, aged 20 to 45 years, with no risk factors or known coronary artery disease were enrolled in a seroepidemiological cross-sectional study. Endothelial function was determined by flow-mediated brachial vasodilation. Serum antibodies consisting of anti-CP IgG and IgM, anti-CMV IgG, anti-EBV nuclear antigen, and anti-HP IgG and markers of inflammation including high-sensitivity C-reactive protein were measured. Average age was 29.3+/-5.5 years. Seroprevalence values were 65.1%, 34.9%, 88.9%, and 14.3% for CP, CMV, EBV, and HP, respectively. Average values for endothelium-dependent and -independent vasodilation were 9.4+/-4.5% and 12.6+/-5.0%. Despite adequate statistical power (82% for the primary end point), no association between endothelial function and seropositivity to individual infectious agents, infectious burden, or C-reactive protein was observed in regression analyses controlling for variables including age, blood pressure, and lipid parameters. Moreover, no dose-response trends between serum titers and endothelial function were found.
Lack of association between chronic infection with CP, CMV, EBV, HP, or pathogen burden and endothelial function was observed, suggesting that these agents are not implicated as early etiologic triggers in the genesis of coronary artery disease. These results do not preclude active involvement at later stages of the pathophysiological process, such as acceleration of existing atherosclerosis and acute plaque rupture.
尽管多项研究报告了感染与冠状动脉疾病之间的相关性，但与内皮功能障碍（其前驱状态）的关联尚未确立。本研究评估了肺炎衣原体（CP）、巨细胞病毒（CMV）、爱泼斯坦-巴尔病毒（EBV）或幽门螺杆菌（HP）感染是否与内皮功能下降有关。
65名年龄在20至45岁之间、无危险因素或已知冠状动脉疾病的男性受试者参与了一项血清流行病学横断面研究。通过血流介导的肱动脉血管舒张来测定内皮功能。检测了包括抗CP IgG和IgM、抗CMV IgG、抗EBV核抗原以及抗HP IgG在内的血清抗体，以及包括高敏C反应蛋白在内的炎症标志物。平均年龄为29.3±5.5岁。CP、CMV、EBV和HP的血清阳性率分别为65.1%、34.9%、88.9%和14.3%。内皮依赖性和非依赖性血管舒张的平均值分别为9.4±4.5%和12.6±5.0%。尽管有足够的统计效力（主要终点的统计效力为82%），但在控制年龄、血压和血脂参数等变量的回归分析中，未观察到内皮功能与个体感染因子血清阳性、感染负担或C反应蛋白之间存在关联。此外，未发现血清滴度与内皮功能之间存在剂量反应趋势。
观察到CP、CMV、EBV、HP慢性感染或病原体负担与内皮功能之间缺乏关联，这表明这些病原体并非冠状动脉疾病发生早期的病因触发因素。这些结果并不排除它们在病理生理过程后期的积极参与，如加速现有的动脉粥样硬化和急性斑块破裂。
