Posttraumatic stress disorder (PTSD) may contribute to heightened cardiovascular disease risk by promoting a proinflammatory state and impaired endothelial function. Previous research has demonstrated associations of PTSD with inflammatory and endothelial function biomarkers, but most work has been cross-sectional and does not separate the effects of trauma exposure from those of PTSD. We investigated associations of trauma exposure and chronic PTSD with biomarkers of inflammation (C-reactive protein and tumor necrosis factor alpha receptor II) and endothelial function (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) in 524 middle-aged women in the Nurses’ Health Study II. Using linear mixed models, we examined associations of trauma/PTSD status with biomarkers measured twice, 10 to 16 years apart, in cardiovascular disease–free women, considering either average levels over time (cross-sectional) or change in levels over time (longitudinal). Biomarker levels were log-transformed. Trauma/PTSD status (based on structured diagnostic interviews) was defined as no trauma at either blood draw ( = 175), trauma at blood draw 1 but no PTSD at either draw ( = 175), and PTSD that persisted beyond blood draw 1 (chronic PTSD; = 174). The reference group was women without trauma. In models adjusted for known potential confounders, women with chronic PTSD had higher average C-reactive protein ( = 0.27, < .05), tumor necrosis factor alpha receptor II ( = 0.07, < .01), and intercellular adhesion molecule-1 ( = 0.04, < .05) levels. Women with trauma but without PTSD had higher average tumor necrosis factor alpha receptor II levels ( = 0.05, < .05). In addition, women with chronic PTSD had a greater increase in vascular cell adhesion molecule-1 over time ( = 0.003, < .05). Increased inflammation and impaired endothelial function may be pathways by which chronic PTSD increases cardiovascular disease risk.

中文翻译：

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女性慢性创伤后应激障碍与炎症和内皮功能标志物的横断面和纵向关联


创伤后应激障碍（PTSD）可能通过促进促炎状态和受损的内皮功能而导致心血管疾病风险增加。先前的研究已经证明了 PTSD 与炎症和内皮功能生物标志物的关联，但大多数工作都是横向的，并且没有将创伤暴露的影响与 PTSD 的影响分开。我们对 524 名中年女性进行了创伤暴露和慢性 PTSD 与炎症生物标志物（C 反应蛋白和肿瘤坏死因子 α 受体 II）和内皮功能（细胞间粘附分子-1 和血管细胞粘附分子-1）的关联研究。护士健康研究 II。使用线性混合模型，我们研究了在无心血管疾病的女性中，创伤/PTSD状态与两次测量的生物标志物（相隔10至16年）之间的关联，考虑随时间的平均水平（横截面）或随时间的水平变化（纵向） ）。生物标志物水平进行对数转换。创伤/PTSD 状态（基于结构化诊断访谈）被定义为两次抽血时均无创伤 ( = 175)、抽血 1 时有创伤但两次抽血均无 PTSD (= 175) 以及抽血 1 后持续存在的 PTSD (慢性创伤后应激障碍；= 174）。参考组是没有外伤的女性。在针对已知潜在混杂因素进行调整的模型中，患有慢性 PTSD 的女性具有较高的平均 C 反应蛋白 (= 0.27，< .05)、肿瘤坏死因子 α 受体 II (= 0.07，< .01) 和细胞间粘附分子-1 ( = 0.04, < .05) 水平。患有创伤但没有 PTSD 的女性的肿瘤坏死因子 α 受体 II 平均水平较高 (= 0.05，< .05)。此外，患有慢性 PTSD 的女性的血管细胞粘附分子-1 随着时间的推移有更大的增加 ( = 0.003，< .05)。炎症增加和内皮功能受损可能是慢性创伤后应激障碍增加心血管疾病风险的途径。