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首页> 外文期刊>Psychosomatic Medicine: Journal of the American Psychosomatic Society >Altered blood coagulation in patients with posttraumatic stress disorder.
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Altered blood coagulation in patients with posttraumatic stress disorder.

机译：创伤后应激障碍患者的凝血功能改变。

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OBJECTIVE: Posttraumatic stress disorder (PTSD) has been associated with an increased cardiovascular risk, though the pathophysiologic mechanisms involved are elusive. A hypercoagulable state before occurrence of coronary thrombosis contributes to atherosclerosis development. We investigated whether PTSD would be associated with increased coagulation activity. METHODS: We measured resting plasma levels of clotting factor VII activity (FVII:C), FVIII:C, FXII:C, fibrinogen, and D-dimer in 14 otherwise healthy patients with PTSD and in 14 age- and gender-matched, trauma-exposed non-PTSD controls. Categorical and dimensional diagnoses of PTSD were made using the Clinician-Administered PTSD Scale (CAPS) interview. We also investigated to what extent the relationship between PTSD and coagulation measures would be confounded by demographics, cardiovascular risk factors, lifestyle variables, time since trauma, and mood. RESULTS: Coagulation factor levels did not significantly differ between patients with a categorical diagnosis of PTSD and controls while controlling for covariates. In all subjects, FVIII:C was predicted by hyperarousal severity (beta = 0.46, p = .014) independent of covariates and by overall PTSD symptom severity (beta = 0.38, p = .045); the latter association was of borderline significance when separately controlling for gender, smoking, exercise, and anxiety (p values <.07). In patients, fibrinogen was predicted by hyperarousal severity (beta = 0.70, p = .005) and by overall PTSD symptom severity (beta = 0.61, p = .020), with mood partially affecting these associations. FVII:C, fibrinogen, and D-dimer showed no independent association with PTSD symptoms. CONCLUSIONS: PTSD may elicit hypercoagulability, even at subthreshold levels, offering one psychobiological pathway by which posttraumatic stress might contribute to atherosclerosis progression and clinical cardiovascular disease.
机译：目的：创伤后应激障碍（PTSD）与心血管风险增加有关，尽管所涉及的病理生理机制尚不清楚。冠状动脉血栓形成之前的高凝状态有助于动脉粥样硬化的发展。我们调查了PTSD是否与凝血活性增加有关。方法：我们测量了14例健康的PTSD患者以及14例年龄和性别相匹配的创伤患者的血浆静息凝血因子VII活性（FVII：C），FVIII：C，FXII：C，纤维蛋白原和D-二聚体水平暴露的非PTSD控件。 PTSD的分类和尺寸诊断是使用临床医生管理的PTSD量表（CAPS）进行的。我们还调查了人口统计学，心血管疾病危险因素，生活方式变量，自创伤以来的时间和情绪在多大程度上会混淆PTSD与凝血措施之间的关系。结果：在确诊为PTSD的患者和控制协变量的对照组之间，凝血因子水平无显着差异。在所有受试者中，FVIII：C均通过独立于协变量的高声调严重度（β= 0.46，p = .014）和整体PTSD症状严重度（β= 0.38，p = .045）预测。当分别控制性别，吸烟，运动和焦虑时，后一种关联具有临界意义（p值<.07）。在患者中，纤维蛋白原是由过度躁动的严重程度（β= 0.70，p = .005）和整体PTSD症状严重程度（β= 0.61，p = .020）预测的，情绪会部分影响这些关联。 FVII：C，纤维蛋白原和D-二聚体与PTSD症状无独立关联。结论：PTSD即使在阈值以下水平也可能引起高凝性，提供了一种心理生物学途径，创伤后应激可能通过该途径促进动脉粥样硬化的进展和临床心血管疾病。

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