Grenon S Marlene, Owens Christopher D, Alley Hugh, Perez Sandra, Whooley Mary A, Neylan Thomas C, Aschbacher Kirstin, Gasper Warren J, Hilton Joan F, Cohen Beth E
Department of Surgery, University of California San Francisco, San Francisco, CA Department of Surgery, Veterans Affairs Medical Center, San Francisco, CA Viperx Lab, San Francisco, CA
Department of Surgery, University of California San Francisco, San Francisco, CA Department of Surgery, Veterans Affairs Medical Center, San Francisco, CA Viperx Lab, San Francisco, CA.
J Am Heart Assoc. 2016 Mar 23;5(3):e003010. doi: 10.1161/JAHA.115.003010.
Current research in behavioral cardiology reveals a significant association between posttraumatic stress disorder (PTSD) and increased risk for cardiovascular disease and mortality; however, the underlying mechanisms remain poorly understood. We hypothesized that patients with PTSD would exhibit endothelial dysfunction, a potential mechanism involved in the development and progression of cardiovascular disease.
A total of 214 outpatients treated at the San Francisco Veterans Affairs Medical Center underwent tests of endothelial function and evaluation for PTSD. Flow-mediated vasodilation of the brachial artery was performed to assess endothelial function, and current PTSD status was defined by the PTSD Checklist, based on the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition), with a score ≥40. Multivariable linear regression models were used to estimate the association between PTSD status and endothelial function. Patients with PTSD (n=67) were more likely to be male (99% versus 91%, P=0.04) and to have depression (58% versus 8%, P<0.0001) and were less likely to be on an angiotensin-converting enzyme inhibitor (17% versus 36%, P=0.007) or β-blocker treatment (25% versus 41%, P=0.03). Univariate analysis demonstrated that patients with PTSD had significantly lower flow-mediated vasodilation (5.8±3.4% versus 7.5±3.7%; P=0.003); furthermore, lower flow-mediated vasodilation was associated with increasing age (P=0.008), decreasing estimated glomerular filtration rate (P=0.003), hypertension (P=0.002), aspirin (P=0.03), and β-blocker treatments (P=0.01). In multivariable analysis, PTSD remained independently associated with lower flow-mediated vasodilation (P=0.0005).
After adjusting for demographic, comorbidity, and treatment characteristics, PTSD remained associated with worse endothelial function in an outpatient population. Whether poor endothelial function contributes to the higher risk of cardiovascular disease in patients with PTSD deserves further study.
行为心脏病学的当前研究揭示了创伤后应激障碍（PTSD）与心血管疾病风险增加及死亡率之间存在显著关联；然而，其潜在机制仍知之甚少。我们推测，PTSD患者会出现内皮功能障碍，这是心血管疾病发生和发展过程中的一个潜在机制。
共有214名在旧金山退伍军人事务医疗中心接受治疗的门诊患者接受了内皮功能测试和PTSD评估。通过测量肱动脉血流介导的血管舒张来评估内皮功能，根据《精神疾病诊断与统计手册》（第四版），使用PTSD检查表来定义当前的PTSD状态，得分≥40。采用多变量线性回归模型来估计PTSD状态与内皮功能之间的关联。PTSD患者（n = 67）更有可能为男性（99%对91%，P = 0.04）且患有抑郁症（58%对8%，P < 0.0001），而服用血管紧张素转换酶抑制剂（17%对36%，P = 0.007）或β受体阻滞剂治疗的可能性较小（25%对41%，P = 0.03）。单变量分析表明，PTSD患者的血流介导的血管舒张显著降低（5.8±3.4%对7.5±3.7%；P = 0.003）；此外，较低的血流介导的血管舒张与年龄增长（P = 0.008）、估计肾小球滤过率降低（P = 0.003）、高血压（P = 0.002）、阿司匹林（P = 0.03）和β受体阻滞剂治疗（P = 0.01）相关。在多变量分析中，PTSD仍然与较低的血流介导的血管舒张独立相关（P = 0.0005）。
在调整了人口统计学、合并症和治疗特征后，PTSD在门诊患者中仍然与较差的内皮功能相关。内皮功能不良是否导致PTSD患者心血管疾病风险较高值得进一步研究。
Zotero 插件