Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, 55 Fruit St, Yawkey 5E, Boston, MA 02114-2750, USA.
BioMedical Engineering and Imaging Institute, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, Box 1234, New York, NY 10029-6574, USA.
Eur Heart J. 2024 May 21;45(19):1753-1764. doi: 10.1093/eurheartj/ehae149.
Chronic stress associates with cardiovascular disease, but mechanisms remain incompletely defined. Advanced imaging was used to identify stress-related neural imaging phenotypes associated with atherosclerosis.
Twenty-seven individuals with post-traumatic stress disorder (PTSD), 45 trauma-exposed controls without PTSD, and 22 healthy controls underwent 18F-fluorodeoxyglucose positron emission tomography/magnetic resonance imaging (18F-FDG PET/MRI). Atherosclerotic inflammation and burden were assessed using 18F-FDG PET (as maximal target-to-background ratio, TBR max) and MRI, respectively. Inflammation was assessed using high-sensitivity C-reactive protein (hsCRP) and leucopoietic imaging (18F-FDG PET uptake in spleen and bone marrow). Stress-associated neural network activity (SNA) was assessed on 18F-FDG PET as amygdala relative to ventromedial prefrontal cortex (vmPFC) activity. MRI diffusion tensor imaging assessed the axonal integrity (AI) of the uncinate fasciculus (major white matter tract connecting vmPFC and amygdala).
Median age was 37 years old and 54% of participants were female. There were no significant differences in atherosclerotic inflammation between participants with PTSD and controls; adjusted mean difference in TBR max (95% confidence interval) of the aorta 0.020 (-0.098, 0.138), and of the carotids 0.014 (-0.091, 0.119). Participants with PTSD had higher hsCRP, spleen activity, and aorta atherosclerotic burden (normalized wall index). Participants with PTSD also had higher SNA and lower AI. Across the cohort, carotid atherosclerotic burden (standard deviation of wall thickness) associated positively with SNA and negatively with AI independent of Framingham risk score.
In this study of limited size, participants with PTSD did not have higher atherosclerotic inflammation than controls. Notably, impaired cortico-limbic interactions (higher amygdala relative to vmPFC activity or disruption of their intercommunication) associated with carotid atherosclerotic burden. Larger studies are needed to refine these findings.
慢性应激与心血管疾病相关，但机制仍不完全明确。本研究采用先进的影像学方法来识别与动脉粥样硬化相关的应激相关神经影像学表型。
27 名创伤后应激障碍（PTSD）患者、45 名无 PTSD 的创伤暴露对照者和 22 名健康对照者接受 18F-氟代脱氧葡萄糖正电子发射断层扫描/磁共振成像（18F-FDG PET/MRI）检查。采用 18F-FDG PET（最大靶/背景比，TBRmax）和 MRI 分别评估动脉粥样硬化炎症和负荷。采用高敏 C 反应蛋白（hsCRP）和白细胞成像（脾脏和骨髓中 18F-FDG 摄取）评估炎症。18F-FDG PET 评估应激相关神经网络活动（SNA），即杏仁核与腹内侧前额皮质（vmPFC）的相对活性。磁共振弥散张量成像评估钩束（连接 vmPFC 和杏仁核的主要白质束）的轴突完整性（AI）。
中位年龄为 37 岁，54%的参与者为女性。PTSD 患者与对照组之间的动脉粥样硬化炎症无显著差异；主动脉 TBRmax 的调整均值差异（95%置信区间）为 0.020（-0.098，0.138），颈动脉 TBRmax 的调整均值差异为 0.014（-0.091，0.119）。PTSD 患者的 hsCRP、脾脏活性和主动脉粥样硬化负荷（归一化壁指数）较高。PTSD 患者的 SNA 较高，AI 较低。在整个队列中，颈动脉粥样硬化负荷（壁厚度标准差）与 SNA 呈正相关，与 AI 呈负相关，与弗雷明汉风险评分无关。
在这项规模有限的研究中，PTSD 患者的动脉粥样硬化炎症并不比对照组高。值得注意的是，皮质-边缘相互作用受损（杏仁核与 vmPFC 活动的相对活性增加或相互通讯中断）与颈动脉粥样硬化负荷相关。需要更大规模的研究来进一步证实这些发现。
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