Jakub Toczek1,2, Ansel T Hillmer3,4,5, Jinah Han1,2, Chi Liu3,4, Dana Peters3, Hamed Emami1, Jing Wu3,4, Irina Esterlis2,4,5, Kelly P Cosgrove3,4,5, Mehran M Sadeghi6,7. 1. Cardiovascular Molecular Imaging Laboratory, Section of Cardiovascular Medicine and Yale Cardiovascular Research Center, Yale University School of Medicine, 300 George Street, #770G, New Haven, CT, 06511, USA. 2. Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA. 3. Department of Radiology and Biomedical Imaging, Yale University School of Medicine, New Haven, CT, USA. 4. Yale PET Center, Yale University School of Medicine, New Haven, CT, USA. 5. Department of Psychiatry, Yale University School of Medicine, New Haven, CT, USA. 6. Cardiovascular Molecular Imaging Laboratory, Section of Cardiovascular Medicine and Yale Cardiovascular Research Center, Yale University School of Medicine, 300 George Street, #770G, New Haven, CT, 06511, USA. mehran.sadeghi@yale.edu. 7. Veterans Affairs Connecticut Healthcare System, West Haven, CT, USA. mehran.sadeghi@yale.edu.
Abstract
The prevalence of cardiovascular diseases (CVD) is increased in subjects with post-traumatic stress disorder (PTSD). Vascular inflammation mediates CVD and may be assessed by 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. In this pilot study, we investigated whether subjects with PTSD have enhanced vascular and systemic inflammation compared to healthy controls, as assessed by FDG PET imaging. METHODS: A prospective group of 16 subjects (9 PTSD and 7 controls, age 34 ± 7) without prior history of CVD underwent FDG PET/CT imaging. The presence of PTSD symptoms at the time of the study was confirmed using PTSD checklist for DSM-5 (PCL5) questionnaire. Blood samples were collected to determine blood glucose, lipid and inflammatory biomarkers (tumor necrosis factor α, interleukin-1β, and interleukin-6) levels. FDG signal in the ascending aorta, amygdala, spleen and bone marrow was quantified. RESULTS: The two groups matched closely with regards to cardiovascular risk factors. The inflammatory biomarkers were all within the normal range. There was no significant difference in FDG signal in the aorta (target to background ratio: 2.40 ± 0.29 and 2.34 ± 0.29 for control and PTSD subjects, difference: - 0.06, 95% confidence interval of difference: - 0.38 to 0.26), spleen, bone marrow, or amygdala between control and PTSD subjects. There was no significant correlation between aortic and amygdala FDG signal. However, a significant positive correlation existed between amygdala, splenic, and bone marrow FDG signal. CONCLUSION: This pilot, small study did not reveal any difference in vascular or systemic inflammation as assessed by FDG PET imaging between PTSD and healthy control subjects. Because of the small number of subjects, a modest increase in vascular inflammation, which requires larger scale studies to establish, cannot be excluded. The correlation between FDG signal in amygdala, spleen and bone marrow may reflect a link between amygdala activity and systemic inflammation.
The prevalence of cardiovascular diseases (CVD) is increased in subjects with post-traumatic stress disorder (PTSD). Vascular inflammation mediates CVD and may be assessed by 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) imaging. In this pilot study, we investigated whether subjects with PTSD have enhanced vascular and systemic inflammation compared to healthy controls, as assessed by FDG PET imaging. METHODS: A prospective group of 16 subjects (9 PTSD and 7 controls, age 34 ± 7) without prior history of CVD underwent FDG PET/CT imaging. The presence of PTSD symptoms at the time of the study was confirmed using PTSD checklist for DSM-5 (PCL5) questionnaire. Blood samples were collected to determine blood glucose, lipid and inflammatory biomarkers (tumor necrosis factor α, interleukin-1β, and interleukin-6) levels. FDG signal in the ascending aorta, amygdala, spleen and bone marrow was quantified. RESULTS: The two groups matched closely with regards to cardiovascular risk factors. The inflammatory biomarkers were all within the normal range. There was no significant difference in FDG signal in the aorta (target to background ratio: 2.40 ± 0.29 and 2.34 ± 0.29 for control and PTSD subjects, difference: - 0.06, 95% confidence interval of difference: - 0.38 to 0.26), spleen, bone marrow, or amygdala between control and PTSD subjects. There was no significant correlation between aortic and amygdala FDG signal. However, a significant positive correlation existed between amygdala, splenic, and bone marrow FDG signal. CONCLUSION: This pilot, small study did not reveal any difference in vascular or systemic inflammation as assessed by FDG PET imaging between PTSD and healthy control subjects. Because of the small number of subjects, a modest increase in vascular inflammation, which requires larger scale studies to establish, cannot be excluded. The correlation between FDG signal in amygdala, spleen and bone marrow may reflect a link between amygdala activity and systemic inflammation.
Authors: Ahmed Tawakol; Amorina Ishai; Richard Ap Takx; Amparo L Figueroa; Abdelrahman Ali; Yannick Kaiser; Quynh A Truong; Chloe Je Solomon; Claudia Calcagno; Venkatesh Mani; Cheuk Y Tang; Willem Jm Mulder; James W Murrough; Udo Hoffmann; Matthias Nahrendorf; Lisa M Shin; Zahi A Fayad; Roger K Pitman Journal: Lancet Date: 2017-01-12 Impact factor: 79.321
Authors: Hamed Emami; Parmanand Singh; Megan MacNabb; Esad Vucic; Zachary Lavender; James H F Rudd; Zahi A Fayad; Joshua Lehrer-Graiwer; Magnus Korsgren; Amparo L Figueroa; Jill Fredrickson; Barry Rubin; Udo Hoffmann; Quynh A Truong; James K Min; Amos Baruch; Khurram Nasir; Matthias Nahrendorf; Ahmed Tawakol Journal: JACC Cardiovasc Imaging Date: 2015-01-07
Authors: Jakub Toczek; Jing Wu; Ansel T Hillmer; Jinah Han; Irina Esterlis; Kelly P Cosgrove; Chi Liu; Mehran M Sadeghi Journal: J Nucl Cardiol Date: 2020-02-10 Impact factor: 5.952