Viola Vaccarino1, Amit J Shah2, Valeria Moncayo3, Jonathon Nye3, Marina Piccinelli3, Yi-An Ko4, Xin Ma4, Nancy Murrah5, Lucy Shallenberger5, Emily Driggers5, Oleksiy M Levantsevych5, Muhammad Hammadah6, Bruno B Lima6, An Young6, Wesley O'Neal6, Mhmtjamil Alkhalaf5, Ammer Haffar5, Paolo Raggi7, Jack Goldberg8, Nicholas L Smith9, Ernest V Garcia3, Arshed A Quyyumi6, J Douglas Bremner10. 1. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia; Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia. Electronic address: viola.vaccarino@emory.edu. 2. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia; Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia; Atlanta Veterans Affairs Health Care System, Decatur, Georgia. 3. Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Georgia. 4. Department of Biostatistics and Bioinformatics, Rollins School of Public Health, Emory University, Atlanta, Georgia. 5. Department of Epidemiology, Rollins School of Public Health, Emory University, Atlanta, Georgia. 6. Division of Cardiology, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia. 7. Mazankowski Alberta Heart Institute, University of Alberta, Edmonton, Alberta, Canada. 8. Seattle Epidemiologic Research and Information Center, United States Department of Veterans Affairs Office of Research and Development, Seattle, Washington. 9. Seattle Epidemiologic Research and Information Center, United States Department of Veterans Affairs Office of Research and Development, Seattle, Washington; Department of Epidemiology, University of Washington, Seattle, Washington. 10. Department of Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Georgia; Department of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, Georgia; Atlanta Veterans Affairs Health Care System, Decatur, Georgia.
Abstract
BACKGROUND: The link between posttraumatic stress disorder (PTSD) and ischemic heart disease remains elusive owing to a shortage of longitudinal studies with a clinical diagnosis of PTSD and objective measures of cardiac compromise. METHODS: We performed positron emission tomography in 275 twins who participated in two examinations approximately 12 years apart. At both visits, we obtained a clinical diagnosis of PTSD, which was classified as long-standing (both visit 1 and visit 2), late onset (only visit 2), and no PTSD (no PTSD at both visits). With positron emission tomography, we assessed myocardial flow reserve (MFR), which, in absence of significant coronary stenoses, indexes coronary microvascular function. We compared positron emission tomography data at visit 2 across the three categories of longitudinally assessed PTSD and examined changes between the two visits. RESULTS: Overall, 80% of the twins had no or minimal obstructive coronary disease. Yet, MFR was depressed in twins with PTSD and was progressively lower across groups with no PTSD (2.13), late-onset PTSD (1.97), and long-standing PTSD (1.93) (p = .01). A low MFR (a ratio <2.0) was present in 40% of the twins without PTSD, in 56% of those with late-onset PTSD, and in 72% of those with long-standing PTSD (p < .001). Associations persisted in multivariable analysis, when examining changes in MFR between visit 1 and visit 2, and within twin pairs. Results were similar by zygosity. CONCLUSIONS: Longitudinally, PTSD is associated with reduced coronary microcirculatory function and greater deterioration over time. The association is especially noted among twins with chronic, long-standing PTSD and is not confounded by shared environmental or genetic factors.
BACKGROUND: The link between posttraumatic stress disorder (PTSD) and ischemic heart disease remains elusive owing to a shortage of longitudinal studies with a clinical diagnosis of PTSD and objective measures of cardiac compromise. METHODS: We performed positron emission tomography in 275 twins who participated in two examinations approximately 12 years apart. At both visits, we obtained a clinical diagnosis of PTSD, which was classified as long-standing (both visit 1 and visit 2), late onset (only visit 2), and no PTSD (no PTSD at both visits). With positron emission tomography, we assessed myocardial flow reserve (MFR), which, in absence of significant coronary stenoses, indexes coronary microvascular function. We compared positron emission tomography data at visit 2 across the three categories of longitudinally assessed PTSD and examined changes between the two visits. RESULTS: Overall, 80% of the twins had no or minimal obstructive coronary disease. Yet, MFR was depressed in twins with PTSD and was progressively lower across groups with no PTSD (2.13), late-onset PTSD (1.97), and long-standing PTSD (1.93) (p = .01). A low MFR (a ratio <2.0) was present in 40% of the twins without PTSD, in 56% of those with late-onset PTSD, and in 72% of those with long-standing PTSD (p < .001). Associations persisted in multivariable analysis, when examining changes in MFR between visit 1 and visit 2, and within twin pairs. Results were similar by zygosity. CONCLUSIONS: Longitudinally, PTSD is associated with reduced coronary microcirculatory function and greater deterioration over time. The association is especially noted among twins with chronic, long-standing PTSD and is not confounded by shared environmental or genetic factors.
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