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From the Department of General Internal Medicine, Division of Psychosomatic Medicine (R.v.K.) and Psychocardiology Unit, Cardiovascular Prevention and Rehabilitation, Swiss Cardiovascular Center (R.v.K.), University Hospital Berne, Berne, Switzerland; Department of Psychiatry (U.H., U.S.), Division of Psychosocial Medicine (C.B.), and Department of Trauma Surgery (M.K., L.M.), University Hospital Zurich, Zurich, Switzerland; Department of Psychiatry, University of California, San Diego, California (K.A.).
Address correspondence and reprint requests to Roland von Känel, MD, Professor of Medicine/Head, Division of Psychosomatic Medicine, Department of General Internal Medicine, Freiburgstrasse 4, University Hospital/INSELSPITAL, CH-3010 Berne, Switzerland. E-mail: roland.vonkaenel{at}insel.ch
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 (ß = 0.46, p = .014) independent of covariates and by overall PTSD symptom severity (ß = 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 (ß = 0.70, p = .005) and by overall PTSD symptom severity (ß = 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.
Key Words: atherosclerosis • blood coagulation • posttraumatic stress disorder • risk factor
Abbreviations: BMI = body mass index; CAD = coronary artery disease; CAPS = Clinician-Administered PTSD Scale; DSM-IV = Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition; FVII:C = clotting factor VII activity; FVIII:C = clotting factor VIII activity; FXII:C = clotting factor XII activity; MBP = mean arterial blood pressure; MI = myocardial infarction; PTSD = posttraumatic stress disorder; SNS = sympathetic nervous system; IL = interleukin; HADS = Hospital Anxiety and Depression Scale.
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