Key result
After controlling for depression, post-MI patients with PTSD had higher interleukin-6 (p=0.041), lower C-reactive protein (p=0.022), and lower soluble CD40 ligand (p=0.016) than those without PTSD.
Why the study?
Does PTSD caused by myocardial infarction alter inflammatory biomarkers in post-MI patients?
Observational (n=44)
Does PTSD caused by myocardial infarction alter inflammatory biomarkers in post-MI patients?
PTSD following myocardial infarction is associated with altered systemic inflammation, but comorbid depressive symptoms must be accounted for to understand this relationship.
Requires depression adjustment in post-MI inflammation assessment; leaves open causal links to outcomes.
OBJECTIVE: Inflammation might link posttraumatic stress disorder (PTSD) with an increased risk of cardiovascular events. We explored the association between PTSD and inflammatory biomarkers related to cardiovascular morbidity and the role of co-morbid depressive symptoms in this relationship. METHODS: We investigated 15 patients with interviewer-rated PTSD caused by myocardial infarction (MI) and 29 post-MI patients with no PTSD. All patients completed the depression subscale of the Hospital Anxiety and Depression Scale and had blood collected to determine inflammatory markers of increased cardiovascular risk. RESULTS: Controlling for demographic and medical covariates, patients with PTSD had higher leptin levels than patients with no PTSD (p = 0.038, explained variance 10.4%); this difference became nonsignificant when controlling for depressive symptoms. After controlling for depressive symptoms, PTSD patients had higher interleukin-6 (p = 0.041; explained variance 10%), lower C-reactive protein (p = 0.022, explained variance 12.1%), and lower soluble CD40 ligand (p = 0.016, explained variance 13.4%) than patients without PTSD. After controlling for PTSD status, depressive symptoms correlated with soluble CD40 ligand (r = 0.45, p = 0.002) and with C-reactive protein (r = 0.29, p < 0.07). CONCLUSIONS: The findings provide further evidence for altered inflammation in PTSD. Comorbid depressive symptoms ought to be considered to disentangle the unique associations of PTSD caused by MI and systemic inflammation.
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Känel et al. (2009) conducted an observational in Posttraumatic stress disorder post-myocardial infarction (n=44). Posttraumatic stress disorder vs. No PTSD was evaluated on Inflammatory biomarkers (leptin, interleukin-6, C-reactive protein, soluble CD40 ligand). After controlling for depression, post-MI patients with PTSD had higher interleukin-6 (p=0.041), lower C-reactive protein (p=0.022), and lower soluble CD40 ligand (p=0.016) than those without PTSD.
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