Background: Depressive disorder in the post-myocardial infarction (MI) period has been associated with increased cardiac morbidity and mortality. Possible pathophysiological mechanisms behind this association are not clear. Major depression in physically healthy subjects has been related to immune abnormalities including increased plasma levels of interleukin-6 (IL-6), tumor necrosis factor alfa (TNF-alpha) and C-reactive protein (CRP). In patients with MI, increased inflammatory markers, such as CRP and TNF-alpha, have been associated with increased cardiovascular events. It was the aim of this study to test the hypothesis that depression in post-MI patients is associated with increased inflammation as compared to non-depressed post-MI patients.
Methods: The cytokines IL-6 and TNF-alpha ; the soluble cytokine receptors sIL-6R, sTNF-RI and sTNF-RII; neopterin; and the inflammation-sensitive plasma proteins (ISPs) CRP and haptoglobin were assessed in a group of 57 patients with a diagnosis of depression post-MI and in a control group of 46 non-depressed post-MI patients, matched for age, gender and time elapsed since MI.
Results: Cytokine, neopterin and ISP levels were not statistically different in the depressed post-MI group as compared to the non-depressed post-MI group. Several inflammatory markers were however elevated in both cohorts when compared with levels reported in healthy subjects, indicating persistent inflammation several months after MI.
Conclusions: There was no indication of increased inflammation in depressed post-MI patients as compared to non-depressed post-MI patients.