Abstract
Background: Depression increases the risk of coronary artery disease (CAD) by about 1.5 times among healthy individuals. The mechanisms underlying this association, however, are still unclear. Although traditional cardiovascular risk factors tend to cluster in depressed patients as a consequence of an unhealthy lifestyle, part of the excess risk remains unexplained. Inflammation has been pointed as a possible mechanistic link between depression and CAD. We intended to assess the role of depression as an independent predictor of subclinical inflammation onset in a cohort study. Methods: We studied 4,222 asymptomatic individuals (mean age: 42.1 years; 20.6% female) who underwent two consecutive routine health evaluations between 2007 and 2012. All the participants were submitted to an extensive baseline clinical and laboratory evaluation and completed the Beck Depression Inventory (BDI). A BDI score >10 was adopted to identify individuals with significant depressive symptoms. Subclinical inflammation was characterized by C-Reactive Protein (hs-CRP) levels >3mg/L. Metabolic syndrome was defined according to the ATP-III criteria. We assessed subclinical inflammation incidence at the following evaluation among those with and without baseline depressive symptoms. Results: Baseline prevalence of depression (BDI>10) was 15%. Depressive symptoms were significantly more frequent among women (21.7% vs. 13.3%; OR 1.8 CI 1.49-2.20; p<0,001). Mean follow-up was 21.7 months (SD 9.6). Baseline BDI>10 was associated with a significantly higher incidence of subclinical inflammation at the following evaluation (RR 1.67; CI 1.22-2.29; p=0.002). Even after adjustment for age, gender, smoking status, physical activity, metabolic syndrome, fatty liver and overweight, baseline BDI>10 remained an independent predictor of future subclinical inflammation onset (RR 1.49; CI 1.02-2.16; p=0.037). Conclusion: Depression is an independent predictor of future subclinical inflammation onset among healthy individuals. Since depression-related inflammation is only partially driven by behavioral cofactors such as smoking status and the metabolic syndrome, it can represent a mechanistic link between depression and CAD.
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