Several potential pathways such as endothelial function disturbance, inflammation with pro-inflammatory cytokines (IL1β, IL2, IL6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) increase, but also decline in the autonomic nervous system, and platelet abnormalities are involved as pathophysiological mechanisms connecting depression and cardiovascular diseases (CVDs). Here, CRP is linked to depressive symptom measurement.