(2017). 9th International Congress on Psychopharmacology & 5th International Symposium on Child and Adolescent Psychopharmacology. Psychiatry and Clinical Psychopharmacology: Vol. 27, 9th International Congress on Psychopharmacology & 5th International Symposium on Child and Adolescent Psychopharmacology Abstracts, pp. 85-180.

It is well-established that cardiovascular disease and depression are highly comorbid. This study aimed to assess the possible role of the NOD-like receptor protein 3 (NLRP3) inflammasome pathway and the high-sensitivity C-reactive protein (hsCRP) in patients with incident myocardial infarction in the presence or absence of depression. Sixty-eight consecutive patients with incident ST-elevation myocardial infarction and twenty healthy subjects were included. The patients were assessed using the Structured Clinical Interview for DSM-5 Disorders—Clinician Version during their 1–4-day-long hospitalization and were divided into two groups: with and without comorbid depression. Blood samples for the determination of NLRP3, interleukin-18 (IL-18), interleukin-1β (IL-1β), and hsCRP levels were analyzed using ELISA. NLRP3, IL-1β, IL-18, and hsCRP levels were significantly higher in myocardial infarction patients compared to the healthy group (p = 0.02, p < 0.001, p < 0.001, and p < 0.001, respectively). No significant difference was found between the myocardial groups with and without depression. However, in the logistic regression analysis, the NLRP3 variable in myocardial infarction patients was found to have a significant contribution to the likelihood of depression (p = 0.015, OR = 1.72, and CI = 1.11–2.66). The likelihood of depression is associated with increasing NLRP3 levels in myocardial infarction patients. However, this potential role should be further explored in a larger sample.

The comorbidity between cardiovascular disease (CVD) and depression has been observed for many years. Several biological and behavioral hypotheses have been proposed to explain this comorbidity. However, the underlying common mechanisms are still unclear. Evidence suggests a bidirectional relationship between depression and CVD. Inflammation has been implicated in the etiology of both depression and CVD. In this review, we aim to increase awareness for CVD and depression comorbidity and provide some insights about the possible role of inflammation.