Molecular signaling pathways that link depression and heart disease.
Patients with clinical depression and coronary artery disease (CAD) risk factors have chronic, persistent activation of potentially toxic mediators optimized for short-term survival from ischemia, infection, and hemorrhage. The mediators and pathways involved in these processes are beginning to be elucidated. This basic research has uncovered novel potential therapeutic targets to prevent or attenuate adverse cardiovascular consequences of clinical depression. Well-designed randomized controlled studies will be required to definitively demonstrate that treating depression decreases cardiac mortality and morbidity. The results of controlled clinical trials support the use of selective serotonin reuptake inhibitors (SSRIs) for patients with CAD. The possibility that the use of an SSRI may confer additional benefit through a platelet inhibitory effect independent of the level of depression warrants further investigation.
Finkel
Mitchell S
MS
Department of Medicine, West Virginia University School of Medicine, Morgantown, WV 26506-9157, USA. mfinkel@hsc.wvu.edu
D000222:Adaptation, Physiological; D000818:Animals; D003324:Coronary Artery Disease / Q000150:complications* / Q000453:epidemiology / Q000503:physiopathology; D016207:Cytokines / Q000502:physiology; D003863:Depression / Q000150:complications* / Q000503:physiopathology; D004195:Disease Models, Animal; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D032383:Myocytes, Cardiac / Q000378:metabolism; D009569:Nitric Oxide / Q000378:metabolism; D010349:Patient Compliance / Q000523:psychology; D015539:Platelet Activation / Q000502:physiology; D017382:Reactive Oxygen Species; D012307:Risk Factors; D015398:Signal Transduction; D014481:United States / Q000453:epidemiology
D016207:Cytokines; D017382:Reactive Oxygen Species; D009569:Nitric Oxide; D020928:Mitogen-Activated Protein Kinases