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An Unpredictable Chronic Mild Stress Protocol for Instigating Depressive Symptoms, Behavioral Changes and Negative Health Outcomes in Rodents
Published on: December 2, 2015
Comorbidity between depression and cardiovascular disease
1Department of Psychiatry, Loyola University Stritch School of Medicine, Maywood, IL 60153, USA. ahalaris@lumc.edu
Insights
Depression significantly increases cardiovascular disease (CVD) risk and mortality. Treating depression, particularly with selective serotonin reuptake inhibitors (SSRIs), may reduce CVD morbidity and mortality by addressing underlying biological mechanisms.
Area of Science:
- Cardiology
- Psychiatry
- Psychoneuroimmunology
Background:
- Cardiovascular disease (CVD) is a leading cause of death globally.
- Depression is a prevalent psychiatric disorder with significant comorbidity with CVD.
- Individuals with depression exhibit a two-fold higher risk of developing CVD and poorer outcomes post-myocardial infarction.
Purpose of the Study:
- To explore the complex mechanisms underlying the comorbidity of depression and CVD.
- To identify potential biological links and therapeutic targets for managing comorbid depression and CVD.
Main Methods:
- Review of epidemiological studies and pathophysiological research.
- Examination of neuroendocrine, autonomic, inflammatory, and platelet function in depression.
- Analysis of the role of serotonergic pathways in linking depression and CVD.
Main Results:
- Depression is associated with sympathoadrenal activation, HPA axis dysregulation, and inflammation.
- Platelet activation and hypercoagulability are observed in depression, potentially reversible with SSRIs.
- Endothelial dysfunction may serve as a trait marker for depression.
Conclusions:
- Shared pathophysiological mechanisms, including autonomic imbalance and inflammation, link depression and CVD.
- Selective serotonin reuptake inhibitors (SSRIs) show promise in ameliorating depression and reducing cardiovascular risk.
- Vigorous treatment of comorbid depression is crucial for improving cardiovascular outcomes.
Abstract:
Morbidity and mortality of cardiovascular disease (CVD) is exceedingly high worldwide. Depressive illness is a serious psychiatric illness that afflicts a significant portion of the population in all countries. Numerous epidemiological studies have confirmed that high comorbidity exists between these two conditions. Apparently healthy individuals with depression have at least a two-fold higher risk of developing CVD. Following myocardial infarction the emergence of clinical depression poses heightened risk of morbidity and mortality. To understand the complex mechanisms accountable for this comorbidity, several factors have been considered. They include pathophysiologic factors, such as sympathoadrenal activation, homeostatic imbalance between the sympathetic and the parasympathetic systems with diminished vagal tone and loss of heart rate variability in depression. Neuroendocrine factors consist mainly of hypothalamic-pituitary-adrenal axis activation resulting in hypercortisolemia with associated sequelae. Platelet activation and hypercoaguability have been demonstrated in depression and appear to normalize with selective serotonin reuptake inhibitor (SSRI) treatment. Inflammatory processes and release of proinflammatory cytokines have also been described whether or not depression is comorbid with another disease entity. Endothelial dysfunction has been detected in depression and may prove to be a trait marker for this illness. Central and peripheral serotonergic transmission may be one common link between the two disease entities. Comorbid depression must be treated vigorously and SSRIs exert beneficial action not only in ameliorating depression but also in reversing platelet activation and inflammation, thereby reducing cardiovascular morbidity and mortality.
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