Abstract
Major depressive disorder (MDD) represents a serious health problem estimated to affect 350 million people globally. Importantly, MDD has repeatedly emerged as an etiological or prognostic factor in cardiovascular disease (CVD) development, including vascular pathology. Several linking pathomechanisms between MDD and CVD involve abnormal autonomic regulation, inflammation, and endothelial dysfunction as an early preclinical stage of atherosclerosis. However, the cause of accelerated atherosclerosis in MDD patients remains unclear. Recently, the causal relationships between MDD and mediator (e.g., inflammation and/or endothelial dysfunction), as well as the causal pathways from the mediator to atherosclerosis, were discussed. Specifically, MDD is accompanied by immune dysregulation, resulting in increased production of proinflammatory cytokines (e.g., interleukin (IL)-6 and tumor necrosis factor (TNF)-α), which could lead to depression-linked abnormalities in brain function. Further, MDD has an adverse effect on endothelial function; for example, circulating markers of endothelial dysfunction (e.g., soluble adhesion molecules, von Willebrand factor) have been linked with depression. Additionally, MDD-linked autonomic dysregulation, which is characterized by disrupted sympathovagal balance associated with excessive circulating catecholamines, can contribute to CVD. Taken together, activated inflammatory response, endothelial dysfunction, and autonomic dysregulation could affect gradual atherosclerosis progression, resulting in a higher risk of developing CVD in MDD. This review focused on the pathomechanisms linking MDD and CVD with respect to neuroimmune regulation, and the description of promising biomarkers, which is important for the early diagnosis and personalized prevention of CVD in major depression.
Highlights
Depression is a common and serious medical illness that negatively affects emotional and cognitive functions, leading to feelings of sadness and/or a loss of interest in once-enjoyed activities
The aim of this study was to summarize potential direct and associated pathophysiological mechanisms leading to depression-linked cardiovascular disease (CVD) with respect to immune, vascular, and autonomic dysfunction, as well as to emphasize potential promising biomarkers that could be used in the personalized prevention of CVD in major depression
In flow-mediated dilation (FMD), changes of the diameter of the brachial artery are evaluated from a single side recording, but in peripheral-artery tonometry (PAT), plethysmographic curves are simultaneously recorded at the index fingers of both hands
Summary
Depression (major depressive disorder, MDD) is a common and serious medical illness that negatively affects emotional and cognitive functions, leading to feelings of sadness and/or a loss of interest in once-enjoyed activities. Depressive disorder has been suggested as a risk factor for the development of cardiovascular disease (CVD) In this aspect, atherosclerosis and depression are listed in the most common medical conditions related to increased mortality and morbidity [1]. Inflammation is closely associated with endothelial dysfunction as a preamble to atherosclerosis [3] In this context, immune response is regulated by the autonomic nervous system via a sympathetic-cholinergic anti-inflammatory pathway that inhibits the release of proinflammatory cytokines [4,5]. The aim of this study was to summarize potential direct and associated pathophysiological mechanisms leading to depression-linked CVD with respect to immune, vascular, and autonomic dysfunction, as well as to emphasize potential promising biomarkers that could be used in the personalized prevention of CVD in major depression
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