MAJOR DEPRESSIVE, DISORDERS AND CORONARY ARTERY DISEASE: A REVIEW ON COMMON PATHOPHYSIOLOGICAL PATHWAYS

被引:0
|
作者
Perini, Giulia Ida [1 ]
Di Florio, Arianna [1 ,2 ]
Pavan, Chiara [1 ]
机构
[1] Univ Padua, Dipartimento Neurosci, Clin Psichiatr, Padua, Italy
[2] Univ Padua, Dipartimento Neurosci, Via Giustiniani 2, I-35128 Padua, Italy
来源
CLINICAL NEUROPSYCHIATRY | 2008年 / 5卷 / 03期
关键词
Major Depressive Disorder; Coronary Artery disease; Autonomic Nervous System; Hypothalamic Pituitary Adrenal Axis;
D O I
暂无
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Patients with Major Depressive Disorder (MDD) have an increased risk of developing or worsening coronary artery disease (CAD). The pathophysiology of this increased risk is only partially understood: six different but not opposing hypotheses have been proposed, involving hypothalamic pituitary adrenal axis (HPA) and autonomic nervous system (ANS) dysregulation., platelet activation, endothelial dysftinction, inflammation and behavioural factors, including treatment adherence and lifestyle habits. A simple model, based on a link between depression and bio-behavioural alteration, seems oversimplified and is not supported by data. Moreover, the lihk between coronary artery disease and depression represents the typical "chicken-egg" dilemma. Epidemiological studies clearly show that MDD or depressive symptoms are risk factors for CAD; conversely, CAD induces a depressive syndrome in 20-47% of acute cases, suggesting that MDD and CAD may share common pathophysiological pathways. In this review we attempt to verify the five above-mentioned mechanisms and propose that a central alteration could represent a link between depression and coronary artery disease, altering the peripheral response to stress via the HPA-axis, ANS, an immune response and platelet function. The relevant literature was sought through MEDLINE, PubMed, PsycINFO and EMBA.SE. The following search words were used alone or in combination, as appropriate: depression, myocardial infarction, coronary artery disease, endothelial dysfunction, inflammation, neurobiological aetiology. Further articles were sourced from the reference lists of articles ascertained through the search.
引用
收藏
页码:151 / 161
页数:11
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