Abstract:
:Patients experiencing an acute myocardial infarction (AMI) have a three times higher chance to develop depression. Vice versa, depressive symptoms increase the risk of cardiovascular events. The co-existence of both conditions is associated with substantially worse prognosis. Although the underlying mechanism of the interaction is largely unknown, inflammation is thought to be of pivotal importance. AMI-induced peripheral cytokines release may cause cerebral endothelial leakage and hence induces a neuroinflammatory reaction. The neuroinflammation may persist even long after the initial peripheral inflammation has subsided. Among those selected brain regions that are prone to blood-brain barrier dysfunction, the paraventricular nucleus of the hypothalamus (PVN), a major center for cardiovascular autonomic regulation, is indicated to play a mediating role. Optimal cardiovascular therapy improves cardiovascular prognosis without major effects on depression. By the same token, antidepressant therapy in cardiovascular disease is associated with modest improvement in depressive symptoms, however without improvement in cardiac outcome. The failure of current antidepressants and the growing number of patients suffering from both conditions legitimize the search for better antidepressive therapies, from patients as well as society perspectives. Though we appreciate the mutual character of the interaction between depression and AMI, the present review focuses on the side of AMI induced depression and discusses the role of inflammation, represented by the proinflammatory cytokine TNF-α, as potential underlying mechanism. It is conceivable that inhibition of the inflammatory response post-AMI, through targeted anti-inflammatory pharmacotherapeutical agents may prevent the development of depressive symptoms and ultimately may improve cardiovascular outcomes.
journal_name
Neurosci Biobehav Revjournal_title
Neuroscience and biobehavioral reviewsauthors
Liu H,Luiten PG,Eisel UL,Dejongste MJ,Schoemaker RGdoi
10.1016/j.neubiorev.2013.02.004subject
Has Abstractpub_date
2013-05-01 00:00:00pages
561-72issue
4eissn
0149-7634issn
1873-7528pii
S0149-7634(13)00039-0journal_volume
37pub_type
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