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Cardiovascular abnormalities in patients with major depressive disorder: Autonomic mechanisms and implications for treatment

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dc.contributor.authorBrown, A.D.H.
dc.contributor.authorBarton, D.A.
dc.contributor.authorLambert, G.W.
dc.date.issued2009
dc.description.abstractThis article provides a detailed review of the association of major depression with coronary heart disease (CHD), examines the biological variables underpinning the linkage and discusses the clinical implications for treatment. When considering the co-morbidity between major depressive disorder (MDD) and CHD it is important to differentiate between (i) the prevalence and impact of MDD in those with existing CHD and (ii) MDD as a risk factor for the development of CHD. Whether the same biological mechanisms are at play in these two instances remains unknown. Depression is common in patients with CHD. Importantly, depression in these patients increases mortality. There is also consistent evidence that MDD is a risk factor for the development of CHD. The relative risk of developing CHD is proportional to the severity of depression and is independent of smoking, obesity, hypercholesterolaemia, diabetes mellitus and hypertension. There is a clear need to identify the underlying neurochemical mechanisms responsible for MDD and their linkage to the heart and vascular system. Of particular interest are activation of stress pathways, including both the sympathetic nervous system and hypothalamic-pituitary-adrenal axis, and inflammatory-mediated atherogenesis. Elevated sympathetic activity, reduced heart rate variability and increased plasma cortisol levels have been documented in patients with MDD. In addition to direct effects on the heart and vasculature, activation of stress pathways may also be associated with increased release of inflammatory cytokines such as interleukin-6 and tumour necrosis factor-α. Elevated levels of C-reactive protein are commonly observed in patients with MDD. The majority of investigations examining treatment of depression following myocardial infarction have focused on safety and efficacy; there is little evidence to indicate that treating depression in these patients improves survival. Given that strategies for preventive therapy remain incompletely formulated, future research should focus on generating a better understanding of the neurobiology of MDD and heart disease as a basis for rational and effective therapy.
dc.identifier.citationCNS Drugs, 2009; 23(7):583-602
dc.identifier.doi10.2165/00023210-200923070-00004
dc.identifier.issn1172-7047
dc.identifier.issn1179-1934
dc.identifier.orcidBrown, A.D.H. [0000-0003-2112-3918]
dc.identifier.urihttps://hdl.handle.net/1959.8/163275
dc.language.isoen
dc.publisherAdis International
dc.relation.fundingNHMRC
dc.relation.fundingNational Heart Foundation of Australia
dc.rightsCopyright 2009 Adis Data Information BV
dc.source.urihttps://doi.org/10.2165/00023210-200923070-00004
dc.subjectdepressive symptom
dc.subjectcoronary heart disease
dc.subjectheart rate variability
dc.subjectmajor depressive disorder
dc.subjectOxytocin
dc.subjectAutonomic Nervous System
dc.subjectHumans
dc.subjectCardiovascular Abnormalities
dc.subjectDepressive Disorder, Major
dc.titleCardiovascular abnormalities in patients with major depressive disorder: Autonomic mechanisms and implications for treatment
dc.typeJournal article
pubs.publication-statusPublished
ror.mmsid9915910760801831

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