title: Characterising acute coronary syndrome-associated depression: Let the data speak.
abstract: Depression in the context of acute coronary syndrome (ACS) is understood to confer increased morbidity and mortality risk. The pathophysiological mechanisms underlying this association remain poorly understood, although several candidates including inflammation, cardiac autonomic dysregulation, and behavioural factors are viewed as of key importance. No single bio-behavioural explanatory model of ACS-associated depression has emerged, likely due the substantial heterogeneity across both conditions. We studied 344 patients with ACS; 45 fulfilled diagnostic (DSM-IV) criteria for a major depressive episode occurring within 1-month of ACS, and 13 had ongoing major depression that pre-dated ACS and continued through to 1 month post-ACS. We employed two statistical methods (multinomial logistic regression; and latent class analysis) and a range of immunological, autonomic and nutritional markers in an attempt to characterise a biological basis for ACS-associated depression. Regression modelling failed to accurately predict categorical group membership of ACS-associated depression. An alternative data-driven approach produced a three-class solution, with the derived classes differing on measure of C-reactive protein, vitamin D, omega-6:omega-3 ratio, heart rate variability, and age (all p⩽0.004). The majority of participants with ACS-associated and ongoing depression were members of the class characterised by the greatest biological disturbance. Patients with depression differed from those without depression on a range of psychological trait and state variables; additionally reporting poorer sleep quality, higher levels of social isolation, and functional impairment, but had similar biological profiles. Patients with ongoing depression generally had higher scores on these psychological/behavioural measures. Our novel analytic approach identified a combination of biomarkers suggestive of a role for immune, autonomic, and nutritional pathways in the manifestation of depression during ACS, in the context of additional psychosocial and behavioural vulnerabilities. Further studies are required to confirm the causal role of these factors in perpetuating depression and increasing risk of poor-health outcomes.
authors.affiliation: School of Psychiatry, University of New South Wales, Australia. Electronic address: ute@unsw.edu.au.
authors.forename: Uté
authors.initials: U
authors.lastname: Vollmer-Conna
authors.affiliation: School of Psychiatry, University of New South Wales, Australia.
authors.forename: Erin
authors.initials: E
authors.lastname: Cvejic
authors.affiliation: School of Psychiatry, University of New South Wales, Australia.
authors.forename: Isabelle
authors.initials: I
authors.lastname: Granville Smith
authors.affiliation: School of Psychiatry, University of New South Wales, Australia.
authors.forename: Dusan
authors.initials: D
authors.lastname: Hadzi-Pavlovic
authors.affiliation: School of Psychiatry, University of New South Wales, Australia.
authors.forename: Gordon
authors.initials: G
authors.lastname: Parker
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000150:complications* / Q000503:physiopathology / Q000523:psychology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001341:Autonomic Nervous System / Q000503:physiopathology*; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D016207:Cytokines / Q000097:blood; D003866:Depressive Disorder / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology / Q000523:psychology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000097:blood; D008297:Male; D008875:Middle Aged; D011569:Psychiatric Status Rating Scales; D012720:Severity of Illness Index; D055815:Young Adult
chemical_list: D015415:Biomarkers; D016207:Cytokines; D002097:C-Reactive Protein
keywords: Acute coronary syndrome; Biological profiling; Depression; Heart rate variability; Inflammation