Examining Depression as a Risk Factor for Cardiovascular Disease in People with HIV: A Systematic Review.

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Title: Examining Depression as a Risk Factor for Cardiovascular Disease in People with HIV: A Systematic Review.
Authors: Polanka, Brittanny M (AUTHOR), Gupta, Samir K (AUTHOR), So-Armah, Kaku A (AUTHOR), Freiberg, Matthew S (AUTHOR), Zapolski, Tamika C B (AUTHOR), Hirsh, Adam T (AUTHOR), Stewart, Jesse C (AUTHOR)
Source: Annals of Behavioral Medicine. Jan2023, Vol. 57 Issue 1, p1-25. 25p.
Subjects: Disease risk factors, Cardiovascular diseases, HIV-positive persons, HIV, Psychoneuroimmunology, Mental depression, CINAHL database
Abstract: Background People with human immunodeficiency virus (HIV) have an increased risk of cardiovascular disease (CVD) not fully accounted for by traditional or HIV-specific risk factors. Successful management of HIV does not eliminate this excess risk. Thus, there is a need to identify novel risk factors for CVD among people with HIV (PWH). Purpose Our objective was to systematically review the literature on one such candidate CVD risk factor in PWH—depression. Methods A systematic literature search of PubMed, PsycINFO, EMBASE, Web of Science, and CINAHL was performed to identify published English-language studies examining associations of depression with clinical CVD, subclinical CVD, and biological mechanisms (immune activation, systemic inflammation, altered coagulation) among PWH between the earliest date and June 22, 2021. Results Thirty-five articles were included. For clinical CVD (k = 8), findings suggests that depression is consistently associated with an increased risk of incident CVD. For subclinical CVD (k = 5), one longitudinal analysis reported a positive association, and four cross-sectional analyses reported null associations. For immune activation (k = 13), systemic inflammation (k = 17), and altered coagulation (k = 5), findings were mixed, and there was considerable heterogeneity in sample characteristics and methodological quality across studies. Conclusions Depression may be an independent risk factor for CVD among PWH. Additional research is needed to confirm depression's association with clinical CVD and to determine whether depression is consistently and meaningfully associated with subclinical CVD and biological mechanisms of CVD in HIV. We propose a research agenda for this emerging area. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
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Abstract:Background People with human immunodeficiency virus (HIV) have an increased risk of cardiovascular disease (CVD) not fully accounted for by traditional or HIV-specific risk factors. Successful management of HIV does not eliminate this excess risk. Thus, there is a need to identify novel risk factors for CVD among people with HIV (PWH). Purpose Our objective was to systematically review the literature on one such candidate CVD risk factor in PWH—depression. Methods A systematic literature search of PubMed, PsycINFO, EMBASE, Web of Science, and CINAHL was performed to identify published English-language studies examining associations of depression with clinical CVD, subclinical CVD, and biological mechanisms (immune activation, systemic inflammation, altered coagulation) among PWH between the earliest date and June 22, 2021. Results Thirty-five articles were included. For clinical CVD (k = 8), findings suggests that depression is consistently associated with an increased risk of incident CVD. For subclinical CVD (k = 5), one longitudinal analysis reported a positive association, and four cross-sectional analyses reported null associations. For immune activation (k = 13), systemic inflammation (k = 17), and altered coagulation (k = 5), findings were mixed, and there was considerable heterogeneity in sample characteristics and methodological quality across studies. Conclusions Depression may be an independent risk factor for CVD among PWH. Additional research is needed to confirm depression's association with clinical CVD and to determine whether depression is consistently and meaningfully associated with subclinical CVD and biological mechanisms of CVD in HIV. We propose a research agenda for this emerging area. [ABSTRACT FROM AUTHOR]
ISSN:08836612
DOI:10.1093/abm/kaab119