Browsing by Author "Polanka, Brittanny M."
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Item Are Cardiovascular Risk Factors Stronger Predictors of Incident Cardiovascular Disease in U.S. Adults With Versus Without a History of Clinical Depression?(Oxford University Press, 2018-12) Polanka, Brittanny M.; Berntson, Jessica; Vrany, Elizabeth A.; Stewart, Jesse C.; Psychology, School of ScienceBackground Several mechanisms underlying the depression-to-cardiovascular disease (CVD) relationship have been proposed; however, few studies have examined whether depression promotes CVD through potentiating traditional cardiovascular risk factors. Purpose To test the combined influence of three cardiovascular risk factors and lifetime depressive disorder on incident CVD in a large, diverse, and nationally representative sample of U.S. adults. Methods Respondents were 26,840 adults without baseline CVD who participated in Waves 1 (2001–2002) and 2 (2004–2005) of the National Epidemiologic Survey on Alcohol and Related Conditions. Lifetime depressive disorder, tobacco use, hypertension, and incident CVD were determined from structured interviews, and body mass index (BMI) was computed from self-reported height and weight. Results Logistic regression models predicting incident CVD (1,046 cases) revealed evidence of moderation, as the interactions between lifetime depressive disorder and current tobacco use (p = .002), hypertension (p < .001), and BMI (p = .031) were significant. The Former Tobacco Use × Lifetime Depressive Disorder interaction was not significant (p = .85). In models stratified by lifetime depressive disorder, current tobacco use (OR = 1.78, 95% CI = 1.36–2.32, p < .001 vs. OR = 1.41, 95% CI = 1.24–1.60, p < .001), hypertension (OR = 2.46, 95% CI = 1.98–3.07, p < .001 vs. OR = 1.39, 95% CI = 1.28–1.51, p < .001), and BMI (OR = 1.10, 95% CI = 1.01–1.20, p = .031 vs. OR = 1.03, 95% CI = 0.99–1.07, p = .16) were stronger predictors of incident CVD in adults with versus without a lifetime depressive disorder. Conclusions Our findings suggest that amplifying the atherogenic effects of traditional cardiovascular risk factors may be yet another candidate mechanism that helps to explain the excess CVD risk of people with depression.Item Associations of Total, Cognitive/Affective, and Somatic Depressive Symptoms and Antidepressant Use With Cardiovascular Disease–Relevant Biomarkers in HIV: Veterans Aging Cohort Study(Wolters Kluwer, 2020) Stewart, Jesse C.; Polanka, Brittanny M.; So-Armah, Kaku A.; White, Jessica R.; Gupta, Samir K.; Kundu, Suman; Chang, Chung-Chou H.; Freiberg, Matthew S.; Psychology, School of ScienceObjective We sought to determine the associations of total, cognitive/affective, and somatic depressive symptoms and antidepressant use with biomarkers of processes implicated in cardiovascular disease in HIV (HIV-CVD). Methods We examined data from 1546 HIV-positive and 843 HIV-negative veterans. Depressive symptoms were assessed using the Patient Health Questionnaire-9, and past-year antidepressant use was determined from Veterans Affair pharmacy records. Monocyte (soluble CD14 [sCD14]), inflammatory (interleukin-6 [IL-6]), and coagulation (D-dimer) marker levels were determined from previously banked blood specimens. Linear regression models with multiple imputation were run to estimate the associations between depression-related factors and CVD-relevant biomarkers. Results Among HIV-positive participants, greater somatic depressive symptoms were associated with higher sCD14 (exp[b] = 1.02, 95% confidence interval [CI] = 1.00–1.03) and D-dimer (exp[b] = 1.06, 95% CI = 1.00–1.11) after adjustment for demographics and potential confounders. Further adjustment for antidepressant use and HIV factors slightly attenuated these relationships. Associations were also detected for antidepressant use, as selective serotonin reuptake inhibitor use was related to lower sCD14 (exp[b] = 0.95, 95% CI = 0.91–1.00) and IL-6 (exp[b] = 0.86, 95% CI = 0.76–0.96), and tricyclic antidepressant use was related to higher sCD14 (exp[b] = 1.07, 95% CI = 1.03–1.12) and IL-6 (exp[b] = 1.14, 95% CI = 1.02–1.28). Among HIV-negative participants, total, cognitive/affective, and somatic depressive symptoms were associated with higher IL-6, and tricyclic antidepressant use was related to higher sCD14. Conclusions Our novel findings suggest that a) monocyte activation and altered coagulation may represent two pathways through which depression increases HIV-CVD risk and that b) tricyclic antidepressants may elevate and selective serotonin reuptake inhibitors may attenuate HIV-CVD risk by influencing monocyte and inflammatory activation.Item Cardiovascular Risk Factors as Differential Predictors of Incident Atypical and Typical Major Depressive Disorder in U.S. Adults(Wolters Kluwer, 2018-03) Patel, Jay S.; Bernston, Jessica; Polanka, Brittanny M.; Stewart, Jesse C.; Psychology, School of ScienceObjectives While the association between major depressive disorder (MDD) and future cardiovascular disease (CVD) is established, less is known about the relationship between CVD risk factors and future depression, and no studies have examined MDD subtypes. Our objective was to determine whether hypertension, tobacco use, and body mass index (BMI) differentially predict atypical and typical MDD in a national sample of U.S. adults. Methods We examined prospective data from 22,915 adults with no depressive disorder history at baseline who participated in Wave 1 (2001-2002) and Wave 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). CVD risk factors (Wave 1) and incident MDD subtypes (Wave 2) were determined by structured interviews. Results There were 252 atypical and 991 typical MDD cases. In fully-adjusted models, baseline hypertension (OR=0.58, 95% CI: 0.43-0.76), former tobacco use (OR=1.46, 95% CI: 1.20-1.78), and BMI (OR=1.32, 95% CI: 1.25-1.40; all p’s<0.001) predicted incident atypical MDD versus no MDD, whereas no CVD risk factor predicted incident typical MDD. Baseline hypertension (OR=0.52, 95% CI: 0.39-0.70), former tobacco use (OR=1.53, 95% CI: 1.22-1.93), and BMI (OR=1.26, 95% CI: 1.18-1.36; all p’s<0.001) also predicted incident atypical MDD versus typical MDD. Conclusions Our study is the first to report that CVD risk factors differentially predict MDD subtypes, with hypertension (protective factor), former tobacco use (risk factor), and BMI (risk factor) being stronger predictors of incident atypical versus typical MDD. Such evidence could provide insights into the etiologies of MDD subtypes and inform interventions tailored to MDD subtype.Item Contribution of Behavioral Health Factors to Non-AIDS-Related Comorbidities: an Updated Review(SpringerLink, 2020-08) Chichetto, Natalie E.; Polanka, Brittanny M.; So-Armah, Kaku A.; Sung, Minhee; Stewart, Jesse C.; Koethe, John R.; Edelman, E. Jennifer; Tindle, Hilary A.; Freiberg, Matthew S.; Psychology, School of SciencePurpose of review: We summarize recent literature on the contribution of substance use and depression to non-AIDS-related comorbidities. Discussion of recent randomized clinical trials and implementation research to curtail risk attributed to each behavioral health issue is provided. Recent findings: Smoking, unhealthy alcohol use, opioid use, and depression are common among PWH and individually contribute to increased risk for non-AIDS-related comorbidities. The concurrence of these conditions is notable, yet understudied, and provides opportunity for linked-screening and potential treatment of more than one behavioral health factor. Current results from randomized clinical trials are inconsistent. Investigating interventions to reduce the impact of these behavioral health conditions with a focus on implementation into clinical care is important. Non-AIDS-defining cancers, cardiovascular disease, liver disease, and diabetes are leading causes of morbidity in people with HIV. Behavioral health factors including substance use and mental health issues, often co-occurring, likely contribute to the excess risk of non-AIDS-related comorbidities.Item Depressive Disorder Subtypes as Predictors of Incident Obesity in US Adults: Moderation by Race/Ethnicity(Oxford, 2017-05-01) Polanka, Brittanny M.; Vrany, Elizabeth A.; Patel, Jay; Stewart, Jesse C.; Psychology, School of ScienceWe compared the relative importance of atypical major depressive disorder (MDD), nonatypical MDD, and dysthymic disorder in predicting 3-year obesity incidence and change in body mass index and determined whether race/ethnicity moderated these relationships. We examined data from 17,787 initially nonobese adults in the National Epidemiologic Survey on Alcohol and Related Conditions waves 1 (2001-2002) and 2 (2004-2005) who were representative of the US population. Lifetime subtypes of depressive disorders were determined using a structured interview, and obesity outcomes were computed from self-reported height and weight. Atypical MDD (odds ratio (OR) = 1.68, 95% confidence interval (CI): 1.43, 1.97; P < 0.001) and dysthymic disorder (OR = 1.66, 95% CI: 1.29, 2.12; P < 0.001) were stronger predictors of incident obesity than were nonatypical MDD (OR = 1.11, 95% CI: 1.01, 1.22; P = 0.027) and no history of depressive disorder. Atypical MDD (B = 0.41 (standard error, 0.15); P = 0.007) was a stronger predictor of increases in body mass index than were dysthymic disorder (B = -0.31 (standard error, 0.21); P = 0.142), nonatypical MDD (B = 0.007 (standard error, 0.06); P = 0.911), and no history of depressive disorder. Race/ethnicity was a moderator; atypical MDD was a stronger predictor of incident obesity in Hispanics/Latinos (OR = 1.97, 95% CI: 1.73, 2.24; P < 0.001) than in non-Hispanic whites (OR = 1.54, 95% CI: 1.25, 1.91; P < 0.001) and blacks (OR = 1.72, 95% CI: 1.31, 2.26; P < 0.001). US adults with atypical MDD are at particularly high risk of weight gain and obesity, and Hispanics/Latinos may be especially vulnerable to the obesogenic consequences of depressions.Item Effect of Modernized Collaborative Care for Depression on Depressive Symptoms and Cardiovascular Disease Risk Biomarkers: eIMPACT Randomized Controlled Trial(Elsevier, 2023) Stewart, Jesse C.; Patel, Jay S.; Polanka, Brittanny M.; Gao, Sujuan; Nurnberger, John I., Jr.; MacDonald, Krysha L.; Gupta, Samir K.; Considine, Robert V.; Kovacs, Richard J.; Vrany, Elizabeth A.; Berntson, Jessica; Hsueh, Loretta; Shell, Aubrey L.; Rollman, Bruce L.; Callahan, Christopher M.; Psychology, School of ScienceAlthough depression is a risk and prognostic factor for cardiovascular disease (CVD), clinical trials treating depression in patients with CVD have not demonstrated cardiovascular benefits. We proposed a novel explanation for the null results for CVD-related outcomes: the late timing of depression treatment in the natural history of CVD. Our objective was to determine whether successful depression treatment before, versus after, clinical CVD onset reduces CVD risk in depression. We conducted a single-center, parallel-group, assessor-blinded randomized controlled trial. Primary care patients with depression and elevated CVD risk from a safety net healthcare system (N = 216, Mage = 59 years, 78% female, 50% Black, 46% with income <$10,000/year) were randomized to 12 months of the eIMPACT intervention (modernized collaborative care involving internet cognitive-behavioral therapy [CBT], telephonic CBT, and/or select antidepressants) or usual primary care for depression (primary care providers supported by embedded behavioral health clinicians and psychiatrists). Outcomes were depressive symptoms and CVD risk biomarkers at 12 months. Intervention participants, versus usual care participants, exhibited moderate-to-large (Hedges' g = -0.65, p < 0.01) improvements in depressive symptoms. Clinical response data yielded similar results - 43% of intervention participants, versus 17% of usual care participants, had a ≥ 50% reduction in depressive symptoms (OR = 3.73, 95% CI: 1.93-7.21, p < 0.01). However, no treatment group differences were observed for the CVD risk biomarkers - i.e., brachial flow-mediated dilation, high-frequency heart rate variability, interleukin-6, high-sensitivity C-reactive protein, β-thromboglobulin, and platelet factor 4 (Hedges' gs = -0.23 to 0.02, ps ≥ 0.09). Our modernized collaborative care intervention - which harnessed technology to maximize access and minimize resources - produced clinically meaningful improvements in depressive symptoms. However, successful depression treatment did not lower CVD risk biomarkers. Our findings indicate that depression treatment alone may not be sufficient to reduce the excess CVD risk of people with depression and that alternative approaches are needed. In addition, our effective intervention highlights the utility of eHealth interventions and centralized, remote treatment delivery in safety net clinical settings and could inform contemporary integrated care approaches.Item Examining Depression as a Risk Factor for Cardiovascular Disease in People with HIV: A Systematic Review(Oxford University Press, 2023) Polanka, Brittanny M.; Gupta, Samir K.; So-Armah, Kaku A.; Freiberg, Matthew S.; Zapolski, Tamika C. B.; Hirsh, Adam T.; Stewart, Jesse C.; Medicine, School of MedicineBackground: 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.Item Insomnia and mechanistic pathways to atherosclerotic CVD in HIV(2020-08) Polanka, Brittanny M.; Stewart, Jesse; Zapolski, Tamika; Hirsh, Adam; Gupta, SamirStudy 1: Background: Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. Methods: We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people living with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, “Difficulty falling or staying asleep?,” with the following response options: “I do not have this symptom” or “I have this symptom and…” “it doesn’t bother me,” “it bothers me a little,” “it bothers me,” “it bothers me a lot.” Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI). Results: For sCD14 and D-dimer, we observed no significant associations. For IL-6, veterans in the “bothers a lot” group had 15% higher IL-6 than veterans in the “I do not have this symptom” group in the demographic-adjusted model (exp[b]=1.15, 95%CI=1.02-1.29, p=.03). This association was nonsignificant in the fully-adjusted model (exp[b]=1.07, 95%CI=0.95-1.19, p=.25). Conclusion: We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted. Study 2: Background: While insomnia has been identified as a potential risk factor for cardiovascular disease in HIV (HIV-CVD), research on the underlying pathophysiological mechanisms is scarce. Methods: We examined associations between 0-to-12-week changes in sleep disturbance and the concurrent 0-to-12-week changes and the subsequent 12-to-24-week changes in markers of systemic inflammation, coagulation, and endothelial dysfunction among people living with HIV (n = 33-38) enrolled in a depression clinical trial. Sleep disturbance was measured using the Pittsburgh Sleep Quality Index. Inflammatory markers interleukin-6 (IL-6) and C-reactive protein (CRP) and coagulation marker D-dimer were determined from blood specimens; endothelial dysfunction marker brachial flow-mediated dilation (FMD) was determined by ultrasound. 0-to-12-week variables were calculated as 12-week visit minus baseline, and 12-to-24-week variables were calculated as 24-week minus 12-week. We constructed multivariate linear regression models for each outcome adjusting for age, sex, race/ethnicity, Framingham risk score, and baseline depressive symptoms. Results: We did not observe statistically significant associations between 0-to-12-week changes in sleep disturbance and 0-to-12-week or 12-to-24-week changes in IL-6, CRP, D-dimer, or FMD. However, we did observe potentially meaningful associations, likely undetected due to low power. For 0-to-12-weeks, every 1-standard deviation (SD) increase, or worsening, in the sleep disturbance change score was associated with a 0.41 pg/mL and 80 ng/mL decease in IL-6 and D-dimer, respectively. For 12-to-24-weeks, every 1-SD increase in sleep disturbance change score was associated with a 0.63 mg/L, 111 ng/mL, and 0.82% increase in CRP, D-dimer, and FMD, respectively. Conclusion: We observed potentially meaningful, though not statistically significant, associations between changes in sleep disturbance and changes in biological mechanisms underlying HIV-CVD over time. Some associations were in the expected direction, but others were not. Additional studies are needed that utilize larger samples and validated, comprehensive assessments of insomnia.Item Insomnia as an Independent Predictor of Incident Cardiovascular Disease in HIV: Data from the Veterans Aging Cohort Study(Wolters Kluwer, 2019-02) Polanka, Brittanny M.; Kundu, Suman; So-Armah, Kaku A.; Freiberg, Matthew S.; Gupta, Samir K.; Bedimo, Roger J.; Budoff, Matthew J.; Butt, Adeel A.; Chang, Chung-Chou H.; Gottlieb, Stephen S.; Marconi, Vincent C.; Womack, Julie A.; Stewart, Jesse C.; Psychology, School of ScienceBackground: Insomnia is associated with increased cardiovascular disease (CVD) risk in the general population and is highly prevalent in people with HIV. The CVD risk conferred by insomnia in the HIV population is unknown. Methods: Using the Veterans Aging Cohort Study-Survey Cohort, insomnia symptoms were measured and dummy coded with the item, “Difficulty falling or staying asleep?” (5-point scale from no difficulty to bothers a lot). Incident CVD event ICD-9 codes (acute myocardial infarction, stroke, or coronary artery revascularization) were identified with VA and Medicare administrative data and VA fee-for-service data. Those with baseline CVD were excluded. Results: HIV-infected (N=3,108) veterans had a median follow-up time of 10.8 years, during which 267 CVD events occurred. Compared to HIV-infected veterans with no difficulty falling or staying asleep, HIV-infected veterans bothered a lot by insomnia symptoms had an increased risk of incident CVD after adjusting for demographics (HR=1.64, 95%CI=1.16-2.31, p=.005), CVD risk factors (HR=1.62, 95%CI=1.14-2.30, p=.007), additional potential confounders (hepatitis C infection, renal disease, anemia, alcohol use, cocaine use; HR=1.70, 95%CI=1.19-2.43, p=.003), and HIV-specific factors (HIV-1 RNA, CD4+ T-cell count, ART; HR=1.66, 95%CI=1.16-2.37, p=.005). Additional adjustment for non-benzodiazepine sleep medication (HR=1.62, 95%CI=1.13-2.32, p=.009) did not attenuate the association; however, it fell short of significance at p < .01 after adjustment for depressive symptoms (HR=1.51, 95%CI=0.98-2.32, p=.060) or antidepressant medication (HR=1.51, 95%CI=1.04-2.19, p=.031). Conclusion: Highly bothersome insomnia symptoms were significantly associated with incident CVD in HIV-infected veterans, suggesting that insomnia may be a novel, modifiable risk factor for CVD in HIV.Item Insomnia symptoms and biomarkers of monocyte activation, systemic inflammation, and coagulation in HIV: Veterans Aging Cohort Study(PLOS, 2021-02-09) Polanka, Brittanny M.; Kundu, Suman; So-Armah, Kaku A.; Freiberg, Matthew S.; Gupta, Samir K.; Zapolski, Tamika C. B.; Hirsh, Adam T.; Bedimo, Roger J.; Budoff, Matthew J.; Butt, Adeel A.; Chang, Chung-Chou H.; Gottlieb, Stephen S.; Marconi, Vincent C.; Womack, Julie A.; Stewart, Jesse C.; Medicine, School of MedicineBackground: Insomnia may be a risk factor for cardiovascular disease in HIV (HIV-CVD); however, mechanisms have yet to be elucidated. Methods: We examined cross-sectional associations of insomnia symptoms with biological mechanisms of HIV-CVD (immune activation, systemic inflammation, and coagulation) among 1,542 people with HIV from the Veterans Aging Cohort Study (VACS) Biomarker Cohort. Past-month insomnia symptoms were assessed by the item, "Difficulty falling or staying asleep?," with the following response options: "I do not have this symptom" or "I have this symptom and…" "it doesn't bother me," "it bothers me a little," "it bothers me," "it bothers me a lot." Circulating levels of the monocyte activation marker soluble CD14 (sCD14), inflammatory marker interleukin-6 (IL-6), and coagulation marker D-dimer were determined from blood specimens. Demographic- and fully-adjusted (CVD risk factors, potential confounders, HIV-related factors) regression models were constructed, with log-transformed biomarker variables as the outcomes. We present the exponentiated regression coefficient (exp[b]) and its 95% confidence interval (CI). Results: We observed no significant associations between insomnia symptoms and sCD14 or IL-6. For D-dimer, veterans in the "Bothers a Lot" group had, on average, 17% higher D-dimer than veterans in the "No Difficulty Falling or Staying Asleep" group in the demographic-adjusted model (exp[b] = 1.17, 95%CI = 1.01-1.37, p = .04). This association was nonsignificant in the fully-adjusted model (exp[b] = 1.09, 95%CI = 0.94-1.26, p = .27). Conclusion: We observed little evidence of relationships between insomnia symptoms and markers of biological mechanisms of HIV-CVD. Other mechanisms may be responsible for the insomnia-CVD relationship in HIV; however, future studies with comprehensive assessments of insomnia symptoms are warranted.