Effect of modernized collaborative care for depression on depressive symptoms and cardiovascular disease risk biomarkers: eIMPACT randomized controlled trial.

Although 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, ß-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. Trial Registration:ClinicalTrials.gov Identifier: NCT02458690.

Are Cardiovascular Risk Factors Stronger Predictors of Incident Cardiovascular Disease in U.S. Adults With Versus Without a History of Clinical Depression?

Background: 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.

Cardiovascular Risk Factors as Differential Predictors of Incident Atypical and Typical Major Depressive Disorder in US Adults.

OBJECTIVE: Although 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 US 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. CVD risk factors (Wave 1) and incident MDD subtypes (Wave 2) were determined by structured interviews. RESULTS: There were 252 patients with atypical MDD and 991 patients with typical MDD. In fully adjusted models, baseline hypertension (odds ratio [OR] = 0.57, 95% confidence interval [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 < .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 < .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.

Number of recent stressful life events and incident cardiovascular disease: Moderation by lifetime depressive disorder.

OBJECTIVE: We investigated whether number of recent stressful life events is associated with incident cardiovascular disease (CVD) and whether this relationship is stronger in adults with a history of clinical depression. METHODS: Prospective data from 28,583 U.S. adults (mean age=45years) initially free of CVD who participated in Waves 1 (2001-2002) and 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were examined. Number of past-year stressful life events (Wave 1), lifetime depressive disorder (Wave 1), and incident CVD (Wave 2) were determined by structured interviews. RESULTS: There were 1069 cases of incident CVD. Each additional stressful life event was associated with a 15% increased odds of incident CVD [Odds Ratio (OR)=1.15, 95% Confidence Interval (CI): 1.11, 1.19]. As hypothesized, a stressful life events by lifetime depressive disorder interaction was detected (P=0.003). Stratified analyses indicated that stressful life events had a stronger association with incident CVD among adults with (OR=1.18, 95% CI: 1.10, 1.27, n=4908) versus without (OR=1.10, 95% CI: 1.07, 1.14, n=23,675) a lifetime depressive disorder. CONCLUSION: Our findings suggest that a greater number of recent stressful life events elevate the risk of new-onset CVD and that this risk is potentiated in adults with a history of clinical depression.

Depressive Symptoms Clusters and Insulin Resistance: Race/Ethnicity as a Moderator in 2005-2010 NHANES Data.

BACKGROUND: Although depression has been linked to insulin resistance, few studies have examined depressive symptom clusters. PURPOSE: We examined whether certain depressive symptom clusters are more strongly associated with insulin resistance in a nationally representative sample, and we evaluated potential moderators and mediators. METHODS: Respondents were 4487 adults from NHANES 2005-2010. Depressive symptoms were measured with the Patient Health Questionnaire-9 (PHQ-9), and insulin resistance was indexed by the homeostatic model assessment (HOMA) score. RESULTS: Positive relationships between PHQ-9 total, somatic, and cognitive-affective scores and HOMA score were detected (ps <0.001). In a simultaneous model, the somatic (p = 0.017), but not the cognitive-affective (p = 0.071), score remained associated with HOMA score. We observed evidence of (a) moderation by race/ethnicity (relationships stronger in non-Hispanic Whites) and (b) mediation by body mass and inflammation. CONCLUSIONS: The depressive symptoms-insulin resistance link may be strongest among non-Hispanic Whites and may be driven slightly more by the somatic symptoms.

Depressive symptoms and self-reported adherence to medical recommendations to prevent cardiovascular disease: NHANES 2005-2010.

UNLABELLED: This study's aim was to examine the relationships between depressive symptom severity and adherence to medication and lifestyle recommendations intended to prevent cardiovascular disease (CVD) in a large, diverse sample of men and women representative of the U.S. POPULATION: Participants were adults from the National Health and Nutrition Examination Survey (NHANES) 2005-2010 with a self-reported history of hypertension and/or hypercholesterolemia, but no CVD. The Patient Health Questionnaire-9 (PHQ-9) was used to assess depressive symptoms, and the Blood Pressure and Cholesterol interview was used to assess self-reported adherence to five medical recommendations: take antihypertensive medication (n = 3313), eat fewer high fat/cholesterol foods (n = 2924), control/lose weight (n = 2177), increase physical activity (n = 2540), and take cholesterol medication (n = 2266). Logistic regression models (adjusted for demographics, diabetes, body mass index, smoking, and alcohol intake) revealed that a 1-SD increase in PHQ-9 score was associated with a 14% lower odds of adherence to the control/lose weight recommendation (OR = 0.86, 95% CI: 0.75-0.98, p = .02) and a 25% lower odds of adherence to the increase physical activity recommendation (OR = 0.75, 95% CI: 0.65-0.86, p < .001). PHQ-9 score, however, was not related to the odds of adherence to the take antihypertensive medication (p = .21), eat fewer high fat/cholesterol foods (p = .40), or take cholesterol medication (p = .90) recommendations. Our findings suggest that poor adherence to provider recommendations to control/lose weight and to increase physical activity may partially explain the excess risk of CVD among depressed persons.