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1.
Psychol Med ; : 1-14, 2024 Sep 10.
Artigo em Inglês | MEDLINE | ID: mdl-39252547

RESUMO

BACKGROUND: Depression is an independent risk factor for cardiovascular disease (CVD), but it is unknown if successful depression treatment reduces CVD risk. METHODS: Using eIMPACT trial data, we examined the effect of modernized collaborative care for depression on indicators of CVD risk. A total of 216 primary care patients with depression and elevated CVD risk were randomized to 12 months of the eIMPACT intervention (internet cognitive-behavioral therapy [CBT], telephonic CBT, and select antidepressant medications) or usual primary care. CVD-relevant health behaviors (self-reported CVD prevention medication adherence, sedentary behavior, and sleep quality) and traditional CVD risk factors (blood pressure and lipid fractions) were assessed over 12 months. Incident CVD events were tracked over four years using a statewide health information exchange. RESULTS: The intervention group exhibited greater improvement in depressive symptoms (p < 0.01) and sleep quality (p < 0.01) than the usual care group, but there was no intervention effect on systolic blood pressure (p = 0.36), low-density lipoprotein cholesterol (p = 0.38), high-density lipoprotein cholesterol (p = 0.79), triglycerides (p = 0.76), CVD prevention medication adherence (p = 0.64), or sedentary behavior (p = 0.57). There was an intervention effect on diastolic blood pressure that favored the usual care group (p = 0.02). The likelihood of an incident CVD event did not differ between the intervention (13/107, 12.1%) and usual care (9/109, 8.3%) groups (p = 0.39). CONCLUSIONS: Successful depression treatment alone is not sufficient to lower the heightened CVD risk of people with depression. Alternative approaches are needed. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02458690.

2.
Brain Behav Immun ; 112: 18-28, 2023 08.
Artigo em Inglês | MEDLINE | ID: mdl-37209779

RESUMO

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.


Assuntos
Doenças Cardiovasculares , Terapia Cognitivo-Comportamental , Humanos , Feminino , Pessoa de Meia-Idade , Masculino , Depressão/terapia , Antidepressivos/uso terapêutico , Terapia Cognitivo-Comportamental/métodos , Biomarcadores
3.
J Health Psychol ; : 13591053241270630, 2024 Aug 15.
Artigo em Inglês | MEDLINE | ID: mdl-39148313

RESUMO

We assess associations of somatic and cognitive/affective depressive symptom clusters with monocyte activation (soluble (s)CD14, sCD163), systemic inflammation (interleukin-6 (IL-6), high-sensitivity C-reactive protein (hsCRP)), and coagulation (D-dimer, fibrinogen) in people with HIV (PWH) on suppressive antiretroviral therapy with depression. Utilizing baseline data from a randomized controlled trial, we found no significant associations in linear regression models examining individual depressive symptom clusters; however, models examining both clusters simultaneously showed that the somatic cluster was positively associated with inflammation biomarkers, while the cognitive/affective cluster was negatively associated with inflammation and coagulation biomarkers (suggesting a cooperative suppression effect). Our findings indicate a differential association with depressive symptom clusters and biological mechanisms underlying cardiovascular disease (CVD) in HIV, which may be driven by unique components of each depressive symptom cluster. This line of research could identify subgroups of PWH with depression at elevated CVD risk needing early CVD prevention approaches. Supported by R01 HL126557.

4.
Psychiatry Res ; 330: 115581, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37931480

RESUMO

Brain-derived neurotrophic factor (BDNF) levels are lower in people with depression and are normalized following pharmacological treatment. However, it is unknown if psychological treatments for depression improve BDNF and if change in BDNF is a mediator of intervention effects on depressive symptoms. Therefore, using data from the eIMPACT trial, we sought to determine the effect of modernized collaborative care for depression on 12-month changes in BDNF and cognitive/affective and somatic depressive symptom clusters and to examine whether BDNF changes mediate intervention effects on depressive symptoms. 216 primary care patients with depression from a safety net healthcare system were randomized to 12 months of the eIMPACT intervention (internet cognitive-behavioral therapy [CBT], telephonic CBT, and select antidepressant medications) or usual primary care. Plasma BDNF was measured with commercially available kits, and depressive symptom clusters were assessed by the Patient Health Questionnaire-9. The intervention did not influence BDNF but did improve both the cognitive/affective and somatic clusters over 12 months. Changes in BDNF did not mediate the intervention effect on either cluster. Our findings suggest that modernized collaborative care is an effective treatment for both the cognitive/affective and somatic symptoms of depression and that the mechanism of action is not improvements in BDNF. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT02458690.


Assuntos
Terapia Cognitivo-Comportamental , Depressão , Humanos , Depressão/terapia , Fator Neurotrófico Derivado do Encéfalo , Antidepressivos/uso terapêutico , Resultado do Tratamento
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