Browsing by Author "Crawford, Christopher A."

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    Adolescents with Congenital Heart Disease: a Patient and Parental Perspective of Genetic Information and Genetic Risk
    (Cambridge University Press, 2020-02) Crawford, Christopher A.; Vujakovich, Courtney E.; Elmore, Lindsey; Fleming, Emily; Landis, Benjamin J.; Spoonamore, Katie G.; Ware, Stephanie M.; Pediatrics, School of Medicine
    Congenital heart defects (CHDs) occur in 8 of 1000 live-born children, making them common birth defects in the adolescent population. CHDs may have single gene, chromosomal, or multifactorial causes. Despite evidence that patients with CHD want information on heritability and genetics, no studies have investigated the interest or knowledge base in the adolescent population. This information is necessary as patients in adolescence take greater ownership of their health care and discuss reproductive risks with their physicians. The objectives of this survey-based study were to determine adolescents' recall of their own heart condition, to assess patient and parent perception of the genetic contribution to the adolescent's CHD, and to obtain information about the preferred method(s) for education. The results show that adolescent patients had good recall of their type of CHD. Less than half of adolescents and parents believed their CHD had a genetic basis or was heritable; however, adolescents with a positive family history of CHD were more likely to believe that their condition was genetic (p = 0.0005). The majority of patients were interested in receiving additional genetics education and preferred education in-person and in consultation with both parents and a physician. The adolescents who felt most competent to have discussions with their doctors regarding potential causes of their heart defect previously had a school science course which covered topics in genetics. These results provide insight into adolescents' perceptions and understanding about their CHD and genetic risk and may inform the creation and provision of additional genetic education.
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    Associations between affective factors and high-frequency heart rate variability in primary care patients with depression
    (Elsevier, 2022-10) Shell, Aubrey L.; Gonzenbach , Virgilio; Sawhney , Manisha; Crawford, Christopher A.; Stewart, Jesse C.; Psychology, School of Science
    Objective Depression is a risk factor for cardiovascular disease (CVD), and subgroups of people with depression may be at particularly elevated CVD risk. Lower high-frequency heart rate variability (HF HRV), which reflects diminished parasympathetic activation, is a candidate mechanism underlying the depression-CVD relationship and predicts cardiovascular events. Few studies have examined whether certain depression subgroups – such as those with co-occurring affective factors – exhibit lower HF HRV. The present study sought to assess associations between co-occurring affective factors and HF HRV in people with depression. Methods Utilizing baseline data from the 216 primary care patients with depression in the eIMPACT trial, we examined cross-sectional associations of depression's co-occurring affective factors (i.e., anxiety symptoms, hostility/anger, and trait positive affect) with HF HRV. HF HRV estimates were derived by spectral analysis from electrocardiographic data obtained during a supine rest period. Results Individual regression models adjusted for demographics and depressive symptoms revealed that anxiety symptoms (standardized regression coefficient β = −0.24, p = .002) were negatively associated with HF HRV; however, hostility/anger (β = 0.02, p = .78) and trait positive affect (β = −0.05, p = .49) were not. In a model further adjusted for hypercholesterolemia, hypertension, diabetes, body mass index, current smoking, CVD prevention medication use, and antidepressant medication use, anxiety symptoms remained negatively associated with HF HRV (β = −0.19, p = .02). Conclusion Our findings suggest that, in adults with depression, those with comorbid anxiety symptoms have lower HF HRV than those without. Co-occurring anxiety may indicate a depression subgroup at elevated CVD risk on account of diminished parasympathetic activation.
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    Examining Relationships Among Depression Treatment, Brain-Derived Neurotrophic Factor (BDNF), and Depressive Symptom Clusters in Primary Care Patients with Depression
    (2023-05) Crawford, Christopher A.; Stewart, Jesse; Rand, Kevin; Wu, Wei
    Depression is a heterogeneous mental health condition, varying in presentation across individuals. A candidate etiology that may help account for this heterogeneity is the neurotrophin hypothesis of depression, which proposes that stress downregulates brain-derived neurotrophic factor (BDNF) expression, leading to aberrant neurogenesis and depression. This etiology may manifest in a distinct symptom profile that may be reflected in depressive symptoms or symptom clusters. The effect of psychological interventions on BDNF is not known. Additionally, it is not known if BDNF levels mediate intervention effects on depressive symptom clusters. Using data from the eIMPACT trial (NCT02458690, supported by R01 HL122245), I examined baseline associations of BDNF with depressive symptoms and depressive symptom clusters. Also, I examined if the modernized collaborative care intervention for depression (internet CBT, telephonic CBT, and select antidepressant medications) affected BDNF and if changes in BDNF mediated intervention effects on cognitive/affective and somatic depressive symptom clusters. 216 participants (primary care patients with depression and elevated cardiovascular disease risk ≥50 years from a safety net healthcare system) were randomized to 12 months of the eIMPACT intervention (n=107) or usual primary care for depression (primary care providers supported by embedded behavioral health clinicians and affiliated psychiatrists; n=109). Plasma BDNF was measured with commercial ELISA kits. Depressive symptoms were assessed by the PHQ-9 (M=15.1, SD=5.0) from which cognitive/affective and somatic subscale scores were computed. No significant baseline associations were observed between BDNF and individual depressive symptoms or depressive symptom clusters. The intervention did not improve BDNF over 12 months. Similarly, 12-month changes in BDNF were not associated with 12-month changes in PHQ-9 cognitive/affective or somatic subscale scores. However, the intervention significantly improved PHQ-9 cognitive/affective and somatic subscale scores over 12 months. 12-month changes in BDNF did not mediate the effect of the intervention on 12-month changes in the PHQ-9 subscale scores. These findings suggest that modernized collaborative care for depression does not improve BDNF. Modernized collaborative care does yield improvements in both cognitive/affective and somatic depressive symptom clusters, albeit not via changes in BDNF.