@misc{TschornKuhlmannRieckmannetal.2020, author = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas}, title = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease}, series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, journal = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, number = {1}, issn = {1866-8364}, doi = {10.25932/publishup-55731}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557315}, pages = {11}, year = {2020}, abstract = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.}, language = {en} } @article{TschornKuhlmannRieckmannetal.2020, author = {Tschorn, Mira and Kuhlmann, Stella Linnea and Rieckmann, Nina and Beer, Katja and Grosse, Laura and Arolt, Volker and Waltenberger, Johannes and Haverkamp, Wilhelm and M{\"u}ller-Nordhorn, Jacqueline and Hellweg, Rainer and Str{\"o}hle, Andreas}, title = {Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease}, series = {Acta Neuropsychiatrica}, volume = {33}, journal = {Acta Neuropsychiatrica}, number = {1}, publisher = {Cambridge Univ. Press}, address = {Cambridge}, issn = {1601-5215}, doi = {10.1017/neu.2020.31}, pages = {22 -- 30}, year = {2020}, abstract = {Objective: Depression and coronary heart disease (CHD) are highly comorbid conditions. Brain-derived neurotrophic factor (BDNF) plays an important role in cardiovascular processes. Depressed patients typically show decreased BDNF concentrations. We analysed the relationship between BDNF and depression in a sample of patients with CHD and additionally distinguished between cognitive-affective and somatic depression symptoms. We also investigated whether BDNF was associated with somatic comorbidity burden, acute coronary syndrome (ACS) or congestive heart failure (CHF). Methods: The following variables were assessed for 225 hospitalised patients with CHD: BDNF concentrations, depression [Patient Health Questionnaire-9 (PHQ-9)], somatic comorbidity (Charlson Comorbidity Index), CHF, ACS, platelet count, smoking status and antidepressant treatment. Results: Regression models revealed that BDNF was not associated with severity of depression. Although depressed patients (PHQ-9 score >7) had significantly lower BDNF concentrations compared to non-depressed patients (p = 0.04), this was not statistically significant after controlling for confounders (p = 0.15). Cognitive-affective symptoms and somatic comorbidity burden each closely missed a statistically significant association with BDNF concentrations (p = 0.08, p = 0.06, respectively). BDNF was reduced in patients with CHF (p = 0.02). There was no covariate-adjusted, significant association between BDNF and ACS. Conclusion: Serum BDNF concentrations are associated with cardiovascular dysfunction. Somatic comorbidities should be considered when investigating the relationship between depression and BDNF.}, language = {en} }