@article{HeringerWaltherMoreiraWesseletal.2006, author = {Heringer-Walther, Silvia and Moreira, Maria da Consolacao V. and Wessel, Niels and Wang, Yong and Ventura, Pago Moreira and Schultheiss, Heinz-Peter and Walther, Thomas}, title = {Does the C-type natriuretic peptide have prognostic value in Chagas disease and other dilated cardiomyopathies}, series = {Journal of cardiovascular pharmacology}, volume = {48}, journal = {Journal of cardiovascular pharmacology}, number = {6}, publisher = {Lippincott Williams \& Wilkins}, address = {Philadelphia}, issn = {0160-2446}, doi = {10.1097/01.fjc.0000249892.22635.46}, pages = {293 -- 298}, year = {2006}, abstract = {Atrial natriuretic peptides (ANP) and brain natriuretic peptides (BNP) are powerful neurohormonal indicators of left-ventricular function and prognosis in heart failure (HF). Chagas disease (CD) caused by the protozoan Trypanosoma cruzi. remains a major cause of HF in Latin America. We assessed whether the plasma concentration of the third natriuretic peptide, C-type natnuretic peptide (CNP), also has diagnostic and prognostic properties in patients with CD or other dilated cardiomyopathies (DCM). Blood samples were obtained from 66 patients with CD, 50 patients with DCM from other causes, and 30 gender- and age-matched healthy subjects. Patients were subdivided according to the New York Heart Association (NYHA) class. The CNP concentration was determined by radioimmunoassay (Immundiagnostik, Bensheim, Germany). The main duration of follow-up was 31.4 months (range 13 to 54 months), 19 patients had died and 11 patients received a heart transplant. CNP concentrations were only significantly altered in patients with DCM or CD of the NYHA classes III and IV (P < 0.05). The Pearson correlation of echocardiographic data with CNP revealed an association only with the left-ventricular end systolic volume (P = 0.03) in patients with DCM. Furthermore, CNP did not predict mortality or the necessity for heart transplant. Our data are the first to demonstrate the raised levels of the third natriuretic peptide CNP in CD and other DCM Whereas ANP and BNP have a high predictive value for mortality in both diseases, CNP is without any predictive potency.}, language = {en} } @misc{ReibisSalzwedelBonaventuraetal.2017, author = {Reibis, Rona Katharina and Salzwedel, Annett and Bonaventura, Klaus and V{\"o}ller, Heinz and Wegscheider, Karl}, title = {Improvement of left ventricular ejection fraction in revascularized postmyocardial patients}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch Naturwissenschaftliche Reihe}, number = {882}, issn = {1866-8372}, doi = {10.25932/publishup-43509}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-435093}, pages = {10}, year = {2017}, abstract = {BACKGROUND: Reduced left ventricular ejection fraction (LVEF) ≤30\% is the most powerful prognostic indicator for sudden cardiac death (SCD) in patients after myocardial infarction (MI), but there are little data about long-term changes of LVEF after revascularization and the following implantation of a cardioverter defibrillator (ICD). METHODS: We performed a retrospective analysis of 277 patients with reduced LVEF at least 1month after MI and complete revascularization. Patients (median time post-MI 23.4months; 74.3\% after PCI, 25.7\% after CABG were assigned either to group 1 (LVEF<30\%) or group 2 (LVEF 30-40\%). Biplane echocardiography was redone after a mean follow-up of 441±220days. RESULTS: LVEF increased significantly in both two groups (group 1: 26.2±4.8\% to 32.4±8.5\%; p<0.001; group 2: 38.2±2.5\% to 44.4±9.6\%; p<0.001). However, statistical analysis of first and second LVEF measurement by means of a LOWESS regression and with an appropriate correction of the regression towards the mean effect revealed only a moderate increase of the mean LVEF from 35 to 37\% (p<0.001) with a large interindividual variation. CONCLUSIONS: The impact of early revascularization on LVEF appears to be low in the majority of post-MI heart failure patients. Owing to the high variability, a single measurement may not be reliable enough to justify a decision on ICD indication.}, language = {en} } @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} }