TY - JOUR A1 - Heringer-Walther, Silvia A1 - Moreira, Maria da Consolacao V. A1 - Wessel, Niels A1 - Wang, Yong A1 - Ventura, Pago Moreira A1 - Schultheiss, Heinz-Peter A1 - Walther, Thomas T1 - Does the C-type natriuretic peptide have prognostic value in Chagas disease and other dilated cardiomyopathies JF - Journal of cardiovascular pharmacology N2 - 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. KW - cardiomyopathy KW - heart failure KW - natriuretic peptide system KW - Trypanosoma cruzi Y1 - 2006 U6 - https://doi.org/10.1097/01.fjc.0000249892.22635.46 SN - 0160-2446 VL - 48 IS - 6 SP - 293 EP - 298 PB - Lippincott Williams & Wilkins CY - Philadelphia ER - TY - GEN A1 - Reibis, Rona Katharina A1 - Salzwedel, Annett A1 - Bonaventura, Klaus A1 - Völler, Heinz A1 - Wegscheider, Karl T1 - Improvement of left ventricular ejection fraction in revascularized postmyocardial patients BT - indication for statistical fallacy T2 - Postprints der Universität Potsdam : Mathematisch Naturwissenschaftliche Reihe N2 - 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. T3 - Zweitveröffentlichungen der Universität Potsdam : Mathematisch-Naturwissenschaftliche Reihe - 882 KW - cardioverter-defibrillator KW - heart failure KW - myocardial infarction KW - regression toward the mean Y1 - 2017 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-435093 SN - 1866-8372 IS - 882 ER - TY - GEN A1 - Tschorn, Mira A1 - Kuhlmann, Stella Linnea A1 - Rieckmann, Nina A1 - Beer, Katja A1 - Grosse, Laura A1 - Arolt, Volker A1 - Waltenberger, Johannes A1 - Haverkamp, Wilhelm A1 - Müller-Nordhorn, Jacqueline A1 - Hellweg, Rainer A1 - Ströhle, Andreas T1 - Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease T2 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe N2 - 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. T3 - Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe - 850 KW - depression KW - BDNF KW - coronary heart disease KW - heart failure KW - somatic comorbidity KW - acute coronary syndrome Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:kobv:517-opus4-557315 SN - 1866-8364 IS - 1 ER - TY - JOUR A1 - Tschorn, Mira A1 - Kuhlmann, Stella Linnea A1 - Rieckmann, Nina A1 - Beer, Katja A1 - Grosse, Laura A1 - Arolt, Volker A1 - Waltenberger, Johannes A1 - Haverkamp, Wilhelm A1 - Müller-Nordhorn, Jacqueline A1 - Hellweg, Rainer A1 - Ströhle, Andreas T1 - Brain-derived neurotrophic factor, depressive symptoms and somatic comorbidity in patients with coronary heart disease JF - Acta Neuropsychiatrica N2 - 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. KW - depression KW - BDNF KW - coronary heart disease KW - heart failure KW - somatic comorbidity KW - acute coronary syndrome Y1 - 2020 U6 - https://doi.org/10.1017/neu.2020.31 SN - 1601-5215 SN - 0924-2708 VL - 33 IS - 1 SP - 22 EP - 30 PB - Cambridge Univ. Press CY - Cambridge ER -