Haarmann, Helge

[["dc.bibliographiccitation.artnumber","46"],["dc.bibliographiccitation.journal","BMC Pulmonary Medicine"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Mohrlang, Cordula"],["dc.contributor.author","Tschiesner, Uta"],["dc.contributor.author","Rubin, David B."],["dc.contributor.author","Bornemann, Thore"],["dc.contributor.author","Rueter, Karin"],["dc.contributor.author","Bonev, Slavtcho"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:44:26Z"],["dc.date.available","2017-09-07T11:44:26Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Neurohumoral activation is present in COPD and might provide a link between pulmonary and systemic effects, especially cardiovascular disease. Because long acting inhaled beta-agonists reduce hyperinflation, they could reduce sympathoexcitation by improving the inflation reflex. We aimed to evaluate if inhaled therapy with salmeterol reduces muscle sympathetic nerve activity (MSNA) evaluated by microneurography. Methods: MSNA, heart rate, blood pressure, and respiration were continually measured. After baseline recording of 20 minutes, placebo was administered; after further 45 minutes salmeterol (50 mu g) was administered which was followed by a further 45 minutes of data recording. Additionally, lung function, plasma catecholamine levels, arterial pulse wave velocity, heart rate variability, and baroreflex sensitivity were evaluated. Following 4 weeks of treatment with salmeterol 50 mu g twice daily, measurements were repeated without placebo administration. Results: A total of 32 COPD patients were included. Valid MSNA signals were obtained from 18 patients. Change in MSNA (bursts/100 heart beats) following acute administration of salmeterol did not differ significantly from the change following placebo (-1.96 +/- 9.81 vs. -0.65 +/- 9.07; p = 0.51) although hyperinflation was significantly reduced. Likewise, no changes in MSNA or catecholamines were observed after 4 weeks. Heart rate increased significantly by 3.8 +/- 4.2 (p < 0.01) acutely and 3.9 +/- 4.3 bpm (p < 0.01) after 4 weeks. Salmeterol treatment was safe and well tolerated. Conclusions: By using microneurography as a gold standard to evaluate sympathetic activity we found no change in MSNA following salmeterol inhalation. Thus, despite an attenuation of hyperinflation, the long acting beta-agonist salmeterol does not appear to reduce nor incite sympathoexcitation."],["dc.identifier.doi","10.1186/s12890-015-0054-7"],["dc.identifier.gro","3141919"],["dc.identifier.isi","000356211900001"],["dc.identifier.pmid","25924990"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12294"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2533"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: GlaxoSmithKline, Munich, Germany [SCO114520]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2466"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Inhaled beta-agonist does not modify sympathetic activity in patients with COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3437"],["dc.bibliographiccitation.issue","36"],["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.lastpage","3447"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Willems, Rik"],["dc.contributor.author","Lubinski, Andrzej"],["dc.contributor.author","Bauer, Axel"],["dc.contributor.author","Brugada, Josep"],["dc.contributor.author","Conen, David"],["dc.contributor.author","Flevari, Panagiota"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Harden, Markus"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Tichelbäcker, Tobias"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Harden, Markus"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.authorgroup","EU-CERT-ICD Study Investigators"],["dc.date.accessioned","2020-05-07T07:50:46Z"],["dc.date.accessioned","2021-10-27T13:22:10Z"],["dc.date.available","2020-05-07T07:50:46Z"],["dc.date.available","2021-10-27T13:22:10Z"],["dc.date.issued","2020"],["dc.description.abstract","Aims: The EUropean Comparative Effectiveness Research to Assess the Use of Primary ProphylacTic Implantable Cardioverter-Defibrillators (EU-CERT-ICD), a prospective investigator-initiated, controlled cohort study, was conducted in 44 centres and 15 European countries. It aimed to assess current clinical effectiveness of primary prevention ICD therapy. Methods and results: We recruited 2327 patients with ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and guideline indications for prophylactic ICD implantation. Primary endpoint was all-cause mortality. Clinical characteristics, medications, resting, and 12-lead Holter electrocardiograms (ECGs) were documented at enrolment baseline. Baseline and follow-up (FU) data from 2247 patients were analysable, 1516 patients before first ICD implantation (ICD group) and 731 patients without ICD serving as controls. Multivariable models and propensity scoring for adjustment were used to compare the two groups for mortality. During mean FU of 2.4 ± 1.1 years, 342 deaths occurred (6.3%/years annualized mortality, 5.6%/years in the ICD group vs. 9.2%/years in controls), favouring ICD treatment [unadjusted hazard ratio (HR) 0.682, 95% confidence interval (CI) 0.537–0.865, P = 0.0016]. Multivariable mortality predictors included age, left ventricular ejection fraction (LVEF), New York Heart Association class

[["dc.bibliographiccitation.firstpage","1242"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Journal of Cachexia, Sarcopenia and Muscle"],["dc.bibliographiccitation.lastpage","1249"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Haehling, Stephan"],["dc.contributor.author","Garfias Macedo, Tania"],["dc.contributor.author","Valentova, Miroslava"],["dc.contributor.author","Anker, Markus S."],["dc.contributor.author","Ebner, Nicole"],["dc.contributor.author","Bekfani, Tarek"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Schefold, Joerg C."],["dc.contributor.author","Lainscak, Mitja"],["dc.contributor.author","Cleland, John G. F."],["dc.contributor.author","Doehner, Wolfram"],["dc.contributor.author","Hasenfuss, Gerd"],["dc.contributor.author","Anker, Stefan D."],["dc.date.accessioned","2021-04-14T08:24:54Z"],["dc.date.available","2021-04-14T08:24:54Z"],["dc.date.issued","2020"],["dc.description.abstract","Abstract Background Skeletal muscle wasting is an extremely common feature in patients with heart failure, affecting approximately 20% of ambulatory patients with even higher values during acute decompensation. Its occurrence is associated with reduced exercise capacity, muscle strength, and quality of life. We sought to investigate if the presence of muscle wasting carries prognostic information. Methods Two hundred sixty‐eight ambulatory patients with heart failure (age 67.1 ± 10.9 years, New York Heart Association class 2.3 ± 0.6, left ventricular ejection fraction 39 ± 13.3%, and 21% female) were prospectively enrolled as part of the Studies Investigating Co‐morbidities Aggravating Heart Failure. Muscle wasting as assessed using dual‐energy X‐ray absorptiometry was present in 47 patients (17.5%). Results During a mean follow‐up of 67.2 ± 28.02 months, 95 patients (35.4%) died from any cause. After adjusting for age, New York Heart Association class, left ventricular ejection fraction, creatinine, N‐terminal pro‐B‐type natriuretic peptide, and iron deficiency, muscle wasting remained an independent predictor of death (hazard ratio 1.80, 95% confidence interval 1.01–3.19, P = 0.04). This effect was more pronounced in patients with heart failure with reduced than in heart failure with preserved ejection fraction. Conclusions Muscle wasting is an independent predictor of death in ambulatory patients with heart failure. Clinical trials are needed to identify treatment approaches to this co‐morbidity."],["dc.identifier.doi","10.1002/jcsm.12603"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81461"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2190-6009"],["dc.relation.issn","2190-5991"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Muscle wasting as an independent predictor of survival in patients with chronic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1038"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Biochemical and Biophysical Research Communications"],["dc.bibliographiccitation.lastpage","1044"],["dc.bibliographiccitation.volume","450"],["dc.contributor.author","N'Guessan, Philippe Dje"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Steiner, Tamara"],["dc.contributor.author","Heyl, Kerstin A."],["dc.contributor.author","Schreiber, Frauke"],["dc.contributor.author","Heinrich, Annina"],["dc.contributor.author","Slevogt, Hortense"],["dc.date.accessioned","2018-11-07T09:37:30Z"],["dc.date.available","2018-11-07T09:37:30Z"],["dc.date.issued","2014"],["dc.description.abstract","Background: Chronic lower airway inflammation is considered to be a major cause of pathogenesis and disease progression in chronic obstructive pulmonary disease (COPD). Moraxella catarrhalis is a COPD-associated pathogen causing exacerbations and bacterial colonization in the lower airways of patients, which may contribute to chronic inflammation. Increasing evidence suggests that the epidermal growth factor receptor (EGFR) modulates inflammatory processes in the human airways. The goal of this study was to investigate the role of EGFR in the M. catarrhalis-induced pro-inflammatory immune response in airway epithelial cells. Methods: The effects of inhibition and gene silencing of EGFR on M. catarrhalis-dependent pro-inflammatory cytokine expression in human primary bronchial epithelial cells (NHBEs), as well as the pulmonary epithelial cell lines BEAS-2B and A549 were analyzed. We also assessed the involvement of EGFR-dependent ERR and NF-kappa B signaling pathways. Results: The M. catarrhalis-induced pro-inflammatory immune response depends, at least in part, on the phosphorylation and activation of the EGF receptor. Interaction of M. catarrhalis with EGFR increases the secretion of pro-inflammatory cytokines, which is mediated via ERK and NF-kappa B activation. Conclusion: The interaction between M. catarrhalis and EGFR increases airway inflammation caused by this pathogen. Our data suggest that the inhibition of EGFR signaling in COPD could be an interesting target for reducing M. catarrhalis-induced airway inflammation. (C) 2014 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/3.0/)."],["dc.identifier.doi","10.1016/j.bbrc.2014.06.102"],["dc.identifier.isi","000339861200019"],["dc.identifier.pmid","24978309"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11375"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32859"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","1090-2104"],["dc.relation.issn","0006-291X"],["dc.rights","CC BY-NC-ND 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/3.0"],["dc.title","The Moraxella catarrhalis-induced pro-inflammatory immune response is enhanced by the activation of the epidermal growth factor receptor in human pulmonary epithelial cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S34"],["dc.bibliographiccitation.journal","Journal of Electrocardiology"],["dc.bibliographiccitation.lastpage","S39"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Schlögl, Simon"],["dc.contributor.author","Lubinski, Andrzej"],["dc.contributor.author","Svendsen, Jesper Hastrup"],["dc.contributor.author","Bauer, Axel"],["dc.contributor.author","Arbelo, Elena"],["dc.contributor.author","Brusich, Sandro"],["dc.contributor.author","Conen, David"],["dc.contributor.author","Cygankiewicz, Iwona"],["dc.contributor.author","Dommasch, Michael"],["dc.contributor.author","Flevari, Panagiota"],["dc.contributor.author","Galuszka, Jan"],["dc.contributor.author","Hansen, Jim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Hatala, Robert"],["dc.contributor.author","Huikuri, Heikki V."],["dc.contributor.author","Kenttä, Tuomas"],["dc.contributor.author","Kucejko, Tomasz"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Harden, Markus"],["dc.contributor.author","Iovev, Svetoslav"],["dc.contributor.author","Kääb, Stefan"],["dc.contributor.author","Kaliska, Gabriela"],["dc.contributor.author","Katsimardos, Andreas"],["dc.contributor.author","Kasprzak, Jaroslaw D."],["dc.contributor.author","Qavoq, Dariusz"],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Malik, Marek"],["dc.contributor.author","Novotný, Tomáš"],["dc.contributor.author","Pavlović, Nikola"],["dc.contributor.author","Perge, Peter"],["dc.contributor.author","Röver, Christian"],["dc.contributor.author","Schmidt, Georg"],["dc.contributor.author","Shalganov, Tchavdar"],["dc.contributor.author","Sritharan, Rajeeva"],["dc.contributor.author","Svetlosak, Martin"],["dc.contributor.author","Sallo, Zoltan"],["dc.contributor.author","Szavits-Nossan, Janko"],["dc.contributor.author","Traykov, Vassil"],["dc.contributor.author","Vandenberk, Bert"],["dc.contributor.author","Velchev, Vasil"],["dc.contributor.author","Vos, Marc A."],["dc.contributor.author","Willich, Stefan N."],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Willems, Rik"],["dc.contributor.author","Merkely, Béla"],["dc.contributor.author","Sticherling, Christian"],["dc.date.accessioned","2020-12-10T14:25:06Z"],["dc.date.available","2020-12-10T14:25:06Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.jelectrocard.2019.09.001"],["dc.identifier.issn","0022-0736"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16386"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72436"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Present criteria for prophylactic ICD implantation: Insights from the EU-CERT-ICD (Comparative Effectiveness Research to Assess the Use of Primary ProphylacTic Implantable Cardioverter Defibrillators in EUrope) project"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","submitted_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","26"],["dc.bibliographiccitation.journal","Tobacco Induced Diseases"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Haarmann, Helge"],["dc.contributor.author","Gossler, Alexandra"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Bonev, Slavtcho"],["dc.contributor.author","Xuan Phuc Nguyen, Xuan Phuc Nguyen"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.contributor.author","Raupach, Tobias"],["dc.date.accessioned","2017-09-07T11:44:44Z"],["dc.date.available","2017-09-07T11:44:44Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Varenicline is an effective smoking cessation medication. Some concern has been raised that its use may precipitate adverse cardiovascular events although no patho-physiological mechanism potentially underlying such an effect has been reported. The aim of this study was to test the hypothesis that varenicline impacts on sympatho-vagal balance during smoking withdrawal. Methods: In this randomised, placebo-controlled trial, muscle sympathetic nerve activity (MSNA), baroreflex sensitivity (BRS), heart rate, and blood pressure were assessed in 17 smokers four weeks before a quit attempt (baseline) and again on the third day of that quit attempt (acute smoking withdrawal). Results: Regarding the primary endpoint of our study, we did not find a significant effect of varenicline compared to placebo on changes in MSNA burst incidence between baseline and acute smoking withdrawal (-3.0 +/- 3.3 vs.-3.9 +/- 5.0 bursts/100 heart beats; p = 0.308). However, heart rate and systolic blood pressure significantly decreased in the placebo group only, while no significant changes in these parameters were observed in the varenicline group. Exposure to smoking cues during acute withdrawal lead to a significant increase of heart rate in the placebo group, while heart rate decreased in the varenicline group, and the difference in these changes was significant between groups (+ 2.7 +/- 1.0 vs.-1.8 +/- 0.5 1/min; p = 0.002). In all 17 participants combined, a significant increase in heart rate during smoking cue exposure was detected in subjects who relapsed in the course of six weeks after the quit date compared to those who stayed abstinent (+ 2.5 +/- 1.2 vs.-1.1 +/- 0.7; p = 0.018). Six-week abstinence rates were higher in the varenicline group compared to placebo (88 vs. 22 % p = 0.015). Conclusion: We did not find evidence of adverse effects of varenicline on sympatho-vagal balance. Varenicline probably blunts the heart rate response to smoking cues, which may be linked to improved cessation outcome."],["dc.identifier.doi","10.1186/s12971-016-0091-x"],["dc.identifier.gro","3141637"],["dc.identifier.isi","000381574200001"],["dc.identifier.pmid","27507930"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13863"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/3900"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Pfizer(R)"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1617-9625"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Effects of varenicline on sympatho-vagal balance and cue reactivity during smoking withdrawal: a randomised placebo-controlled trial"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]