Lüthje, Lars

[["dc.bibliographiccitation.firstpage","102"],["dc.bibliographiccitation.journal","International Journal of Cardiology"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","272"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Willems, Rik"],["dc.contributor.author","Sprenkeler, David J."],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Flevari, Panayota"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Katsaras, Dimitrios"],["dc.contributor.author","Kirova, Aleksandra"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Röver, Christian"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Sossalla, Samuel"],["dc.contributor.author","Dunnink, Albert"],["dc.contributor.author","Sritharan, Rajevaa"],["dc.contributor.author","Tuinenburg, Anton E."],["dc.contributor.author","Vandenberk, Bert"],["dc.contributor.author","Vos, Marc A."],["dc.contributor.author","Wijers, Sofieke C."],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2019-07-09T11:50:23Z"],["dc.date.available","2019-07-09T11:50:23Z"],["dc.date.issued","2018"],["dc.description.abstract","BACKGROUND AND OBJECTIVE: We prospectively investigated combinations of risk stratifiers including multiple EP diagnostics in a cohort study of ICD patients. METHODS: For 672 enrolled patients, we collected history, LVEF, EP study and T-wave alternans testing, 24-h Holter, NT-proBNP, and the eGFR. All-cause mortality and first appropriate ICD shock were predefined endpoints. RESULTS: The 635 patients included in the final analyses were 63 ± 13 years old, 81% were male, LVEF averaged 40 ± 14%, 20% were inducible at EP study, 63% had a primary prophylactic ICD. During follow-up over 4.3 ± 1.5 years, 108 patients died (4.0% per year), and appropriate shock therapy occurred in n = 96 (3.9% per year). In multivariate regression, age (p < 0.001), LVEF (p < 0.001), NYHA functional class (p = 0.007), eGFR (p = 0.024), a history of atrial fibrillation (p = 0.011), and NT-pro-BNP (p = 0.002) were predictors of mortality. LVEF (p = 0.002), inducibility at EP study (p = 0.007), and secondary prophylaxis (p = 0.002) were identified as independent predictors of appropriate shocks. A high annualized risk of shocks of about 10% per year was prevalent in the upper quintile of the shock score. In contrast, a low annual risk of shocks (1.8% per year) was found in the lower two quintiles of the shock score. The lower two quintiles of the mortality score featured an annual mortality <0.6%. CONCLUSIONS: In a prospective ICD patient cohort, a very good approximation of mortality versus arrhythmic risk was possible using a multivariable diagnostic strategy. EP stimulation is the best test to assess risk of arrhythmias resulting in ICD shocks."],["dc.identifier.doi","10.1016/j.ijcard.2018.06.103"],["dc.identifier.pmid","29983251"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15929"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59764"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15360 but duplicate"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241526/EU//EUTRIGTREAT"],["dc.relation.issn","1874-1754"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.access","openAccess"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Aged, 80 and over"],["dc.subject.mesh","Arrhythmias, Cardiac"],["dc.subject.mesh","Cohort Studies"],["dc.subject.mesh","Death, Sudden, Cardiac"],["dc.subject.mesh","Defibrillators"],["dc.subject.mesh","Defibrillators, Implantable"],["dc.subject.mesh","Female"],["dc.subject.mesh","Follow-Up Studies"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Mortality"],["dc.subject.mesh","Multivariate Analysis"],["dc.subject.mesh","Natriuretic Peptide, Brain"],["dc.subject.mesh","Peptide Fragments"],["dc.subject.mesh","Prospective Studies"],["dc.subject.mesh","Risk Factors"],["dc.title","Differential multivariable risk prediction of appropriate shock versus competing mortality - A prospective cohort study to estimate benefits from ICD therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","7"],["dc.bibliographiccitation.journal","Respiratory Research"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Michels, Hellmuth"],["dc.contributor.author","Unsoeld, Bernhard W."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:34Z"],["dc.date.available","2017-09-07T11:47:34Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: Systemic effects of chronic obstructive pulmonary disease (COPD) significantly contribute to severity and mortality of the disease. We aimed to develop a COPD/emphysema model exhibiting systemic manifestations of the disease. Methods: Female NMRI mice were treated 5 times intratracheally with porcine pancreatic elastase (emphysema) or phosphate-buffered saline (control). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, diaphragm dysfunction using isolated muscle strips, pulmonary hypertension by measuring right ventricular pressure, and neurohumoral activation by determining urinary norepinephrine concentration. Results: Mean linear intercept was higher in emphysema (260.7 +/- 26.8 mu m) than in control lungs (24.7 +/- 1.7 mu m). Emphysema mice lost body weight, controls gained weight. Running distance was shorter in emphysema than in controls. Diaphragm muscle length was shorter in controls compared to emphysema. Fatigue tests of muscle strips revealed impaired relaxation in emphysema diaphragms. Maximum right ventricular pressure and norepinephrine were elevated in emphysema compared to controls. Linear correlations were observed between running distance changes and intercept, right ventricular weight, norepinephrine, and diaphragm length. Conclusion: The elastase mouse model exhibited severe emphysema with consecutive exercise limitation, and neurohumoral activation. The model may deepen our understanding of systemic aspects of COPD."],["dc.identifier.doi","10.1186/1465-9921-10-7"],["dc.identifier.gro","3143160"],["dc.identifier.isi","000263727200001"],["dc.identifier.pmid","19175913"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13854"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/643"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1465-9921"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Exercise intolerance and systemic manifestations of pulmonary emphysema in a mouse model"],["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","416"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","EP Europace"],["dc.bibliographiccitation.lastpage","422"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Vos, Marc A."],["dc.contributor.author","Flevari, Panagiota"],["dc.contributor.author","Willems, Rik"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Kremastinos, Dimitrios T."],["dc.contributor.author","Flore, Vincent"],["dc.contributor.author","Meine, Mathias"],["dc.contributor.author","Tuinenburg, Anton"],["dc.contributor.author","Myles, Rachel C."],["dc.contributor.author","Simon, Dirk"],["dc.contributor.author","Brockmöller, Jürgen"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Lehnart, Stephan E."],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2017-09-07T11:48:57Z"],["dc.date.available","2017-09-07T11:48:57Z"],["dc.date.issued","2012"],["dc.description.abstract","Aims The EUTrigTreat clinical study has been designed as a prospective multicentre observational study and aims to (i) risk stratify patients with an implantable cardioverter defibrillator (ICD) for mortality and shock risk using multiple novel and established risk markers, (ii) explore a link between repolarization biomarkers and genetics of ion (Ca-2, Na, K) metabolism, (iii) compare the results of invasive and non-invasive electrophysiological (EP) testing, (iv) assess changes of non-invasive risk stratification tests over time, and (v) associate arrythmogenomic risk through 19 candidate genes. Methods and results Patients with clinical ICD indication are eligible for the trial. Upon inclusion, patients will undergo non-invasive risk stratification, including beat-to-beat variability of repolarization (BVR), T-wave alternans, T-wave morphology variables, ambient arrhythmias from Holter, heart rate variability, and heart rate turbulence. Non-invasive or invasive programmed electrical stimulation will assess inducibility of ventricular arrhythmias, with the latter including recordings of monophasic action potentials and assessment of restitution properties. Established candidate genes are screened for variants. The primary endpoint is all-cause mortality, while one of the secondary endpoints is ICD shock risk. A mean follow-up of 3.3 years is anticipated. Non-invasive testing will be repeated annually during follow-up. It has been calculated that 700 patients are required to identify risk predictors of the primary endpoint, with a possible increase to 1000 patients based on interim risk analysis. Conclusion The EUTrigTreat clinical study aims to overcome current shortcomings in sudden cardiac death risk stratification and to answer several related research questions. The initial patient recruitment is expected to be completed in July 2012, and follow-up is expected to end in September 2014. Clinicaltrials.gov identifier: NCT01209494."],["dc.identifier.doi","10.1093/europace/eur352"],["dc.identifier.gro","3142572"],["dc.identifier.isi","000300717700021"],["dc.identifier.pmid","22117037"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7031"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8937"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Community [HEALTH-F2-2009-241526, EUTrigTreat]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1099-5129"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Rationale, objectives, and design of the EUTrigTreat clinical study: a prospective observational study for arrhythmia risk stratification and assessment of interrelationships among repolarization markers and genotype"],["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","273"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.lastpage","280"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Renner, Bernd"],["dc.contributor.author","Kessels, Roger"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Gerritse, Bart"],["dc.contributor.author","Tasci, Selcuk"],["dc.contributor.author","Schwab, Joerg O."],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Zenker, Dieter"],["dc.contributor.author","Schott, Peter"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Unterberg-Buchwald, Christina"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:47:31Z"],["dc.date.available","2017-09-07T11:47:31Z"],["dc.date.issued","2009"],["dc.description.abstract","Aims The combined therapeutic impact of atrial overdrive pacing (ACIP) and cardiac resynchronization therapy (CRT) on central steep apnoea (CSA) in chronic heart failure (CHF) so far has not been investigated. We aimed to evaluate the effect of CRT alone and CRT + AOP on CSA in CHF patients and to compare the influence of CRT on CHF between CSA positive and CSA negative patients. Methods and results Thirty patients with CRT indication underwent full night polysomnography, echocardiography, exercise testing, and neurohumoral evaluation before and 3 months after CRT implantation. In CSA positive patients (60%), two additional steep studies were conducted after 3 months of CRT, with CRT alone or CRT + ACIP, in random order. Cardiac resynchronization therapy resulted in significant improvements of NYHA class, left ventricular ejection fraction, N-terminal pro-brain natriuretic peptide, VO(2)max, and quality of life irrespective of the presence of CSA. Cardiac resynchronization therapy also reduced the central apnoea-hypopnoea index (AHI) (33.6 +/- 14.3 vs. 23.8 +/- 16.9 h(-1); P < 0.01) and central apnoea index (17.3 +/- 14.1 vs. 10.9 +/- 13.9 h(-1); P < 0.01) without altering steep stages. Cardiac resynchronization therapy with atrial overdrive pacing resulted in a small but significant additional decrease of the central AHI (23.8 +/- 16.9 vs. 21.5 +/- 16.9 h(-1); P < 0.01). Conclusion In this study, CRT significantly improved CSA without altering sleep stages. Cardiac resynchronization therapy with atrial. overdrive pacing resulted in a significant but minor additional improvement of CSA. Positive effects of CRT were irrespective of the presence of CSA."],["dc.identifier.doi","10.1093/eurjhf/hfn042"],["dc.identifier.gro","3143143"],["dc.identifier.isi","000265845700008"],["dc.identifier.pmid","19147446"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/625"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Bakken Research Center, Maastricht, Netherlands"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1388-9842"],["dc.title","Cardiac resynchronization therapy and atrial overdrive pacing for the treatment of central sleep apnoea"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","424"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Heart Rhythm"],["dc.bibliographiccitation.lastpage","432"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Kowallick, Johannes T."],["dc.contributor.author","Staab, Wieland"],["dc.contributor.author","Schuster, Andreas"],["dc.contributor.author","Backhaus, Sören J."],["dc.contributor.author","Weber-Krüger, Mark"],["dc.contributor.author","Bauer, Lukas"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Bergau, Leonard"],["dc.date.accessioned","2020-12-10T14:24:26Z"],["dc.date.available","2020-12-10T14:24:26Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.hrthm.2018.09.016"],["dc.identifier.issn","1547-5271"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72245"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Reverse left ventricular structural remodeling after catheter ablation of atrial fibrillation in patients with preserved left ventricular function: Insights from cardiovascular magnetic resonance native T1 mapping"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","684"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Heart Journal - Cardiovascular Imaging"],["dc.bibliographiccitation.lastpage","691"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Sohns, Jan Martin"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Dorenkamp, Marc"],["dc.contributor.author","Zwaka, Paul A."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Lotz, Joachim"],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2017-09-07T11:47:40Z"],["dc.date.available","2017-09-07T11:47:40Z"],["dc.date.issued","2013"],["dc.description.abstract","Aims This study aimed to identify whether left atrial (LA) volume assessed by multidetector computed tomography (MDCT) is related to the long-term success of pulmonary vein ablation (PVA). MDCT is used to guide PVA for the treatment of atrial fibrillation (AF). MDCT permits accurate sizing of LA dimensions. Methods and results We analysed data from 368 ablation procedures of 279 consecutive patients referred for PVA due to drug-refractory symptomatic AF (age 62 +/- 10; 58% men; 71% paroxysmal AF). Prior to the procedure, all patients underwent ECG-gated 64-MDCT scan for assessment of LA and PV anatomy, LA thrombus evaluation, LA volume estimation, and electroanatomical mapping integration. Within a mean follow-up of 356 +/- 128 days, 64% of the patients maintained sinus rhythm after the initial ablation, and 84% when including repeat PVA. LA diameter (P = 0.004), LA volume (P = 0.002), and type of AF (P = 0.001) were independent predictors of AF recurrence in univariate analysis. There was a relatively low correlation between the echocardiographic LA diameter and LA volume from MDCT (P = 0.01, r = 0.5). In multivariate analysis, paroxysmal AF (P < 0.006) and LA volume below the median value of 106 mL (P = 0.042) were significantly associated with the success of PVA, whereas LA diameter was not (P = 0.245). Analysing receiver-operator characteristics, the area under the curve for LA volume was 0.73 (P = 0.001) compared with 0.60 (P = 0.09) for LA diameter from echocardiography. Conclusion LA volume assessed by MDCT is a better predictor of AF recurrence after PVA than echocardiograpic LA diameter and can be derived from the pre-procedural imaging data set."],["dc.identifier.doi","10.1093/ehjci/jet017"],["dc.identifier.gro","3142334"],["dc.identifier.isi","000321462600013"],["dc.identifier.pmid","23435593"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7131"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","2047-2404"],["dc.title","Left atrial volumetry from routine diagnostic work up prior to pulmonary vein ablation is a good predictor of freedom from atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","118"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","American Journal of Respiratory and Critical Care Medicine"],["dc.bibliographiccitation.lastpage","122"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Lüthje, L."],["dc.contributor.author","Unterberg-Buchwald, Christina"],["dc.contributor.author","Dajani, D."],["dc.contributor.author","Vollmann, D."],["dc.contributor.author","Hasenfuß, G."],["dc.contributor.author","Andreas, S."],["dc.date.accessioned","2017-09-07T11:54:20Z"],["dc.date.available","2017-09-07T11:54:20Z"],["dc.date.issued","2005"],["dc.description.abstract","Rationale: Atrial overdrive pacing markedly improved sleep-disordered breathing in a recent study. Objectives: Using a single-blind, randomized, crossover design, we aimed to reproduce these findings and investigate the possible underlying mechanisms. Methods: Twenty ambulatory patients with an implanted pacemaker or cardioverter defibrillator were studied by polysomnography on 3 consecutive nights in a randomized, single-blind, crossover study in which devices were programmed for nonpacing or for overdrive pacing at 7 or 15 beats/minute faster than the mean nocturnal heart rate. Ventilation and biomarkers (urinary norepinephrine excretion, amino-terminal portion of the precursor of brain natriuretic peptide, or NT-proBNP, were also evaluated. Measurements and Main Results: Neither the primary endpoint apnea-hypopnea index, nor the apnea index, oxygen desaturation, ventilation, or biomarkers were affected by the nocturnal atrial overdrive pacing. A small, clinically insignificant, rate-dependent reduction in the hypopnea index was evoked by pacing (nonpacing, 13.4 +/- 1.4; pacing 7, 12.9 +/- 1.4, pacing 15, 10.9 +/- 1.0; p < 0.01, analysis of variance). Conclusions:The lack of effect on the apnea-hypopnea index means that atrial overdrive pacing is inappropriate for treating sleep-disordered breathing."],["dc.identifier.doi","10.1164/rccm.200409-1258OC"],["dc.identifier.gro","3143824"],["dc.identifier.isi","000230102400019"],["dc.identifier.pmid","15750043"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1381"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1073-449X"],["dc.title","Atrial overdrive pacing in patients with sleep apnea with implanted pacemaker"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Hnatkova, Katerina"],["dc.contributor.author","Exposito, P. Munoz"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Malik, Marek"],["dc.contributor.author","Zabel, M."],["dc.date.accessioned","2018-11-07T09:35:35Z"],["dc.date.available","2018-11-07T09:35:35Z"],["dc.date.issued","2014"],["dc.format.extent","770"],["dc.identifier.isi","000343001304445"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32419"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.eventlocation","Barcelona, SPAIN"],["dc.relation.issn","1522-9645"],["dc.relation.issn","0195-668X"],["dc.title","T-wave morphology markers from the 12-lead surface ECG for prediction of appropriate implantable cardioverter-defibrillator discharges and all-cause mortality"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","215"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Pulmonary Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","220"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Koegler, Harald"],["dc.contributor.author","Duve, Christian"],["dc.contributor.author","Schweda, Frank"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:44:19Z"],["dc.date.available","2017-09-07T11:44:19Z"],["dc.date.issued","2011"],["dc.description.abstract","Objectives: COPD with emphysema causes marked neurohumoral activation. Angiotensin II receptors are highly expressed within the lung and interfere with mechanisms involved in the progression of emphysema. This study examined the effects of an angiotensin II receptor blocker (ARB) on pulmonary and systemic manifestations of emphysema in a mouse model. Methods: Female NMRI mice received five intratracheal instillations of porcine pancreatic elastase (emphysema; n = 11) or phosphate-buffered saline (PBS; n = 4). Emphysema severity was quantified histologically by mean linear intercept, exercise tolerance by treadmill running distance, and lung biomechanics by compliance. Following emphysema induction, 6 mice were treated with the ARB irbesartan for 8 weeks, while 5 mice receiving standard food served as controls. Results: Following emphysema induction, mean linear intercept was higher in elastase-treated than in PBS-treated lungs (103.0 +/- 6.2 mu m vs. 35.0 +/- 0.6 mu m; p = 0.043) while running distance was shorter in emphysema mice (418.6 +/- 83.5 m vs. 906.6 +/- 244.6 m, p = 0.028). Irbesartan-treated emphysema mice showed a lower mean linear intercept (90.8 +/- 3.8 mu m vs. 121.5 +/- 8.1 mu m; p = 0.005), improved compliance (163.6 +/- 55.9 mu l/cmH(2)O vs. 354.4 +/- 72.5 mu l/cmH(2)O; p = 0.063) and greater running distance (p ANOVA = 0.015) compared to emphysema mice receiving standard food. Conclusions: The ARB irbesartan elicits encouraging beneficial effects on emphysema severity, lung biomechanics and exercise capacity in an emphysema mouse model. These findings might help to understand the corresponding positive effects of angiotensin II receptor blockade noticed in patients with COPD. (C) 2010 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.pupt.2010.12.006"],["dc.identifier.gro","3142753"],["dc.identifier.isi","000289396400006"],["dc.identifier.pmid","21187155"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/192"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Sanofi-Aventis (formerly Sanofi-Synthelabo), Paris, France"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Ltd- Elsevier Science Ltd"],["dc.relation.issn","1094-5539"],["dc.title","Local and systemic effects of angiotensin receptor blockade in an emphysema mouse model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","107"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Respiratory Medicine"],["dc.bibliographiccitation.lastpage","113"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Raupach, Tobias"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Herrmann, Peter"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Andreas, Stefan"],["dc.date.accessioned","2017-09-07T11:46:44Z"],["dc.date.available","2017-09-07T11:46:44Z"],["dc.date.issued","2010"],["dc.description.abstract","Objectives: Neurohumoral. activation has been shown to be present in patients with chronic obstructive pulmonary disease (COPD). The increase in respiratory muscle work might be responsible for the observed elevation of sympathetic tone via a respiratory muscle ergoreflex in these patients. The aim of this study is to investigate whether moderately increasing inspiratory resistive loading will impact on sympathetic activity in healthy subjects and COPD patients. Methods: Efferent muscle sympathetic nerve activity, blood pressure, heart rate and respiratory movements were continuously measured in 15 patients and 15 healthy control subjects. In order to increase work of breathing as evaluated by the tension-time index, inspiratory resistive loading was performed white patients were breathing through a spirometer. Results: At baseline, sympathetic nerve activity was significantly elevated in patients. Resistive loading increased work of breathing (tension-time index) by roughly 110% (COPD) and 130% (controls) but did not significantly alter blood gases or sympathetic activity in either group. Conclusions: Doubting the work of breathing does not affect sympathetic activation in COPD patients or healthy control subjects. Thus in COPD the respiratory muscle ergoreflex does not seem to play a major rote in sympathoexcitation. (C) 2009 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.rmed.2009.06.011"],["dc.identifier.gro","3143004"],["dc.identifier.isi","000274889300015"],["dc.identifier.pmid","19619996"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/471"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0954-6111"],["dc.title","Inspiratory resistive loading does not increase sympathetic tone in COPD"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]