Now showing 1 - 10 of 17
  • 2018Journal Article
    [["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"]]
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  • 2009Journal Article Research Paper
    [["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"]]
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  • 2012Journal Article Research Paper
    [["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"]]
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  • 2009Journal Article Discussion
    [["dc.bibliographiccitation.firstpage","517"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Clinical Research in Cardiology"],["dc.bibliographiccitation.lastpage","520"],["dc.bibliographiccitation.volume","98"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Vollmann, Dirk"],["dc.date.accessioned","2018-11-07T11:25:54Z"],["dc.date.available","2018-11-07T11:25:54Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1007/s00392-009-0040-2"],["dc.identifier.isi","000268511200008"],["dc.identifier.pmid","19554254"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56732"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","1861-0684"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Loss of capture late after right ventricular pacing lead revision: what is the mechanism?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.subtype","letter_note"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article
    [["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The International Journal of Cardiovascular Imaging"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","27"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Sossalla, Samuel T."],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Schmitto, Jan Dieter"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Obenauer, Silvia"],["dc.date.accessioned","2018-11-07T09:01:25Z"],["dc.date.available","2018-11-07T09:01:25Z"],["dc.date.issued","2011"],["dc.description.abstract","The aim of this study was to investigate the prevalence of extracardiac findings diagnosed by 64-multidetector computed tomography (MDCT) examinations prior to circumferential pulmonary vein (PV) ablation of atrial fibrillation (AF). A total of 158 patients (median age, 60.5 years; male 68%) underwent 64-MDCT of the chest and upper abdomen to characterize left atrial and PV anatomy prior to AF ablation. MDCT images were evaluated by a thoracic radiologist and a cardiologist. For additional scan interpretation, bone, lung, and soft tissue window settings were used. CT scans with extra-cardiac abnormalities categorized for the anatomic distribution and divided into two groups: Group 1-exhibiting clinically significant or potentially significant findings, and Group 2-patients with clinically non-significant findings. Extracardiac findings (n = 198) were observed in 113/158 (72%) patients. At least one significant finding was noted in 49/158 patients (31%). Group 1 abnormalities, such as malignancies or pneumonias, were found in 85/198 findings (43%). Group 2 findings, for example mild degenerative spine disease or pleural thickening, were observed in 113/198 findings (72%). 74/198 Extracardiac findings were located in the lung (37%), 35/198 in the mediastinum (18%), 8/198 into the liver (4%) and 81/198 were in other organs (41). There is an appreciable prevalence of prior undiagnosed extracardiac findings detected in patients with AF prior to PV-Isolation by MDCT. Clinically significant or potentially significant findings can be expected in similar to 40% of patients who undergo cardiac MDCT. Interdisciplinary trained personnel is required to identify and interpret both cardiac and extra cardiac findings."],["dc.identifier.doi","10.1007/s10554-010-9653-9"],["dc.identifier.isi","000287142900016"],["dc.identifier.pmid","20549365"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8173"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24422"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1569-5794"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Extra cardiac findings by 64-multidetector computed tomography in patients with symptomatic atrial fibrillation prior to pulmonal vein isolation"],["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"]]
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  • 2020Journal Article
    [["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
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  • 2017Journal Article
    [["dc.bibliographiccitation.artnumber","e0186387"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PloS one"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Tichelbäcker, Tobias"],["dc.contributor.author","Kessel, Barbora"],["dc.contributor.author","Lüthje, Lars"],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2019-07-09T11:44:37Z"],["dc.date.available","2019-07-09T11:44:37Z"],["dc.date.issued","2017"],["dc.description.abstract","BACKGROUND: There is evidence that the benefit of a primary prophylactic ICD therapy is not equal in all patients. PURPOSE: To evaluate risk factors of appropriate shocks and all- cause mortality in patients with a primary prophylactic ICD regarding contemporary studies. DATA SOURCE: PubMed, LIVIVO, Cochrane CENTRAL between 2010 and 2016. STUDY SELECTION: Studies were eligible if at least one of the endpoints of interest were reported. DATA EXTRACTION: All abstracts were independently reviewed by at least two authors. The full text of all selected studies was then analysed in detail. DATA SYNTHESIS: Our search strategy retrieved 608 abstracts. After exclusion of unsuitable studies, 36 papers with a total patient number of 47282 were included in our analysis. All-cause mortality was significantly associated with increasing age (HR 1.41, CI 1.29-1.53), left ventricular function (LVEF; HR 1.21, CI 1.14-1.29), ischemic cardiomyopathy (ICM; HR 1.37, CI 1.14-1.66) and co-morbidities such as impaired renal function (HR 2.30, CI 1.97-2.69). Although, younger age (HR 0.96, CI 0.85-1.09), impaired LVEF (HR 1.26, CI 0.89-1.78) and ischemic cardiomyopathy (HR 2.22, CI 0.83-5.93) were associated with a higher risk of appropriate shocks, none of these factors reached statistical significance. LIMITATIONS: Individual patient data were not available for most studies. CONCLUSION: In this meta-analysis of contemporary clinical studies, all-cause mortality is predicted by a variety of clinical characteristics including LVEF. On the other hand, the risk of appropriate shocks might be associated with impaired LVEF and ischemic cardiomyopathy. Further prospective studies are required to verify risk factors for appropriate shocks other than LVEF to help select appropriate patients for primary prophylactic ICD-therapy."],["dc.identifier.doi","10.1371/journal.pone.0186387"],["dc.identifier.pmid","29040341"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14842"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59051"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602299/EU//EU-CERT-ICD"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.subject.mesh","Age Factors"],["dc.subject.mesh","Aged"],["dc.subject.mesh","Cardiomyopathy, Dilated"],["dc.subject.mesh","Death, Sudden, Cardiac"],["dc.subject.mesh","Defibrillators, Implantable"],["dc.subject.mesh","Female"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Male"],["dc.subject.mesh","Middle Aged"],["dc.subject.mesh","Myocardial Ischemia"],["dc.subject.mesh","Primary Prevention"],["dc.subject.mesh","Prognosis"],["dc.subject.mesh","Prospective Studies"],["dc.subject.mesh","Risk Factors"],["dc.subject.mesh","Survival Analysis"],["dc.subject.mesh","Ventricular Function, Left"],["dc.title","Predictors of mortality and ICD shock therapy in primary prophylactic ICD patients-A systematic review and meta-analysis."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","170"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Therapeutics"],["dc.bibliographiccitation.lastpage","177"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Sossalla, Samuel Tobias"],["dc.contributor.author","Wallisch, Nora"],["dc.contributor.author","Toischer, Karl"],["dc.contributor.author","Sohns, Christian"],["dc.contributor.author","Vollmann, Dirk"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2018-11-07T09:37:19Z"],["dc.date.available","2018-11-07T09:37:19Z"],["dc.date.issued","2014"],["dc.description.abstract","Purpose: Torsades de pointes (TdP) tachycardias are triggered, polymorphic ventricular arrhythmias arising from early afterdepolarizations (EADs) and increased dispersion of repolarization. Ranolazine is a new agent which reduces pathologically elevated late I-Na but also I-Kr. Aim of this study was to evaluate the effects of ranolazine in a validated isolated Langendorff-perfused rabbit heart model. Methods: TdP was reproducibly induced with d-sotalol (10(-4) mol/L) and low potassium (K) (1.0 mmol/L for 5 min, pacing at CL 1000 ms). In 10 hearts, ECG and 8 epi- and endocardial monophasic action potentials were recorded. Action potential duration (APD) was measured at 90% repolarization and dispersion defined as APD max-min. Results: D-sotalol prolonged APD(90) and increased dispersion of APD(90), simultaneously causing EADs and induction of TdP. The combination of d-sotalol and two concentrations of ranolazine did not increase dispersion of ventricular APD(90) as compared to vehicle. Ranolazine at 5 mu mol/L did not cause additional induction of EADs and/or TdP but also did not significantly suppress arrhythmogenic triggers. The higher concentration of ranolazine (10 mu mol/L) in combination with d-sotalol caused further prolongation of APD(90), at the same time reduction in APD(90) dispersion. In parallel, the incidence of EADs was reduced and an antitorsadogenic effect was seen. Conclusions: In the healthy isolated rabbit heart (where late INa is not elevated), ranolazine does not cause proarrhythmia but exerts antiarrhythmic effects in a dose-dependent manner against d-sotalol/low K-induced TdP. This finding-despite additional APD prolongation-supports the safety of a combined use of both drugs and merits clinical investigation."],["dc.identifier.doi","10.1111/1755-5922.12078"],["dc.identifier.isi","000339497100005"],["dc.identifier.pmid","24785406"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32814"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/57"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | A03: Bedeutung CaMKII-abhängiger Mechanismen für die Arrhythmogenese bei Herzinsuffizienz"],["dc.relation.issn","1755-5922"],["dc.relation.issn","1755-5914"],["dc.relation.workinggroup","RG L. Maier (Experimentelle Kardiologie)"],["dc.relation.workinggroup","RG Sossalla (Kardiovaskuläre experimentelle Elektrophysiologie und Bildgebung)"],["dc.relation.workinggroup","RG Toischer (Kardiales Remodeling)"],["dc.rights","CC BY-NC 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/3.0"],["dc.title","Effects of Ranolazine on Torsades de Pointes Tachycardias in a Healthy Isolated Rabbit Heart Model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2018-12Journal Article
    [["dc.bibliographiccitation.firstpage","2110"],["dc.bibliographiccitation.journal","Data in Brief"],["dc.bibliographiccitation.lastpage","2116"],["dc.bibliographiccitation.volume","21"],["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","2019-07-09T11:49:47Z"],["dc.date.available","2019-07-09T11:49:47Z"],["dc.date.issued","2018-12"],["dc.description.abstract","This data article features supplementary figures and tables related to the article \"Differential Multivariable risk prediction of appropriate shock vs. competing mortality - a prospective cohort study to estimate benefits from implantable cardioverter defibrillator therapy\" (Bergau et al., 2018) [1]. The figures show the clinical study CONSORT graph (data that show the number of patients not-analyzable as well as a distribution of patients by outcomes) and the correlation scatter plot for risk scores of appropriate shock vs. mortality (data that show the calculated score values of the two scores plotted against each other). The tables show the results for the univariate Cox regressions for prediction of mortality and appropriate shock. For further information, please see Bergau et al. (2018) [1]."],["dc.identifier.doi","10.1016/j.dib.2018.11.025"],["dc.identifier.pmid","30533459"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15766"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59628"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/241526/EU//EUTRIGTREAT"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602299/EU//EU-CERT-ICD"],["dc.relation.issn","2352-3409"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Data on differential multivariable risk prediction of appropriate shock vs. competing mortality"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2016Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","86"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","The American Journal of Cardiology"],["dc.bibliographiccitation.lastpage","94"],["dc.bibliographiccitation.volume","118"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Bergau, Leonard"],["dc.contributor.author","Exposito, Pascal Munoz"],["dc.contributor.author","Bauer, Axel"],["dc.contributor.author","Fischer, Thomas H."],["dc.contributor.author","Luethje, Lars"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Zabel, Markus"],["dc.date.accessioned","2017-09-07T11:44:49Z"],["dc.date.available","2017-09-07T11:44:49Z"],["dc.date.issued","2016"],["dc.description.abstract","In patients treated with implantable cardioverter defibrillator (ICD), prediction of both overall survival and occurrence of shocks is important if improved patient selection is desired. We prospectively studied the predictive value of biomarkers and indexes of cardiac and renal function and spectral microvolt T-wave alternans testing and 24-hour Holier variables in a population who underwent first ICD implantation. Consecutive patients in sinus rhythm with ischemic or dilated cardiomyopathy scheduled for primary or secondary prophylactic ICD implantation were enrolled. Exercise microvolt T-wave alternans and 24-hour Holler for number of ventricular premature contractions (VPCs), deceleration capacity, heart rate variability, and heart rate turbulence were done. Death of any cause and first appropriate ICD shock were defined as end points. Over 33 +/- 15 months of follow-up, 36 of 253 patients (14%) received appropriate shocks and 39 of 253 patients (15%) died. Only 3 of 253 patients (1%) died after receiving at least 1 appropriate shock. In univariate analyses, New York Heart Association class, ejection fraction, N-terminal pro brain-type natriuretic peptide (NT-proBNP), renal function, ICD indication, deceleration capacity, heart rate variability, and heart rate turbulence were predictive of all-cause mortality and VPC number and deceleration capacity predicted first appropriate shock. NT-proBNP (>= 1,600 pg/ml) was identified as the only independent predictor of all-cause mortality (hazard ratio 3.0, confidence interval 1.3 to 7.3, p = 0.014). In contrast, VPC number predicted appropriate shocks (hazard ratio 2.3, confidence interval 1.0 to 5.5, p = 0.047) as the only independent risk marker. In conclusion, NT-proBNP is a strong independent predictor of mortality in a typical prospective cohort of newly implanted patients with ICD, among many electrocardiographic and clinical variables studied. Number of VPCs was identified as a predictor of appropriate shocks (clinicaltrials.gov: NCT02010515). (C) 2016 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY NC -ND license (http://creativecommons.orgflicenses/by-nc-nd/4.00. (Am J Cardiol 2016;118:86-94)"],["dc.identifier.doi","10.1016/j.amjcard.2016.04.016"],["dc.identifier.gro","3141655"],["dc.identifier.isi","000379632100013"],["dc.identifier.pmid","27189815"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13530"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5898"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Community [HEALTH-F2-2009-241526, 602299]"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Excerpta Medica Inc-elsevier Science Inc"],["dc.relation.eissn","1879-1913"],["dc.relation.issn","0002-9149"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Prediction of Appropriate Shocks Using 24-Hour Holter Variables and T-Wave Alternans After First Implantable Cardioverter-Defibrillator Implantation in Patients With Ischemic or Nonischemic Cardiomyopathy"],["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"]]
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