Now showing 1 - 10 of 106
  • 2009Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","3027"],["dc.bibliographiccitation.issue","24"],["dc.bibliographiccitation.journal","European heart journal"],["dc.bibliographiccitation.lastpage","3036"],["dc.bibliographiccitation.volume","30"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Schmidt-Schweda, Stephan"],["dc.contributor.author","Westermann, Dirk"],["dc.contributor.author","Post, Heiner"],["dc.contributor.author","Edelmann, Frank"],["dc.contributor.author","Kasner, Mario"],["dc.contributor.author","Lueers, Claus"],["dc.contributor.author","Steendijk, Paul"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Tschoepe, Carsten"],["dc.contributor.author","Pieske, Burkert"],["dc.date.accessioned","2017-09-07T11:46:45Z"],["dc.date.available","2017-09-07T11:46:45Z"],["dc.date.issued","2009"],["dc.description.abstract","We tested the hypothesis that, in heart failure with normal ejection fraction (HFNEF), diastolic dysfunction is accentuated at increasing heart rates, and this contributes to impaired frequency-dependent augmentation of cardiac output. In 17 patients with HFNEF (median age 69 years, 13 female) and seven age-matched control patients, systolic and diastolic function was analysed by pressure-volume loops at baseline heart rate and during atrial pacing to 100 and 120 min(-1). At baseline, relaxation was prolonged and end-diastolic left ventricular stiffness was higher in HFNEF, whereas all parameters of systolic function were not different from control patients. This resulted in smaller end-diastolic volumes, higher end-diastolic pressure, and a lower stroke volume and cardiac index in HFNEF vs. control patients. During pacing, frequency-dependent upregulation of contractility indices (+dP/dt(max) and Ees) occurred similarly in HFNEF and control patients, but frequency-dependent acceleration of relaxation (dP/dt(min)) was blunted in HFNEF. In HFNEF, end-diastolic volume and stroke volume decreased with higher heart rates while both remained unchanged in control patients. In HFNEF, frequency-dependent upregulation of cardiac output is blunted. This results from progressive volume unloading of the left ventricle due to limited relaxation reserve in combination with increased LV passive stiffness, despite preserved force-frequency relation."],["dc.identifier.doi","10.1093/eurheartj/ehp341"],["dc.identifier.gro","3143014"],["dc.identifier.isi","000272927300018"],["dc.identifier.pmid","19720638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/482"],["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","0195-668X"],["dc.title","Blunted frequency-dependent upregulation of cardiac output is related to impaired relaxation in diastolic heart failure"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2003Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","996"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cardiovascular Research"],["dc.bibliographiccitation.lastpage","1003"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Schillinger, Wolfgang"],["dc.contributor.author","Ohler, A."],["dc.contributor.author","Embry, S. L."],["dc.contributor.author","Muller, F"],["dc.contributor.author","Christians, Claus"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Kogler, H."],["dc.contributor.author","Teucher, Niels"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Seidler, Tim"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.date.accessioned","2021-06-01T10:50:03Z"],["dc.date.available","2021-06-01T10:50:03Z"],["dc.date.issued","2003"],["dc.description.abstract","Objectives: The functional consequences of Na+/Ca2+ exchanger (NCX) overexpression in heart failure have been controversially discussed. NCX function strongly depends on intracellular sodium which has been shown to be increased in heart failure. Methods and results: We investigated the Na+/K+-ATPase (NKA) inhibitor ouabain (0.5-16 mumol/l) in electrically stimulated, isotonically contracting adult rabbit cardiocytes overexpressing NCX after adenoviral gene transfer (Ad-NCX-GFP, 48 h culture time). Myocytes transfected with adenovirus encoding for green fluorescent protein (Ad-GFP) served as a control. Contractions were analyzed by video-edge detection. In the Ad-NCX-GFP group, the maximum inotropic response was significantly reduced by 50.7% (P < 0.05). This was a result of an enhanced susceptibility to contracture after exposure to the drug (median concentration (25-75%): 4 (4-8) vs. 8 (6-16) mumol/l, P < 0.05). When analyzing relaxation before contracture, the maximum relaxation velocity was reduced (0.15 +/- 0.04 vs. 0.27 +/- 0.04 mum/s, P < 0.05) and the time from peak shortening to 90% of relaxation was increased (298 +/- 39 vs. 185 +/- 15 ms, P < 0.05). No differences in systolic and diastolic parameters were observed with the Na+ channel modulator BDF9198 (1 mumol/l). Conclusions: Inhibition of NKA by ouabain induces a combined diastolic and systolic dysfunction in NCX overexpressing rabbit myocytes. This may be the consequence of cytoplasmic Ca2+ overload due to inhibition of forward mode or induction of reverse mode Na+/Ca2+ exchange. In end-stage failing human myocardium and during digitalis treatment this mechanism may be of major importance. (C) 2003 European Society of Cardiology. Published by Elsevier Science B.V. All rights reserved."],["dc.identifier.doi","10.1016/S0008-6363(02)00829-5"],["dc.identifier.gro","3144121"],["dc.identifier.isi","000181975100014"],["dc.identifier.pmid","12650877"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/86511"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0008-6363"],["dc.title","The functional effect of adenoviral Na+/Ca2+ exchanger overexpression in rabbit myocytes depends on the activity of the Na+/K+-ATPase"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article
    [["dc.bibliographiccitation.firstpage","434"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Circulation Research"],["dc.bibliographiccitation.lastpage","442"],["dc.bibliographiccitation.volume","75"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Reinecke, H."],["dc.contributor.author","Studer, R."],["dc.contributor.author","Meyer, M."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Holtz, J."],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Posival, H."],["dc.contributor.author","Just, Hanjörg"],["dc.contributor.author","Drexler, H."],["dc.date.accessioned","2017-09-07T11:52:59Z"],["dc.date.available","2017-09-07T11:52:59Z"],["dc.date.issued","2012"],["dc.identifier.doi","10.1161/01.res.75.3.434"],["dc.identifier.gro","3145001"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2689"],["dc.notes.intern","Crossref Import"],["dc.notes.status","public"],["dc.publisher","Ovid Technologies (Wolters Kluwer Health)"],["dc.relation.issn","0009-7330"],["dc.title","Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]
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  • 2015Journal Article
    [["dc.bibliographiccitation.artnumber","e000182"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Open Heart"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Seegers, Joachim"],["dc.contributor.author","Zabel, Markus"],["dc.contributor.author","Grüter, Timo"],["dc.contributor.author","Ammermann, Antje"],["dc.contributor.author","Weber-Krüger, Mark"],["dc.contributor.author","Edelmann, Frank"],["dc.contributor.author","Gelbrich, Götz"],["dc.contributor.author","Binder, Lutz"],["dc.contributor.author","Herrmann-Lingen, Christoph"],["dc.contributor.author","Gröschel, Klaus"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Feltgen, Nicolas"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Wachter, Rolf"],["dc.date.accessioned","2017-09-07T11:52:34Z"],["dc.date.available","2017-09-07T11:52:34Z"],["dc.date.issued","2015"],["dc.identifier.doi","10.1136/openhrt-2014-000182"],["dc.identifier.gro","3144967"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2650"],["dc.notes.intern","Crossref Import"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","public"],["dc.relation.issn","2053-3624"],["dc.rights","CC BY-NC 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc/4.0"],["dc.title","Natriuretic peptides for the detection of paroxysmal atrial fibrillation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2004Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","602"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Herz"],["dc.bibliographiccitation.lastpage","608"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Hermann, Hans-Peter"],["dc.contributor.author","Pieske, Burkert"],["dc.date.accessioned","2017-09-07T11:43:17Z"],["dc.date.available","2017-09-07T11:43:17Z"],["dc.date.issued","2004"],["dc.description.abstract","30-50% of patients presenting with symptoms of congestive heart failure exhibit a near normal left ventricular systolic function at rest,and an impaired diastolic function of the heart may be causative. Despite a better prognosis than in systolic heart failure, frequency of hospitalizations due to diastolic heart failure is comparable with systolic heart failure. According to the criteria of Vasan & Levy diagnosis of diastolic heart failure is probable, if symptoms and signs of heart failure are accompanied in proximity (within 72 h) by objective evidence of normal left ventricular systolic function. Newer echocardiographic techniques (e.g., tissue Doppler) aid to confirm the diagnosis and to determine the severity of dysfunction and may substitute invasive demonstration of impaired left ventricular relaxation, filling, compliance or stiffness for standardized diagnosis. Incorporation of biochemical test (BNP [brain natriuretic peptide]) allows differential diagnosis and may increase the accuracy of diagnosis. Due to inconsistent diagnostic criteria, data from prospective randomized controlled trials for the treatment of diastolic heart failure are rare. Basic principles include treatment of the underlying disease, i.e., control of hypertension, diabetes, or obstructive airway disease. Angiotensin 1 antagonists (ARB) have proven effective in regression of left ventricular hypertrophy (LIFE) and may reduce morbidity, but not mortality (CHARM). Maintenance of sinus rhythm, heart rate control (beta-blockers, calcium channel blockers) and anti-ischemic therapy may be indicated in view of pathophysiological aspects. Diuretics should be administered with caution in patients with symptoms of congestion, digitalis is not useful in the treatment of isolated diastolic heart failure. The results of ongoing trials (e.g., I-Preserve) may offer new therapeutic options, and evidence-based guidelines for the so far often unsatisfactory treatment of diastolic dysfunction/heart failure are awaited."],["dc.identifier.doi","10.1007/s00059-004-2621-1"],["dc.identifier.gro","3143951"],["dc.identifier.isi","000224723700006"],["dc.identifier.pmid","15912435"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1521"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Urban & Vogel"],["dc.relation.issn","0340-9937"],["dc.title","Dyspnea and normal systolic function"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 1991Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","8"],["dc.bibliographiccitation.journal","European heart journal"],["dc.bibliographiccitation.lastpage","13"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Holubarsch, Christian"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Thierfelder, L."],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Just, Hanjörg"],["dc.date.accessioned","2017-09-07T11:51:53Z"],["dc.date.available","2017-09-07T11:51:53Z"],["dc.date.issued","1991"],["dc.identifier.gro","3144807"],["dc.identifier.isi","A1991GB44200003"],["dc.identifier.pmid","1833195"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2472"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","W B Saunders Co Ltd"],["dc.relation.issn","0195-668X"],["dc.title","THE HEART IN HEART-FAILURE VENTRICULAR AND MYOCARDIAL ALTERATIONS"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2014Journal Article
    [["dc.bibliographiccitation.firstpage","59"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","ESC Heart Failure"],["dc.bibliographiccitation.lastpage","74"],["dc.bibliographiccitation.volume","1"],["dc.contributor.author","Nolte, Kathleen"],["dc.contributor.author","Schwarz, Silja"],["dc.contributor.author","Gelbrich, Götz"],["dc.contributor.author","Mensching, Steffen"],["dc.contributor.author","Siegmund, Friederike"],["dc.contributor.author","Wachter, Rolf"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Düngen, Hans-Dirk"],["dc.contributor.author","Herrmann-Lingen, Christoph"],["dc.contributor.author","Halle, Martin"],["dc.contributor.author","Pieske, Burkert"],["dc.contributor.author","Edelmann, Frank"],["dc.date.accessioned","2019-07-09T11:41:03Z"],["dc.date.available","2019-07-09T11:41:03Z"],["dc.date.issued","2014"],["dc.description.abstract","Background The long-term effects of exercise training (ET) in diastolic dysfunction (DD) and heart failure with preserved ejection fraction (HFpEF) are unknown. The present study compared the long-term effects of ET on exercise capacity, diastolic function, and quality of life (QoL) in patients with DD vs. HFpEF. Methods A total of n=43 patients with asymptomatic DD (n=19) or HFpEF [DD and New York Heart Association (NYHA) ≥II, n=24] and left ventricular ejection fraction ≥50% performed a combined endurance/resistance training over 6months (2–3/week) on top of usual care. Cardiopulmonary exercise testing, echocardiography, and QoL were obtained at baseline and follow-up. Results Patients were 62±8 years old (37% female). In the HFpEF group, 67% of patients were in NYHA class II (33% in NYHA III). Exercise capacity (peak oxygen consumption, peak VO2) differed at baseline (DD 29.2±8.7mL/min/kg vs. HFpEF 17.8±4.6 mL/min/kg; P=0.004). After 6months, peak VO2 increased significantly (P<0.044) to 19.7±5.8 mL/min/kg in the HFpEF group and also in the DD group (to 32.8±8.5mL/min/kg; P<0.002) with no overall difference between the groups (P=0.217). E/e′ ratio (left ventricular filling index) decreased from 12.2±3.5 to 10.1±3.0 (P<0.002) in patients with HFpEFand also in patients with DD (10.7±3.1 vs. 9.5±2.3; P=0.03; difference between groups P=0.210). In contrast, left atrial volume index decreased in the HFpEF group (P<0.001) but remained stable within the DD group (difference between groups P=0.015). After 6 months, physical QoL (Minnesota living with heart failure Questionnaire, 36-item short form health survey), general health perception, and 9-item patient health questionnaire score only improved in HFpEF (P<0.05). In contrast, vitality improved in both groups (difference between groups P=0.708). Conclusion A structured 6 months ET programme effectively improves exercise capacity and diastolic function in patients with DD and overt HFpEF. Therefore, controlled lifestylemodification with physical activity is effective both in DD and HFpEF."],["dc.identifier.doi","10.1002/ehf2.12007"],["dc.identifier.fs","610857"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11651"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58349"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1879-0844"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Effects of long-term endurance and resistance training on diastolic function, exercise capacity, and quality of life in asymptomatic diastolic dysfunction vs. heart failure with preserved ejection fraction"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2011Conference Abstract
    [["dc.bibliographiccitation.journal","European Heart Journal"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Duvinage, Andre"],["dc.contributor.author","Stahrenberg, Raoul"],["dc.contributor.author","Gelbrich, Goetz"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Wachter, R. Rolf"],["dc.contributor.author","Pieske, Burkert M."],["dc.contributor.author","Edelmann, F."],["dc.date.accessioned","2018-11-07T08:53:55Z"],["dc.date.available","2018-11-07T08:53:55Z"],["dc.date.issued","2011"],["dc.format.extent","907"],["dc.identifier.isi","000208702706476"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22542"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","0195-668X"],["dc.title","Association between neurohormonal activation and submaximal exercise capacity in patients with diastolic dysfunction and diastolic heart failure"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","194"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Circulation"],["dc.bibliographiccitation.lastpage","199"],["dc.bibliographiccitation.volume","105"],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Maier, Lars S."],["dc.contributor.author","Hermann, Hans-Peter"],["dc.contributor.author","Luers, C."],["dc.contributor.author","Hünlich, Mark"],["dc.contributor.author","Zeitz, Oliver"],["dc.contributor.author","Janssen, P. M. L."],["dc.contributor.author","Pieske, Burkert"],["dc.date.accessioned","2017-09-07T11:45:57Z"],["dc.date.available","2017-09-07T11:45:57Z"],["dc.date.issued","2002"],["dc.description.abstract","Background-Application of pyruvate was shown to improve contractile function in isolated animal myocardium and hemodynamics in patients with congestive heart failure. We assessed the influence of pyruvate on systolic and diastolic myocardial function and its subcellular mode of action in isolated myocardium. from end-stage failing human hearts. Methods and Results-In muscle strip preparations, concentration-dependent effects of pyruvate on developed and diastolic force (n=6), aequorin light emission reflecting intracellular Ca2+ transients (n=6), and rapid cooling contractures reflecting sarcoplasmic reticulum (SR) Ca2+ content (n=11) were measured. Pyruvate resulted in a concentration-dependent increase in developed force and a decrease in diastolic force, with a maximum effect of 155% and 21%, respectively, at 20 mmol/L pyruvate (P<0.05). This was associated with a dose-dependent prolongation of time to peak tension and relaxation time. Pyruvate increased rapid cooling contractures by 51% and aequorin light signals by 85% (at 15 and 20 mmol/L; P<0.05). This indicates increased SR Ca2+ content and increased intracellular Ca2+ transients. The inotropic effect of pyruvate was still present after elimination of SR Ca2+ storage function with 10 mumol/L cyclopiazonic acid and I mumol/L ryanodine (n=8). Pyruvate significantly increased intracellular pH from 7.31+/-0.03 to 7.40+/-0.04 by BCECF fluorescence (n=6). Conclusions-The present findings indicate that pyruvate improves contractile performance of failing human myocardium by increasing a intracellular Ca2+ transients as well as myofilament Ca2+ sensitivity. The former seem to result from increased SR Ca2+ accumulation and release, the latter from increased intracellular pH."],["dc.identifier.doi","10.1161/hc0202.102238"],["dc.identifier.gro","3144225"],["dc.identifier.isi","000173330900027"],["dc.identifier.pmid","11790700"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1826"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0009-7322"],["dc.title","Influence of pyruvate on contractile performance and Ca2+ cycling in isolated failing human myocardium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2015Conference Abstract
    [["dc.bibliographiccitation.journal","European Journal of Heart Failure"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Duvinage, Andre"],["dc.contributor.author","Stahrenberg, Raoul"],["dc.contributor.author","Bueren, F. To"],["dc.contributor.author","Nolte, K."],["dc.contributor.author","Mende, Meinhard"],["dc.contributor.author","Pieske, Burkert M."],["dc.contributor.author","Hasenfuß, Gerd"],["dc.contributor.author","Wachter, R. Rolf"],["dc.contributor.author","Edelmann, F."],["dc.date.accessioned","2018-11-07T09:57:28Z"],["dc.date.available","2018-11-07T09:57:28Z"],["dc.date.issued","2015"],["dc.format.extent","420"],["dc.identifier.isi","000366200403599"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37164"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.issn","1879-0844"],["dc.relation.issn","1388-9842"],["dc.title","Combination of neurohormones and clinical signs and symptoms to detect a left ventricular dysfunction"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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