Christoph Bode

University of Freiburg

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Co-Authors

Andreas Zirlik

Medical University of Graz

Martin Moser

Massachusetts General Hospital

Karlheinz Peter

Baker Heart and Diabetes Institute

Peter Stachon

University of Freiburg

Ingo Hilgendorf

University of Freiburg

Dennis Wolf

University of Freiburg

Constantin von zur Mühlen

Universitäts-Herzzentrum Freiburg-Bad Krozingen

Daniel Duerschmied

University Medical Centre Mannheim

Sebastian Grundmann

University Medical Center Freiburg

Natalie Hoppe

University of Freiburg

Cooperative Institutions

University of Freiburg

610

University Medical Center Freiburg

353

Universitäts-Herzzentrum Freiburg-Bad Krozingen

273

Harvard University

169

Heidelberg University

146

Brigham and Women's Hospital

124

University Hospital Heidelberg

Baker Heart and Diabetes Institute

Massachusetts General Hospital

University Medical Center

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Role of striatal NMDA receptor subunits in a model of paroxysmal dystonia

Experimental Neurology (2014)

Yosef Avchalumov Svenja E. Sander Franziska Richter Katrin Porath Melanie Hamann

10.1016/j.expneurol.2014.08.012

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Citations (16)

Severe mitral regurgitation requiring ECMO therapy treated by interventional valve reconstruction using the MitraClip

Catheterization and Cardiovascular Interventions (2013)

Dawid L. Staudacher Christoph Bode Tobias Wengenmayer

Surgical repair is considered the gold standard in severe mitral valve regurgitation. Multi‐organ failure because of acute mitral insufficiency, however, can be challenging to manage as it aggravates to an inoperable state. We report the case of a 59 year old woman who presented with pulmonary oedema because of high grade mitral regurgitation. A recompensation prior to surgery using medical therapy failed and the patient developed a progressive multi‐organ failure including pulmonary, circulatory, and renal failure within days. Symptomatically, our patient could be stabilized employing an extracorporeal membrane oxygenation and an intra‐aortic balloon pump. A surgical mitral valve repair was ruled out because of the multi‐organ failure. We performed an interventional valve reconstruction using the MitraClip™ device continuing the extracorporeal membrane oxygenation and the intra‐aortic balloon counterpulsation therapy during the procedure. After clipping, multi‐organ failure regressed and the extracorporeal membrane oxygenation could be explanted at day two after intervention. © 2013 Wiley Periodicals, Inc.

MitraClip

Extracorporeal

10.1002/ccd.25332

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Citations (28)

ASSOCIATION OF HUB AND SPOKE PRACTICE PATTERNS WITH CORONARY INTERVENTION AND OUTCOMES IN NON ST ELEVATION ACUTE CORONARY SYNDROMES (NSTE ACS): INSIGHTS FROM THE EARLY GLYCOPROTEIN IIB/IIIA INHIBITION IN NSTE ACS (EARLY-ACS) TRIAL

Journal of the American College of Cardiology (2011)

Olga Toleva Cynthia M. Westerhout Manohara Senaratne Christoph Bode Magnus Lindroos

ST elevation

10.1016/s0735-1097(11)61101-7

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Citations (1)

Novel antiplatelet therapies following percutaneous coronary interventions.

PubMed (2009)

Ingo Ahrens Christoph Bode

Drug-eluting stents effectively reduce the incidence of in-stent restenosis; however, the use of these stents has led to the requirement for more effective antiplatelet therapies than are currently available. This requirement primarily arises from the presence of the antiproliferative drug coating of the stents. These coatings cause the prolonged exposure of platelets to stent struts and denuded endothelium, resulting in an increased potential for prothrombotic clinical sequelae. New antiplatelet therapies are also required because of the inter-individual variability in responses to available antiplatelet drugs. Ideally, new drugs would selectively target distinct mechanisms of platelet activation, avoiding increases in bleeding risk. This review discusses novel antiplatelet therapies under clinical investigation.

Antiplatelet drug

Interventional cardiology

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Citations (4)

Construction and In Vitro Testing of a Novel Fab-Hirudin–Based Fusion Protein That Targets Fibrin and Inhibits Thrombin in a Factor Xa–Dependent Manner

Journal of Cardiovascular Pharmacology (2003)

Karlheinz Peter Amitabh Gupta Thomas K. Nordt Simone Bauer Marschall S. Runge

Fibrin targeting of the thrombin inhibitor hirudin via chemical coupling is effective in vitro and in vivo. However, since chemical coupling has limitations, a recombinant approach was taken to improve the fibrin-targeting ability of hirudin. Additionally, to activate hirudin selectively at the target area and thereby limit side effects in an in vivo setting, the authors aimed to construct an inactive precursor molecule that is converted into an active thrombin inhibitor only upon cleavage by factor Xa. Using PCR, the coding region for hirudin was fused to parts of the genomic DNA of the IgG heavy chain that was cloned from the antifibrin antibody-producing hybridoma cell line 59D8. Additionally, a factor Xa recognition site was introduced between the antibody and the hirudin sequence. The fusion construct was then transfected into a heavy-chain loss variant of the hybridoma cell line 59D8. After selection of stable hybridoma clones, the expressed fusion protein was evaluated for its molecular size (57 kd) and its binding ability to the fibrin-specific peptide Bbeta 15-22. The cleavage of the fusion protein by factor Xa was demonstrated by HPLC. The recombinant anticoagulant revealed antithrombin activity only after cleavage by factor Xa. Thus, the newly designed hirudin fusion protein revealed the anticipated functions in vitro. Further experiments are needed to prove whether this precursor anticoagulant allows a highly clot-specific and efficient thrombin inhibition in vivo.

Hirudin

Cleavage (geology)

10.1097/00005344-200308000-00013

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Citations (10)

Mitochondrial sirtuins in the heart

Heart Failure Reviews (2016)

Heiko Bugger Constantin N. Witt Christoph Bode

SIRT3

10.1007/s10741-016-9570-7

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Citations (42)

Direct attenuation of plasminogen activator inhibitor type-1 expression in human adipose tissue by thiazolidinediones

Thrombosis and Haemostasis (2004)

Andreas Zirlik Anne Leugers Jens Lohrmann Sandra Ernst Burton E. Sobel

Summary Adipose tissue produces substantial amounts of plasminogen activator inhibitor type-1 (PAI-1), an established cardiovascular risk factor. This study evaluated PAI-1 expression in human adipose tissue in response to thiazolidinediones, insulin sensitising drugs activating peroxisome proliferator-activated receptorgamma (PPAR-γ). Troglitazone, rosiglitazone, and ciglitazone significantly reduced PAI-1 protein expression in human preadipocytes under basal conditions and after stimulation of the cells with TGF-β. Pioglitazone had no effect. In human adipocytes all four thiazolidinediones significantly attenuated PAI-1 expression. Signalling appeared to be mediated via PPAR-γ and effects reflected, at least in part, changes in transcription. Accordingly, patients with insulin resistance may benefit from treatment with thiazolidinediones with respect to diminution of PAI-1 expression in adipose tissue and consequent potential reduction of cardiovascular risk.

Troglitazone

Rosiglitazone

Pioglitazone

Thiazolidinedione

Plasminogen activator inhibitor-1

Ciglitazone

10.1160/th03-06-0384

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Citations (58)

Hsp70 preventing thrombosis: benefit without burden?

Cardiovascular Research (2016)

Daniel Duerschmied Christoph Bode

This editorial refers to ‘Hsp70 protects from stroke in atrial ﬁbrillation patients by preventing thrombosis without increased bleeding risk’ by M. Allende et al ., pp. 309–318. Thromboembolism is a major killer worldwide and is also involved in debilitating chronic ischaemic disease of heart and brain. Most cases of myocardial infarction, stroke, and pulmonary embolism are caused by a thrombus that contains fibrin and activated platelets. Antithrombotic therapy targets both the coagulation process of fibrin formation and platelet activation. However, any antithrombotic agent that effectively prevents thrombus formation increases the risk for bleeding, because both coagulation and platelets are required for haemostasis. Clinicians generally accept this paradigm as an unavoidable trade-off. Many researchers however refuse to accept this and have tried to …

10.1093/cvr/cvw077

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Citations (2)

Selective Removal of Plasma Low-Density Lipoproteins by Combined Extracorporeal Plasma Separation-Immunoadsorption

Springer eBooks (1983)

W. Stoffel Christoph Bode H. Borberg M. Tauchert K. Oette

Immunoadsorption

Plasma lipoprotein

Extracorporeal

Extracorporeal circulation

10.1007/978-3-642-81817-2_91

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