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Your search keyword '"Theilmeier, Gregor"' showing total 26 results
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26 results on '"Theilmeier, Gregor"'

6. Cell-type-specific downregulation of heme oxygenase-1 by lipopolysaccharide via Bach1 in primary human mononuclear cells

Author

Dorresteijn, Mirrin J., Paine, Ananta, Zilian, Eva, Fenten, Maaike G.E., Frenzel, Eileen, Janciauskiene, Sabina, Figueiredo, Constanca, Eiz-Vesper, Britta, Blasczyk, Rainer, Dekker, Douwe, Pennings, Bas, Scharstuhl, Alwin, Smits, Paul, Larmann, Jan, Theilmeier, Gregor, van der Hoeven, Johannes G., Wagener, Frank A.D.T.G., Pickkers, Peter, and Immenschuh, Stephan

Published
2015
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7. Prospective evaluation of preoperative lung ultrasound for prediction of perioperative outcome and myocardial injury in adult patients undergoing vascular surgery (LUPPO study)

Author

Gillmann, Hans-Jörg, Dieding, Jasmin, Schrimpf, Claudia, Janssen, Henrike, Sahlmann, Bianca, Rustum, Saad, Aper, Thomas, Lichtinghagen, Ralf, Teebken, Omke E, Theilmeier, Gregor, Larmann, Jan, University of Zurich, and Larmann, Jan

Subjects
11548 Clinic for Vascular Surgery, 610 Medicine & health, 2703 Anesthesiology and Pain Medicine
Published
2020

10. Sequential Surgical Procedures in Vascular Surgery Patients Are Associated With Perioperative Adverse Cardiac Events

Author

Janssen, Henrike, Felgner, Larissa, Kummer, Laura, Gillmann, Hans-Joerg, Schrimpf, Claudia, Rustum, Saad, Lichtinghagen, Ralf, Sahlmann, Bianca, Weigand, Markus A., Teebken, Omke E., Theilmeier, Gregor, Larmann, Jan, and University of Zurich

Subjects
VULNERABILITY, OPTICAL COHERENCE TOMOGRAPHY, interleukin-6, 610 Medicine & health, Cardiovascular Medicine, perioperative inflammation, vascular surgery, regulatory T cells, MYOCARDIAL-INFARCTION, RUPTURE, 11548 Clinic for Vascular Surgery, TROPONIN-T, plaque vulnerability, REGULATORY T-CELLS, ATHEROSCLEROTIC PLAQUE, cardiac adverse event, NONCARDIAC SURGERY, NECROTIC CORE, TASK-FORCE, Original Research
Abstract

Patients at elevated cardiovascular risk are prone to perioperative cardiovascular complications, like myocardial injury after non-cardiac surgery (MINS). We have demonstrated in a mouse model of atherosclerosis that perioperative stress leads to an increase in plaque volume and higher plaque vulnerability. Regulatory T cells (Tregs) play a pivotal role in development and destabilization of atherosclerotic plaques. For this exploratory post-hoc analysis we identified 40 patients recruited into a prospective perioperative biomarker study, who within the inclusion period underwent sequential open vascular surgery. On the basis of protein markers measured in the biomarker study, we evaluated the perioperative inflammatory response in patients' plasma before and after index surgery as well as before and after a second surgical procedure. We also analyzed available immunohistochemistry samples to describe plaque vulnerability in patients who underwent bilateral carotid endarterectomy (CEA) in two subsequent surgical procedures. Finally, we assessed if MINS was associated with sequential surgery. The inflammatory response of both surgeries was characterized by postoperative increases of interleukin-6,-10, Pentraxin 3 and C-reactive protein with no clear-cut difference between the two time points of surgery. Plaques from CEA extracted during the second surgery contained less Tregs, as measured by Foxp3 staining, than plaques from the first intervention. The 2nd surgical procedure was associated with MINS. In conclusion, we provide descriptive evidence that sequential surgical procedures involve repeat inflammation, and we hypothesize that elevated rates of cardiovascular complications after the second procedure could be related to reduced levels of intraplaque Tregs, a finding that deserves confirmatory testing and mechanistic exploration in future populations.

Published
2020

11. Prospective evaluation of preoperative lung ultrasound for prediction of perioperative outcome and myocardial injury in adult patients undergoing vascular surgery (LUPPO study)

Author

Gillmann, Hans-Jörg, primary, Dieding, Jasmin, additional, Schrimpf, Claudia, additional, Janssen, Henrike, additional, Sahlmann, Bianca, additional, Rustum, Saad, additional, Aper, Thomas, additional, Lichtinghagen, Ralf, additional, Teebken, Omke E., additional, Theilmeier, Gregor, additional, and Larmann, Jan, additional

Published
2020
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16. Adrenomedullin Is Associated With Surgical Trauma and Impaired Renal Function in Vascular Surgery Patients.

Author

Gillmann, Hans-Jörg, Meinders, Antje, Larmann, Jan, Sahlmann, Bianca, Schrimpf, Claudia, Aper, Thomas, Lichtinghagen, Ralf, Teebken, Omke E., and Theilmeier, Gregor

Subjects
ACUTE kidney failure, CARDIOVASCULAR disease diagnosis, SYSTEMIC inflammatory response syndrome, TRAUMATOLOGY diagnosis, ACADEMIC medical centers, BIOMARKERS, VASCULAR surgery, CARDIOVASCULAR diseases risk factors, LONGITUDINAL method, PATIENTS, PEPTIDE hormones, STATISTICS, SURGERY, MULTIPLE regression analysis, MEDICAL records, PERIOPERATIVE care, DIAGNOSIS, DISEASE risk factors
Abstract

Background: Patients undergoing vascular surgery are prone to perioperative organ injury because of both higher prevalence of cardiovascular risk factors and the extent of surgery. Early detection of organ failure is essential to facilitate appropriate medical care. Midregional pro-adrenomedullin (MR-proADM) has been investigated in acute medical care settings to guide clinical decision-making regarding patient pathways and to identify patients prone to imminent cardiovascular or inflammatory complications. In this study, we evaluated the impact of perioperative MR-proADM levels as an early marker of perioperative cardiovascular and inflammatory stress reactions and kidney injury. Methods: The study was conducted as a monocentric, prospective, noninterventional trial at Hannover Medical School, Germany. A total of 454 consecutive patients who underwent open vascular surgery were followed from the day prior to until 30 days after surgery. The composite primary end point was defined as the occurrence of major adverse cardiac events (MACEs), acute kidney injury (AKI), or systemic inflammatory response syndrome (SIRS). Measurements were correlated with both medical history and postoperative MACE, AKI, or SIRS using univariate and multivariate regression analysis. Results: One hundred thirty-nine (31%) of the patients reached the primary end point within the study interval. Midregional pro-adrenomedullin change was associated with the combined primary end point and with the intensity of surgical trauma. Midregional pro-adrenomedullin change was increased in patients reaching the secondary end points, SIRS (optimal cutoff: 0.2 nmol/L) and AKI (optimal cutoff: 0.7 nmol/L), but not in patients with MACEs. Conclusion: Increased levels of MR-proADM within the perioperative setting (1) were linked to the invasiveness of surgery and (2) identified patients with ongoing loss of renal function. Increased MR-proADM levels may therefore identify a subgroup of patients prone to excessive cardiovascular stress but did not directly correlate with adverse cardiac events. Consistently low levels of MR-proADM may identify a subgroup of patients with acceptable low risk to guide discharge from high-density care units. [ABSTRACT FROM AUTHOR]

Published
2019
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21. Renal Function Interferes with Copeptin in Prediction of Major Adverse Cardiac Events in Patients Undergoing Vascular Surgery

Author

Schrimpf, Claudia, primary, Gillmann, Hans-Joerg, additional, Sahlmann, Bianca, additional, Meinders, Antje, additional, Larmann, Jan, additional, Wilhelmi, Mathias, additional, Aper, Thomas, additional, Rustum, Saad, additional, Lichtinghagen, Ralf, additional, Theilmeier, Gregor, additional, and Teebken, Omke E., additional

Published
2015
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22. Acute perioperative stress-induced increase of plaque volume and vulnerability in apolipoprotein E-deficient mice is amenable to statin treatment and IL-6-inhibition

Author

Janssen, Henrike, primary, Wagner, Christian S., additional, Demmer, Philipp, additional, Callies, Simone, additional, Sölter, Gesine, additional, Kouzhani, Houra Loghmani, additional, Hu, Niandan, additional, Schuett, Harald, additional, Tietge, Uwe J.F., additional, Warnecke, Gregor, additional, Larmann, Jan, additional, and Theilmeier, Gregor, additional

Published
2015
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23. The authors reply

Author

Gillmann, Hans-Jörg, primary, Meinders, Antje, additional, Grohennig, Anika, additional, Larmann, Jan, additional, Bünte, Christoph, additional, Calmer, Simone, additional, Sahlmann, Bianca, additional, Rustum, Saad, additional, Aper, Thomas, additional, Lichtinghagen, Ralf, additional, Koch, Armin, additional, Teebken, Omke E., additional, and Theilmeier, Gregor, additional

Published
2014
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24. Hepatic Overexpression of Soluble Urokinase Receptor (uPAR) Suppresses Diet-Induced Atherosclerosis in Low-Density Lipoprotein Receptor-Deficient (LDLR-/-) Mice.

Author

Larmann, Jan, Jurk, Kerstin, Janssen, Henrike, Müller, Martin, Herzog, Christine, Lorenz, Anika, Schmitz, Martina, Nofer, Jerzy-Roch, and Theilmeier, Gregor

Subjects
ATHEROSCLEROSIS, GENE expression, UROKINASE, LOW density lipoprotein receptors, LABORATORY mice, MONOCYTES
Abstract

Objective: Atherosclerosis, a chronic inflammatory disease, arises from metabolic disorders and is driven by inappropriate recruitment and proliferation of monocytes / macrophages and vascular smooth-muscle-cells. The receptor for the urokinase-type plasminogen activator (uPAR, Plaur) regulates the proteolytic activation of plasminogen. It is also a coactivator of integrins and facilitates leukocyte-endothelial interactions and vascular smooth-muscle-cell migration. The role of uPAR in atherogenesis remains elusive. Methods and Results: We generated C57Bl6/J low-density lipoprotein receptor (LDL) and uPAR double knockout (uPAR-/-/LDLR-/-) mice to test the role of uPAR in two distinct atherosclerosis models. In LDLR-/- mice, hepatic overexpression following hydrodynamic transfection of soluble uPAR that competes with endogenous membrane-bound uPAR was performed as an interventional strategy. Aortic root atherosclerotic lesions induced by feeding a high-fat diet were smaller and comprised less macrophages and vascular smooth-muscle-cells in double knockout mice and animals overexpressing soluble uPAR when compared to controls. In contrast, lesion size, lipid-, macrophage-, and vascular smooth muscle cell content of guide-wire-induced intima lesions in the carotid artery were not affected by uPAR deficiency. Adhesion of uPAR-/--macrophages to TNFα-stimulated endothelial cells was decreased in vitro accompanied by reduced VCAM-1 expression on primary endothelial cells. Hepatic overexpression of soluble full-length murine uPAR in LDLR-/- mice led to a reduction of diet-induced atherosclerotic lesion formation and monocyte recruitment into plaques. Ex vivo incubation with soluble uPAR protein also inhibited adhesion of macrophages to TNFα-stimulated endothelial cells in vitro. Conclusion: uPAR-deficiency as well as competitive soluble uPAR reduced diet-promoted but not guide-wire induced atherosclerotic lesions in mice by preventing monocyte recruitment and vascular smooth-muscle-cell infiltration. Soluble uPAR may represent a therapeutic tool for the modulation of hyperlipidemia-associated atherosclerotic lesion formation. [ABSTRACT FROM AUTHOR]

Published
2015
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25. Acute perioperative-stress-induced increase of atherosclerotic plaque volume and vulnerability to rupture in apolipoprotein-E-deficient mice is amenable to statin treatment and IL-6 inhibition

Author

Janssen, Henrike, Wagner, Christian S., Demmer, Philipp, Callies, Simone, Sölter, Gesine, Loghmani-khouzani, Houra, Hu, Niandan, Schuett, Harald, Tietge, Uwe J. F., Warnecke, Gregor, Larmann, Jan, and Theilmeier, Gregor

Abstract

Myocardial infarction and stroke are frequent after surgical procedures and consume a considerable amount of benefit of surgical therapy. Perioperative stress, induced by surgery, is composed of hemodynamic and inflammatory reactions. The effects of perioperative stress on atherosclerotic plaques are ill-defined. Murine models to investigate the influence of perioperative stress on plaque stability and rupture are not available. We developed a model to investigate the influence of perioperative stress on plaque growth and stability by exposing apolipoprotein-E-deficient mice, fed a high cholesterol diet for 7 weeks, to a double hit consisting of 30 min of laparotomy combined with a substantial blood loss (approximately 20% of total blood volume; 400 µl). The innominate artery was harvested 72 h after the intervention. Control groups were sham and baseline controls. Interleukin-6 (IL-6) and serum amyloid A (SAA) plasma levels were determined. Plaque load, vascular smooth muscle cell (VSMC) and macrophage content were quantified. Plaque stability was assessed using the Stary score and frequency of signs of plaque rupture were assessed. High-dose atorvastatin (80 mg/kg body weight/day) was administered for 6 days starting 3 days prior to the double hit. A single dose of an IL-6-neutralizing antibody or the fusion protein gp130-Fc selectively targeting IL-6 trans-signaling was subcutaneously injected. IL-6 plasma levels increased, peaking at 6 h after the intervention. SAA levels peaked at 24 h (n=4, P<0.01). Plaque volume increased significantly with the double hit compared to sham (n=8, P<0.01). More plaques were scored as complex or bearing signs of rupture after the double hit compared to sham (n=5-8, P<0.05). Relative VSMC and macrophage content remained unchanged. IL-6-inhibition or atorvastatin, but not blocking of IL-6 trans-signaling, significantly decreased plaque volume and complexity (n=8, P<0.01). Using this model, researchers will be able to further investigate the pathophysiology of perioperative plaque stability, which can result in myocardial infarction, and, additionally, to test potential protective strategies.

Published
2015
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