Pawel Burchardt1,2,3, Maura Farinacci4, Magdalena Mayer5, Klaus Luecke6, Thomas Krahn7, Jaroslaw Manczak8, Marek Slomczynski8, Jaroslaw Hiczkiewicz9, Janusz Rzezniczak8. 1. Biology of Lipid Disorders Department, Chair of Biology and Environmental Sciences, Poznan University of Medical Sciences, Poznan, Poland. pab2@tlen.pl. 2. Department of Cardiology, J. Strus Hospital, Szwajcarska 3, 61-285 Poznan, Poland. pab2@tlen.pl. 3. Department of Cardiology, Hospital of Nowa Sol, Poland. pab2@tlen.pl. 4. Institute for Medical Immunology, Berlin-Brandenburg Center für Regenerative Therapies, Core Unit Biomarker, Charité University Medicine, Berlin, Germany. 5. Zablab sp. z o.o, Poznan, Poland. 6. HaimaChek Inc, Santa Monica, Santa Monica, CA,, United States. 7. Bayer AG, Biomarker Research, Berlin, Germany. 8. Department of Cardiology, J. Strus Hospital, Szwajcarska 3, 61-285 Poznan, Poland. 9. Department of Cardiology, Hospital of Nowa Sol, Poland.
Abstract
BACKGROUND: Circulating endothelial cells (CEC) may be used to find new strategies for the early di-agnosis of cardiovascular diseases. The major objective of the project is to broaden knowledge of CEC biology by determining their phenotypic characteristics. The additional aim is to clarify whether on the basis of these information it is possible to identify the origin of CEC release (from various cardiovascular compartments). METHODS: Circulating endothelial cells were collected from arterial blood prior to angiography, as well as from arterial and venous blood obtained after angiography/coronary angioplasty, from 18 patients with non-ST-segment elevation myocardial infarction (NSTEMI). CECs were quantified by flow cytometry and defined as Syto16 (dye)+, CD45dim/neg, CD31+ and CD146+. The additional CD36+ was establish as a marker of endothelial cells released from small vessels of the microcirculation. RESULTS: The total number of CECs increased significantly after the percutaneous transluminal coronary angioplasty (PTCA) in the arterial system. Number of CECs isolated at similar time points (after invasive procedure) did not differ significantly between arteries and veins, but the number of CD36+ CECs after coronary angioplasty was significantly higher in the venous system, than in the arterial system. CONCLUSIONS: The number of CD36+ in artery samples obtained after coronary angioplasty (PTCA) had tendency to be decreased (in comparison to the sample obtained before angiography). It was major difference between those who had PTCA performed vs. those who had not.
BACKGROUND: Circulating endothelial cells (CEC) may be used to find new strategies for the early di-agnosis of cardiovascular diseases. The major objective of the project is to broaden knowledge of CEC biology by determining their phenotypic characteristics. The additional aim is to clarify whether on the basis of these information it is possible to identify the origin of CEC release (from various cardiovascular compartments). METHODS: Circulating endothelial cells were collected from arterial blood prior to angiography, as well as from arterial and venous blood obtained after angiography/coronary angioplasty, from 18 patients with non-ST-segment elevation myocardial infarction (NSTEMI). CECs were quantified by flow cytometry and defined as Syto16 (dye)+, CD45dim/neg, CD31+ and CD146+. The additional CD36+ was establish as a marker of endothelial cells released from small vessels of the microcirculation. RESULTS: The total number of CECs increased significantly after the percutaneous transluminal coronary angioplasty (PTCA) in the arterial system. Number of CECs isolated at similar time points (after invasive procedure) did not differ significantly between arteries and veins, but the number of CD36+ CECs after coronary angioplasty was significantly higher in the venous system, than in the arterial system. CONCLUSIONS: The number of CD36+ in artery samples obtained after coronary angioplasty (PTCA) had tendency to be decreased (in comparison to the sample obtained before angiography). It was major difference between those who had PTCA performed vs. those who had not.
Authors: Jan-Malte Sinning; Jan Losch; Katrin Walenta; Michael Böhm; Georg Nickenig; Nikos Werner Journal: Eur Heart J Date: 2010-12-24 Impact factor: 29.983
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Authors: Gilles Montalescot; Udo Sechtem; Stephan Achenbach; Felicita Andreotti; Chris Arden; Andrzej Budaj; Raffaele Bugiardini; Filippo Crea; Thomas Cuisset; Carlo Di Mario; J Rafael Ferreira; Bernard J Gersh; Anselm K Gitt; Jean-Sebastien Hulot; Nikolaus Marx; Lionel H Opie; Matthias Pfisterer; Eva Prescott; Frank Ruschitzka; Manel Sabaté; Roxy Senior; David Paul Taggart; Ernst E van der Wall; Christiaan J M Vrints; Jose Luis Zamorano; Stephan Achenbach; Helmut Baumgartner; Jeroen J Bax; Héctor Bueno; Veronica Dean; Christi Deaton; Cetin Erol; Robert Fagard; Roberto Ferrari; David Hasdai; Arno W Hoes; Paulus Kirchhof; Juhani Knuuti; Philippe Kolh; Patrizio Lancellotti; Ales Linhart; Petros Nihoyannopoulos; Massimo F Piepoli; Piotr Ponikowski; Per Anton Sirnes; Juan Luis Tamargo; Michal Tendera; Adam Torbicki; William Wijns; Stephan Windecker; Juhani Knuuti; Marco Valgimigli; Héctor Bueno; Marc J Claeys; Norbert Donner-Banzhoff; Cetin Erol; Herbert Frank; Christian Funck-Brentano; Oliver Gaemperli; José R Gonzalez-Juanatey; Michalis Hamilos; David Hasdai; Steen Husted; Stefan K James; Kari Kervinen; Philippe Kolh; Steen Dalby Kristensen; Patrizio Lancellotti; Aldo Pietro Maggioni; Massimo F Piepoli; Axel R Pries; Francesco Romeo; Lars Rydén; Maarten L Simoons; Per Anton Sirnes; Ph Gabriel Steg; Adam Timmis; William Wijns; Stephan Windecker; Aylin Yildirir; Jose Luis Zamorano Journal: Eur Heart J Date: 2013-08-30 Impact factor: 29.983