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J Thorac Cardiovasc Surg 2006;132:291-296
© 2006 The American Association for Thoracic Surgery


Cardiopulmonary Support and Physiology

Circulating endothelial cells demonstrate an attenuation of endothelial damage by minimizing the extracorporeal circulation

Christian A. Skrabal, MD a , * , Yeong H. Choi, MD a , Alexander Kaminski, MD a , Michael Steiner, MD b , Guenther Kundt, PhD c , Gustav Steinhoff, MD, PhD a , Andreas Liebold, MD, PhD a

a Department of Cardiac Surgery, University of Rostock, Rostock, Germany
b Institute of Clinical Chemistry and Laboratory Medicine, University of Rostock, Rostock, Germany
c Institute of Medical Informatics and Biometry, University of Rostock, Rostock, Germany

Received for publication December 22, 2005; accepted for publication March 13, 2006.

* Address for reprints: Christian A. Skrabal, MD, Department of Cardiac Surgery, University of Rostock, Schillingallee 35, D-18057 Rostock, Germany. (Email: cskrabal{at}fastmail.fm).

OBJECTIVE: Detachment of endothelial cells may represent serious injury of the endothelium after cardiopulmonary bypass. We investigated whether the extent of endothelial injury is related to the type of cardiopulmonary bypass system used (conventional or minimized) and determined circulating endothelial cells as well as von Willebrand factor and soluble thrombomodulin.

METHODS: Twenty patients scheduled for elective coronary bypass grafting were randomly assigned to either the minimal extracorporeal circulation system or the standard cardiopulmonary bypass. Ten healthy volunteers served as controls. Circulating endothelial cells per milliliter of full blood were perioperatively determined by immunomagnetic cell separation technique. Endothelial plasma markers were measured by enzyme-linked immunosorbent assay.

RESULTS: Preoperative circulating endothelial cell numbers did not differ between the experimental groups, but were significantly higher than in the healthy controls (18.6 ± 5.6 vs 7.2 ± 3.8, P < .001). At 6 hours, circulating endothelial cell numbers increased significantly compared with baseline in both experimental groups and peaked at 12 hours after cardiopulmonary bypass initiation, each time with significantly lower values in the minimal extracorporeal circulation group (6 hours: 44.0 ± 9.9 vs 29.6 ± 9.8, P = .007; 12 hours: 48.1 ± 6.8 vs 31.8 ± 7.1, P < .001). Likewise, von Willebrand factor and soluble thrombomodulin postoperatively increased in both groups with a tendency toward lower levels in the minimal extracorporeal circulation group. Although circulating endothelial cells gradually declined, continually with lower numbers in the minimal extracorporeal circulation group, the endothelial plasma markers remained elevated during observation time.

CONCLUSIONS: Circulating endothelial cells represent a novel marker of the intrinsic endothelial damage caused by cardiopulmonary bypass. Its analysis facilitates the evaluation of cardiopulmonary bypass modifications as the minimal extracorporeal circulation system could be proven to be less injurious to endothelium and myocardium.








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