RSS-Feed abonnieren
DOI: 10.1055/s-2002-32404
© Georg Thieme Verlag Stuttgart · New York
Elastase Release Following Myocardial Ischemia during Extracorporeal Circulation (ECC) - Marker of Ongoing Systemic Inflammation?
Presented at the 30th Annual Meeting of the German Society of Thoracic and Cardiovascular Surgery, February 18 - 21, 2001, LeipzigPublikationsverlauf
Publikationsdatum:
21. Juni 2002 (online)
![](https://www.thieme-connect.de/media/thoracic/200203/lookinside/thumbnails/10.1055-s-2002-32404-1.jpg)
Abstract
Background: ‚Post-Perfusion Syndrome’ (PPS) after cardiopulmonary bypass (CPB) is known to be evoked by inflammatory reactions. The hypothesis of a pathogenetic role for the neutrophil granulocytes in this inflammation would be strengthened if elevated concentrations of a neutrophil product such as elastase could be demonstrated, particularly in case of a PPS or a systemic inflammatory response syndrome (SIRS). Methods: In a randomized prospective double-blind study, 40 patients undergoing aortocoronary bypass grafting (CABG) were divided into 4 groups of 10 patients each. One group served as the control group, one received prostacyclin (PGl2), the third group was substituted with high-dosed aprotinin and the last group was treated with a combination of PGl2 and aprotinin. 6 blood samples were taken from every patient perioperatively, and plasma elastase (PE), procalcitonin (PCT), C1-esterase inhibitor (CEI) and parameters of coagulation and fibrinolysis were determined. Results: Levels of elastase increased significantly in all intra- and postoperative blood samples compared to the preoperative baseline values (< 30 µg/l, p < 0.05). The elastase release was even more pronounced in the control and aprotinin group (170 ± 23 µg/l; 175 ± 14 µg/l during ECC) compared to patients who received prostacyclin (142 = 21 µg/l, p < 0.05). Duration of myocardial ischemia could be directly correlated to elastase levels at the end of CPB. 10 of the 40 patients suffered postoperatively from a PPS or a SIRS; in these patients, elastase levels at the end of CPB were significantly higher (188 ± 26 µg/l vs. 138 ± 22 µg/l, p < 0.05). Immediately after the operation, these 10 patients also showed significant changes in the cascades of coagulation and fibrinolysis resulting in a hypercoagulatory state. Levels of PCT and CEI did not change significantly during and after ECC. Conclusions: Our results indicate that CPB initiates an elastase release that can be suppressed by prostacyclin. Increased intraoperative elastase levels in patients with PPS show that elastase may be an indicator of ongoing systemic inflammation, possibly causing complications due to a hypercoagulatory state. Myocardial ischemia seems to be one reason for this elastase release. It can be speculated that early PGl2-infusion could be a therapeutic option in inflammatory diseases caused by ECC.
Key words
Cardiopulmonary bypass - Extracorporeal circulation - Systemic inflammatory response syndrome - Myocardial ischemia - Elastase
References
- 1 Utley J R. Early development of cardiopulmonary bypass. Perfusion. 1986; 1 14
- 2 Chenoweth D E, Cooper S W, Hugli T E, Stewart R W, Blackstone E H, Kirklin J W. Complement activation during cardiopulmonary bypass. Evidence for generation of C3a and C5a anaphylotoxins. N Engl J Med. 1981; 304 497-503
- 3 Riegel W, Spillner G, Schlosser V, Horl W H. Plasma levels of main granulocyte components during cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1988; 95 1014-1019
- 4 Plow E. Alternative pathways to fibrinolysis. J Clin Invest. 1975; 56 30-38
- 5 Boeken U, Feindt P, Petzold T, Klein M, Micek M, Seyfert U T, Mohan E, Schulte H D, Gams E. Diagnostic value of procalcitonin: The influence of cardiopulmonary bypass, aprotinin, SIRS and sepsis. Thorac Cardiovasc Surg. 1998; 46 348-351
- 6 American College of Chest Physicians - Society of Critical Care Medicine Consensus Conference . Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis. Crit Care Med. 1992; 20 864-875
- 7 Davis R, Wittington R. Aprotinin. Drugs. 1995; 49 954-983
- 8 Bick R L. Hemostasis defects associated with cardiac surgery, prosthetic devices, and other extracorporea! circuits. Semin Thromb Hemost. 1985; 11 249-280
- 9 Woodman R C, Marker L A. Bleeding complications associated with cardiopulmonary bypass. Blood. 1990; 76 1680-1697
- 10 Royston D. High-dose aprotinin therapy: a review of the first five years' experience. J Cardiothorac Vase Anesth. 1992; 6 76-100
- 11 Kirklin J K, Westaby S, Blackstone E H, Kirklin J W, Chenoweth D E, Pacitico A D. Complement and the damaging effects of cardiopulmonary bypass. J Thorac Cardiovasc Surg. 1983; 86 854-857
- 12 Westaby S. Complement and the damaging effects of cardiopulmonary bypass. Thorax. 1983; 38 321-325
- 13 Ashraf S, Tian Y, Cowan D, Nair U, Chatrath R, Sunders N R. ‘Low-Dose’ Aprotinin modifies hemostasis but not proinflammatoty cytokine release. Ann Thorac Surg. 1997; 63 68-73
- 14 Butler J, Rocker G M, Westaby S. Inflammatory response to cardiopulmonary bypass. Ann Thorac Surg. 1993; 55 552-559
- 15 Hennein H A, Ebba H, Rodriguez J R. Relationship of the proinflammatory cytokines to myocardial ischemia and dysfunction after uncomplicated coronary revascularization. J Thorac Cardiovasc Surg. 1994; 108 626-635
- 16 Nagaoka H, Innami R, Murayama R, Funakoshi N, Hirooka K, Watanabe M, Satoh M. Effects of aprotinin on prostaglandin metabolism and platelet function in open heart surgery. J Cardiovasc Surg. 1991; 32 31-37
- 17 Ditter H, Heinrich D, Matthias F R, Sellmann-Richter R, Wanger W L, Hehrlein F W. Effects of prostacyclin during cardiopulmonary bypass in men plasma levels of (Mhromboglobulin, platelet factor 4, thromboxane B2, 6-keto-prostaglandin F1a and heparin. Thrombosis Research 1983. ; 32 393-408
- 18 Aren C, Feddersen K, Radegran K. Effects of prostacyclin infusion on platelet activation and postoperative blood loss in coronary bypass. Ann Thorac Surg. 1983; 36 49-54
- 19 DiSesa V J, Huval W, Lelcuk S. Disadvantages of prostacyclin infusion during cardiopulmonary bypass: A double-blind study of 50 patients having coronary revascularization. Ann Thorac Surg. 1984; 38 514-519
Dr. Udo Boeken
Department of Thoracic and Cardiovascular Surgery Heinrich Heine University
Moorenstraße 5
07747 Jena
40225 Düsseldorf
Telefon: +49 (211) 811 8331
Fax: +49 (211) 811 8333