Elastase release following myocardial ischemia during extracorporeal circulation (ECC) -- marker of ongoing systemic inflammation?

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 (PGl 2 ), the third group was substituted with high-dosed aprotinin and the last group was treated with a combination of PGl 2 and aprotinin. 6 blood samples were taken from every patient perioperatively, and plasma elastase (PE), procalcitonin (PCT), C 1 -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 microg/l, p < 0.05). The elastase release was even more pronounced in the control and aprotinin group (170 +/- 23 microg/l; 175 +/- 14 microg/l during ECC) compared to patients who received prostacyclin (142 = 21 microg/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 microg/l vs. 138 +/- 22 microg/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.