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J Thorac Cardiovasc Surg 1999;118:422-429
© 1999 Mosby, Inc.

CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

CARDIOPULMONARY BYPASS AND ACTIVATION OF ANTITHROMBOTIC PLASMA PROTEIN C

This work was supported in part by grants from the Sigrid Jusélius Foundation, the Paulo Foundation, the Finnish Cultural Foundation, the Stein Endowment Fund, and the National Institutes of Health (R37HL52246 and R01HL 21544).

Address for reprints: Jari Petäjä, MD, PhD, Children’s Hospital, University of Helsinki, Stenbäckinkatu 11, FIN-00290 Helsinki, Finland (E-mail: jari.petaja{at}dlc.fi).

Objective: We hypothesized that antithrombotic plasma-activated protein C plays a defensive antithrombotic role during coronary ischemia and postischemic reperfusion.
Methods and results: We evaluated protein C activation during cardiopulmonary bypass and coronary reperfusion in 20 patients undergoing coronary bypass surgery. During cardiopulmonary bypass and during the 10 minutes after aortic unclamping, the plasma levels of protein C (mean ± standard error of the mean) decreased from 123% ± 7% to 74% ± 5% of normal mean. In contrast, the levels of activated protein C in plasma increased from 122% ± 8% to 159% ± 21%, and the activated protein C/protein C ratio increased from 1.04 ± 0.08 to 2.29 ± 0.31 (P = .006, 2-tailed Wilcoxon signed rank test). Patients were stratified on the basis of the increase in activated protein C in the coronary sinus plasma at 10 minutes after reperfusion by means of the arbitrary value of 1.5 for the activated protein C/protein C ratio. Within 24 hours, the patients with low increases in activated protein C (ratio < 1.5, n = 8) had a significantly (P < .05) lower cardiac output and mean pulmonary artery pressure, as well as a higher systemic vascular resistance, than patients (n = 11) with high increases in activated protein C (ratio > 1.5). The rapid increase in activated protein C during the first 10 minutes after aortic unclamping indicated protein C activation in the reperfused vascular beds.
Conclusions: The antithrombotic protein C pathway was significantly activated during cardiopulmonary bypass mainly during the minutes after aortic unclamping in the ischemic vascular beds. Suboptimal protein C activation during ischemia may impair the postischemic recovery of human heart and circulation.

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