Detection of a soluble form of the complement membrane attack complex inhibitor CD59 in plasma after acute myocardial infarction

Activation of the complement system has been documented in both experimenta l and clinical studies of acute myocardial infarction (AMI). Our earlier im munohistochemical studies have shown that the deposition of the membrane at tack complex (MAC) of complement is associated with the loss of protectin ( CD59), a glycosyl-phosphatidylinositol (GPI)-anchored sarcolemmal regulator of MAC, from the human and rat infarcted myocardium. In this study we dete cted, using an enzyme immunoassay (EIA), CD59 in the plasma of AMI patients at a concentration of 23.0 +/- 8.4 ng/ml (mean +/- SD; n = 17) at 4 h and 27.3 +/- 11.8 ng/ml (n = 24) at 24 h after AMI. Both values were significan tly higher than in healthy controls (7.8 +/- 6.4 ng/ml; n = 20; P < 0.001). The amount of CD59 correlated with the level of soluble terminal complemen t complexes (SC5b-9; r = 0.84; P < 0.01) in the plasmas of AMI patients. Ou r results suggest that myocardial damage leads to release of CD59 from the sarcolemmal cell membranes during AMI.