Low levels of plasma soluble complement receptor type 1 in patients receiving thrombolytic therapy for acute myocardial infarction.

Background: Administration of recombinant soluble CR1 (sCR1) has been shown to attenuate complement mediated myocardial injury in animal models of acute MI. The plasma level of sCR1 in humans with acute MI is not known. We determined the levels of the complement regulatory protein, complement receptor type-1 (CR1) in plasma and its expression on the surface of leukocytes of patients receiving thrombolysis for acute myocardial infarction (AMI).

Methods: Plasma sCR1 was measured by a sandwich ELISA. The levels in patients with AMI were compared with those in normal controls. Leukocyte surface expression of CR1 was measured by flow cytometry. We correlated these parameters with clinical outcome and left ventricular ejection fraction.

Results: Patients had very low plasma sCR1 levels. Mean plasma sCR1 levels were significantly less than in controls (6 +/- 3.6 ng/mL vs. 44.6 +/- 12.2 ng/mL, P < 0.00001). Patients who had an adverse in-hospital outcome had significantly lower sCR1 levels when compared to those who had an uneventful course (3.8 +/- 2.0 ng/mL and 7.1 +/- 3.8 ng/mL respectively, P = 0.01). The low plasma sCR1 was despite significantly greater lymphocyte and monocyte surface CR1 (which is a potential source of plasma sCR1).

Conclusion: Plasma sCR1 levels are reduced in patients receiving thrombolysis for AMI. Replenishing plasma sCR1 might limit complement-mediated injury in this setting.