The mechanisms by which tissue injury after acute myocardial infarction (AMI) occurs has not been fully elucidated. Recent evidence in experimental models has suggested involvement of the complement system in microvascular and macrovascular injury subsequent to AMI. With respect to angina pectoris, whether or not the complement system is activated is not clear. The present study assessed the role of complement as a mediator of myocardial inflammation by quantifying products of complement activation, including C3d, C4d, Bb, and SC5b-9 complexes, in 31 patients with AMI, 17 patients with unstable angina pectoris, 19 patients with stable angina pectoris, and 20 normal volunteers. The plasma C3d levels increased in patients with AMI and in those with unstable angina pectoris (p<0.01). The plasma levels of C4d, Bb, and SC5b-9 increased only in patients with AMI (p<90.01). The plasma SC5b-9 level was related to peak creatine phosphokinase (r=0.71) and inversely related to the ejection fraction (r= -0.71). The plasma SC5b-9 level of patients with congestive heart failure was higher than that of patients without congestive heart failure in AMI. These results show that activation of complement system occurs after AMI and show an association of myocardial damage with complement activation. With respect to angina pectoris, the complement system is mildly activated in patients with unstable angina pectoris; however, the cardiac function of patients with unstable angina pectoris is not damaged. The complement system of patients with stable angina pectoris is not activated. (Circulation 1990;81:156-163) R ecent studies in experimental models suggest that acute myocardial ischemia is associated with activation of the complement system. First, studies in the baboon have established that C3, C4, and C5 are deposited in most infarction myocardial fibers.12 Second, by inactivating the complement system in vivo with cobra venom factor, a significant reduction in myocardial damage was achieved in an animal model.3 Also, a few studies report the complement activation in vivo in patients with acute myocardial infarction (AMI).4-6 However, it is not clear whether the activated complement system affects the myocardial necrotic size and cardiac function in human myocardial infarction. It is also unknown whether or not the complement system is activated in patients with angina pectoris (AP). This study assessed complement activation in patients with AMI and AP by directly measuring by-products of the reaction. The degree of activation of the complement system was compared with the hemodynamic manifestations and peak creatine phosphokinase (CPK) in patients with AMI.
MethodsThe study group consisted of 31 patients with AMI, 17 patients with unstable angina pectoris (UAP), 19 patients with stable angina pectoris (SAP), and 20 normal volunteers (Table 1). AMI was defined by at least two of the following: 1) angina lasting longer than 30 minutes, unrelieved by rest, 2) serum creatine kinase-MB fraction greater than 5%, 3) inversion or elev...
