Circulation, Vol 81, 156-163, Copyright © 1990 by American Heart Association
M Yasuda, K Takeuchi, M Hiruma, H Iida, A Tahara, H Itagane, I Toda, K Akioka, M Teragaki and H Oku
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 less than
0.01). The plasma levels of C4d, Bb, and SC5b-9 increased only in patients
with AMI (p less than 0.01). 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.
ARTICLES
The complement system in ischemic heart disease
First Department of Internal Medicine, Osaka City University Medical School, Japan.
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