Complement activation in acute coronary syndromes.
The complement system is part of the host defence response. However, considerable evidence suggests that complement plays an important role in the pathophysiology of ischemic heart disease. The aim of this study was to evaluate complement activation in patients with all forms of acute coronary syndromes (ACS) and to examine the relationship between the degree of complement activation and myocardial injury. The study population included 152 subjects (26 females): 82 with ACS (35 acute myocardial infarction (AMI), 22 non-Q wave MI (NQMI), 25 unstable angina (UAP)) (Group A), 35 stable angina (SA) (Group B), and 35 healty control subjects (Group C). Complement 3 (C3), Complement 4 (C4), C-reactive protein (CRP), troponin I (TnI) as well as creatine kinase MB (CK-MB) were evaluated. Patients' blood samples were taken on admission (day 1) and after 2, 3 and 7 days in group A. However, only one measurement was performed in the groups B and C. Plasma C3 and C4 peak levels were significantly higher in patients with AMI (141+/-29 and 35+/-11 mg/dl) and NQMI (136+/-13 and 35+/-7 mg/dl) than in patients with SA (128+/-14 and 27+/-10 mg/dl) and the control subjects (114+/-22 and 22+/-7 mg/dl) (p<0.03). Also, C3 and C4 serum levels in patients with SA and UAP (126+/-16 and 31+/-7 mg/dl) were significantly higher than those in control subjects (p<0.01, p<0.03, respectively). At 1-week follow-up, there were no significant differences between the plasma levels of C3 and C4 in patients with UAP (p>0.05). However, plasma levels of C3 and C4 were significantly different between days in patients with AMI and NQMI (p<0.0001). Plasma C3 and C4 levels in ACS showed a relationship with peak CK-MB and Tn I levels (p<0.01). Plasma CRP level in ACS showed positive correlation with C3 (p<0.01) and C4 (p<0.001). In this study, we determined that plasma C3 and C4 levels were elevated in ACS and SA. Although C3 and C4 were higher in ACS and SA, the systemic levels of inflammatory markers in patients with SA and UAP were lower than those found in the AMI and NQMI groups. The relationship between C3, C4 levels and ACS further suggests that the complement activation is related to necrosis within the myocardium.
Iltumur
Kenan
K
Department of Cardiology, Faculty of Medicine, Dicle University, 21280 Diyarbakýr, Turkey. kencan@cicle.edu.tr
Karabulut
Aziz
A
Toprak
Gülten
G
Toprak
Nizamettin
N
D000208:Acute Disease; D000368:Aged; D003167:Complement Activation; D003176:Complement C3 / Q000032:analysis / Q000378:metabolism; D003181:Complement C4 / Q000032:analysis / Q000378:metabolism; D003327:Coronary Disease / Q000175:diagnosis / Q000276:immunology*; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004562:Electrocardiography; D005260:Female; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000175:diagnosis / Q000276:immunology*; D013577:Syndrome; D019210:Troponin I / Q000097:blood
D003176:Complement C3; D003181:Complement C4; D007527:Isoenzymes; D019210:Troponin I; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form