Complement activation in acute coronary syndromes

Abstract

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.

Acute and long-term effect of percutaneous coronary intervention on serially-measured oxidative, inflammatory, and coagulation biomarkers in patients with stable angina

“…(31) Association of the single nucleotide polymorphism (SNP) Y402H of the CFH gene with increased cardiovascular risk has been controversial. (32),(33),(34),(35) However, complement activation has been shown to be higher in individuals presenting with ACS,(36) and recently to be associated with an anti-coagulant role. (37) The biological activity of CFH binding to MDA-LDL decreased by ~12% post PCI, and there was an increase of ~6% at 3-7 days post PCI that remained until 6 months.…”

High serum C1q-binding adiponectin levels in male patients with acute coronary syndrome

“…Our previous report had reported that stepwise multiple regression analysis did not identify HDL-C as a significant determinant of C1q–APN [17]. Some studies reported that serum complement levels were markedly elevated in ACS compared with SAP patients, suggesting an acute phase and inflammatory response [31,32]. The protein family CTRPs (C1q/TNF-related proteins) has recently been identified as adiponectin paralogs and some CTRP members share adiponectin's metabolic regulatory function and regulate cardiac remodeling after acute myocardial infarction [33,34].…”

Serum complements and heart fatty acid binding protein in Bangladeshi patients with acute myocardial infarction

“…In another study, plasma C3 and C4 levels in ACS showed a relationship with peak creatine kinase (CK)-MB and troponin I levels. The relationship of C3, C4 levels with peak CK-MB and troponin I levels further suggests that complement activation is related to necrosis within the myocardium 7. Lack of significance between some correlations may be due to the small sample size, which was a limitation of this study.…”