Depletion of complement system immunity in patients with myocardial infarction

Abstract

The aim of the present study was to evaluate differences in the expression of complement system genes, and serum levels of CH50, C3 and C4 in peripheral blood mononuclear cells from patients with myocardial infarction (AMI), stable angina pectoris (SA) and controls. A total of 100 patients with AMI, 100 with SA and 100 clinical controls were recruited in the present study. In each group, 20 randomly selected individuals were examined using whole human genome microarray analysis to detect the expression of genes of the complement system. The serum levels of CH50, C3 and C4 were measured in all 300 subjects. In the patients with AMI, the expression levels of genes encoding C1qα, C1qβ, C1qγ, C1r, Factor P, C5a (complement component), CR1, integrin αM, integrin αX, integrin β2, C5aR, CRIg (complement receptors) and CD46, CD55 and CD59 (complement regulators) were significantly higher, compared with the respective genes in the SA patients and controls (P<0.05), whereas the mRNA levels of C1s, C7, C8β and C9 were the lowest in this group (P<0.05). No statistically significant differences were found in the gene expression levels of complement components or regulators between the SA and control groups. The serum levels of CH50, C3 and C4 were significantly increased in the AMI and SA groups, compared with the controls. In the AMI and SA groups, the complement system was activated. However, the differential mRNA expression of complement components, receptors and regulators in the AMI group suggested the dysfunction of the C5b-9 complex. The depression of complement system immunity in the patients with AMI may be associated with the pathogenesis of AMI.

Evaluation of expression levels and mechanism of complement activation

“…The average ages of the subjects ranged from 55±6.54 to 49.4±3.2 years. The diagnostic criteria of acute myocardial infarction were as follows: CT angiography showed that dissection diaphragm divided aorta into true lumen and false lumen ( 3 ). The diagnostic criteria of coronary artery stenosis were the pathological expansion of abdominal aorta exceeding 50% of normal blood vessel diameter ( 12 ).…”

“…The change of serum enzymes included the sequence change of serum enzyme concentration or beginning at first and reducing later on, which was a typical evolution process of myocardial infarction. Six hours after on site, serum creatin phosphokinase (CK or CPK) appeared and reached a peak at 24 h, and disappeared after 48–72 h, with a positive rate of 92.7% ( 3 ). Before surgery, the patients were examined by coronary angiogram and diagnosed as acute myocardial infarction.…”

“…This could induce fatal complications such as rupture and cardiac tamponade. The typical clinical manifestation is sudden lancination of lower back, where the occurrence does not exceed 14 days ( 3 , 4 ). The main pathology manifests as retrogression of artery medial and infiltration of inflammatory cells ( 3 , 5 ).…”

“…The typical clinical manifestation is sudden lancination of lower back, where the occurrence does not exceed 14 days ( 3 , 4 ). The main pathology manifests as retrogression of artery medial and infiltration of inflammatory cells ( 3 , 5 ). In mouse, the application of anti-neutrophil cytoplasmic antibody may markedly reduce the occurrence of acute myocardial infarction ( 6 ).…”

The role of the complement factor B‒arginase‒polyamine molecular axis in uremia‐induced cardiac remodeling in mice

“…Several studies have shown that complement system is involved in a diverse range of pathological cardiac conditions. For example, Yan et al reported that the expression of CP and final path components was upregulated in PBMCs from patients with myocardial infarction, compared with stable angina pectoris and controls [4]. Hertle et al raised a conclusion from a large-sample cohort that the excessive AP activation would promote poor cardiovascular outcomes [5].…”