Levels of toll-like receptors 2 and 4 in serum of men with postinfarction cardiosclerosis and its relationship with antiphospholipid syndrome components
Annotation. There is a tendency for an increase of incidence of coronary heart disease (CHD) among young people, with the development of acute myocardial infarction (MI) in the absence of marked atherosclerosis and obstruction of the coronary arteries. Antiphospholipid syndrome (APS), cellular and humoral mediators of immunoinflammatory activation of endothelium are considered as factors of non-obstructive damage to the coronary vessels. New trigger factors for endothelial dysfunction, cardiac fibrosis, and myocardial hypertrophy include toll-like receptors (TLR2 and TLR4). Antiphospholipid antibodies may act as endogenous activators of toll-like receptors. The study of the association between APS components and expression of toll-like receptors in patients with CHD with postinfarction cardiosclerosis remains relevant. The aim is to study the levels of TLR2 and TLR4 and its relationship with APS components in men with postinfarction cardiosclerosis. 164 patients with stable CHD with postinfarction cardiosclerosis (100% of men, age 53.0±9.14 years) and 48 men of control group (without CHD) were examined. Levels of total antiphospholipid antibodies (aPL), antibodies to β2-glycoprotein 1 (anti-β2-GP 1) IgG and IgM, TLR2, TLR4 in serum were determined by ELISA. The studies were conducted in compliance with bioethical standards. Statistical processing of the results was performed in SPSS Statistics 22.0. Determined that men with postinfarction cardiosclerosis showed higher levels of TLR2 and TLR4 (in 1.8–2.2 times, p<0.001) in serum than control group. Higher (in 1.2–1.4 times) levels of TLR2 and TLR4 were found in patients who underwent Q-MI, recurrent MI and had clinical manifestations of APS (stroke, transient ischemic attacks, livedo reticularis). An increase TLR2 and TLR4 levels was closely associated with an increase of aPL and anti-β2-GP 1 of IgG (r = | 0.31 - 0.51 |, p<0.01). Thus, in men with postinfarction cardiosclerosis who had aPL and anti-β2-GP 1 IgG positivity had an unfavorable immunoinflammatory pattern, that characterized by increased expression of TLR2 and TLR4. The imbalance in TLR2 and TLR4 is more pronounced in young CHD patients and associated with Q-MI and recurrent MI.
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