Coronary heart disease and inflammation.

The increased content of inflammation markers in the blood is a significant prognostic sign of coronary events in persons with stable or asymptomatic course of coronary heart disease (CHD) and suggests that the inflammation underlying the destabilization of CHD has an independent character and is largely independent of the severity of stenotic lesions of coronary vessels. Activation of the local inflammatory process in the atherosclerotic plaque leads to the destruction of the fibrous capsule in combination with an increase in the activity of cellular and plasma factors of the coagulation system and inhibition of the fibrinolytic system. Cytomegalovirus, Chlamydia pneumoniae, pathogens of periodontal disease are nominated for the role of inducers of inflammatory reactions. The synergistic effect of several pathogens is reflected in the concept of burden of infection (“infectious burden”). Immuno-inflammatory rheumatic diseases are characterized by a high risk of cardiovascular complications. An important place in their prevention is an effective anti-inflammatory therapy: methotrexate, suppressing the formation of interleukin 1ft and tumor necrosis factor a, allows not only to modify the course of the disease, but also to reduce the risk of cardiovascular accidents. Chronic inflammation, as a key element of atherosclerosis pathogenesis, can be caused not only by infectious and immune factors, but also by metabolic factors. The activation of inflammasomes induced by cholesterol crystals in macrophages is an important link between cholesterol metabolism and inflammation in atherosclerotic plaques. Confirmation of the important pathogenetic role of inflammation is to reduce the risk of cardiovascular complications (CVD) on the background of anti-inflammatory therapy. In statin therapy, the decrease in The level of C-reactive protein (CRP) was significantly correlated with the suppression of atherosclerosis progression and a decrease in the risk of SSR, regardless of the degree of lowering the low-density lipoprotein cholesterol level. Taking colchicine in a low dose in patients with stable coronary artery disease, who received standard therapy, reduced the risk of acute coronary syndrome and sudden cardiac death. Secondary prevention of cardiovascular complications by human monoclonal antibodies to interleukin 1ft (kanakinumab) led to a decrease in the risk of SSR regardless of sex, Smoking, and lipid levels.