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The study focuses on redox processes in the development of vascular complications in coronary heart disease. The data showed the formation of active oxygen radicals, inducing the process of lipid peroxidation. The development of oxidative stress occurred with a decrease in the activity of the antioxidant protection enzymes of the cells. Inhibition of superoxidecismutase, catalase, and ceruloplasmin occurred. Under these conditions, there was a decrease in the content of total metabolites of nitric oxide, the main vasodilating factor. In violation of the bioavailability of the substrate L-arginine for the NO-forming enzyme, a violation of cholesterol metabolism played a role: an increase in total cholesterol, LDL, and a decrease of HDL cholesterol. In ischemic patients, these metabolic changes were accompanied by hypertension, impaired cardiac activity, which was manifested by ECG changes and anginal attacks. The obtained fundamental data served as the basis for the development and application of therapy, including atorvastatin and Q10, an inhibitor of cholesterol synthesis. Combined therapy with an HMG-CoA reductase inhibitor and coenzyme Q10 had an antioxidant effect and reduced the content of total cholesterol, LDL cholesterol, and such HDL cholesterol increase. These changes served as the basis for increasing the content of nitric oxide, vasodilation, and improving the clinical condition.

Pathogenetic Substantiation of the Endothelial Dysfunction Correction in Ischemic Heart Disease of II Functional Class