Ultra-low dose estradiol plus dydrogesterone: a role in prevention of the development and progression of atherosclerosis

Active development of the "anti-aging medicine", attempts to slow down biological (including vascular) aging led to the creation of new pharmaceuticals including menopausal hormone therapy. The vascular wall protective mechanism of the hormones is not completely clear, but it was shown that natural estrogens are able to control the condition of the vascular wall, prevent platelet adhesion, control a range of metabolic and trophic and energy processes in the endothelium of the vascular wall, producing antithrombogenic factors, namely their inhibition contributes to the development of atherosclerosis. It is known that standard and low-dose estrogen may restore the impaired antithrombogenic potential of the vascular wall, provided its initial reduction does not exceed 20%. The issue of the role and possibilities of correction of the antithrombogenic activity of the vascular wall with ultra-low dose estradiol remained unresolved. As a "clinical model" for the study of this issue, we formed 2 groups of patients: in the study group patients received ultra-low dose estradiol plus dydrogesterone, subjects from the control group received beta-alanine. Three-year follow-up showed a decrease in antithrombogenic activity of the vascular wall in control subjects after 2 and 3 years of follow-up according to the M.V. Baluda's test versus subjects treated with ultra-low dose estrogen plus dydrogesterone. The decrease of the relative risk of reduction of the antithrombogenic activity of the vascular wall with the use of ultra-low dose estrogen plus dydrogesterone during the first two years was 2.3 times, and during the 3 years of follow-up — 3.8 times versus control. Thus, prescribing only ultra-low dose estradiol plus dydrogesterone for patients with normal antithrombogenic activity of the vessel wall at baseline reliably lowers the risk of long-term reduction of antithrombogenic potential of the vascular wall.