[PHARMACOGENETIC ASPECTS OF TREATMENT OF PATIENTS WITH CHRONIC HEART FAILURE (REVIEW)].

This article reviews data for pharmacogenetics findings for treatment for chronic heart insufficiency of heart failure. Also, it discusses connections of genetic polymorphism with a risk of developing heart failure and how it affects the choice of a treatments medicine. The article investigates genetically determined factors of the risk of developing glycoside toxicity. One of the causes is polymorphism of the MDR1 gene encoding glycoprotein P, a transporter, that is involved in the absorption of drugs in the intestines and excretion by the kidneys. Also, the genetic characteristics of ACE in patients with heart failure are discussed. The data is presented from the study of the role of genetic liver metabolism polymorphism regarding efficacy and safety of loop diuretic torasemide. Data for genetic polymorphism of the metabolism of the main beta blocker, used in chronic heart failure metoprolosuccinate is also discussed. Data for roll ß1-AP polymorphism in the clinical use of ß-AB in patients with heart failure. Further observations are needed from longer studies, that will evaluate long-term efficacy and safety outcomes for medicines related to genetic traits.

[CLINICAL CASE: THE SIDE EFFECTS OF STATINS].

The clinical studies, conducted in recent years, suggest that statins increase the activity of telomerase and by that decelerate speed of telomerase shortening. Thus, on one hand, it reduces a risk of cardiovascular diseases development, decelerate aging, but on the other hand, increasing the activity of telomerase, lead to expression rising of gene hTERT, that can make prerequisites for malignancy. That's why, it's necessary to study the subject and develop reliable criteria for safety use of activators-telomerase.