Application of lipid-lowering in patients with coronary artery disease and obesity depending on genotypes of the Met235Thr polymorphism of the angiotensinogen gene
Summary. The aim was to evaluate the efficacy of adding atorvastatin and rosuvastatin to the standard therapy in patients with coronary heart disease (CHD) and obesity, depending on genotypes of the Met235Thr polymorphism of the angiotensinogen (ATG) gene. Materials and methods. Two subgroups of observation were identified: 1 — 116 patients with CHD and obesity receiving atorvastatin at a daily dose of 20 mg (among which T/T-genotype carriers — 34, T/M-genotype — 45 and M/M-genotype — 37), 2 — 108 patients with CHD and obesity who received rosuvastatin in a daily dose of 10 mg (among which T/T-genotype carriers — 30, T/M-genotype — 43 and M/M-genotype — 35). All patients were determined by indicators lipid exchange according to the standard biochemical technique, allelic polymorphism of the Met235Thr of the ATG gene by polymerase chain reaction. Results. The analysis of the efficacy of atorvastatin and rosuvastatin, based on the genotypes of the Met235Thr polymorphism of the ATG gene in patients with CHD and obesity, revealed likely differences in more pronounced lipid-lowering effect of rosuvastatin in T/T-genotype carriers, and it was more appropriate to use atorvastatin in M/M-genotype carriers. Conclusions. Treatment of patients with CHD and obesity with hypolipidemic agents (atorvastatin or rosuvastatin) improved lipid metabolism by reducing the content of proatherogenic fractions. The use of atorvastatin in M/M- and rosuvastatin in T/T-genotype carriers of the Met235Thr-polymorphism of the ATG gene is particularly effective and most preferred.
Key words: rosuvastatin, atorvastatin, coronary heart disease, obesity, polymorphism of the angiotensinogen gene.
- DiNicolantonio J.J., Lavie C.J., Serebruany V.L., O’Keefe J.H. (2013) Statin wars: the heavyweight match — atorvastatin versus rosuvastatin for the treatment of atherosclerosis, heart failure, and chronic kidney disease. Postgrad. Med., 125(1): 7–16.
- Khera A.V., Everett B.M., Caulfield M.P. et al. (2014) Lipoprotein(a) concentrations, rosuvastatin therapy, and residual vascular risk: an analysis from the JUPITER Trial (Justification for the Use of Statins in Prevention: an Intervention Trial Evaluating Rosuvastatin). Circulation, 129(6): 635–642.
- Pelliccia F., Rosano G., Marazzi G. et al. (2014) Pharmacodynamic effects of atorvastatin versus rosuvastatin in coronary artery disease patients with normal platelet reactivity while on dual antiplatelet therapy — the PEARL randomized cross-over study. Eur. J. Pharmacol., 725: 18–22.
- European Association for Cardiovascular Prevention & Rehabilitation, Reiner Z., Catapano A.L. et al.; ESC Committee for Practice Guidelines (CPG) 2008–2010 and 2010–2012 Committees (2011) ESC/EAS Guidelines for the management of dyslipidaemias: the Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and the European Atherosclerosis Society (EAS). Eur. Heart J., 32(14): 1769–1818.
- Stone N.J., Robinson J.G., Lichtenstein A.H. et al.; American College of Cardiology/American Heart Association Task Force on Practice Guidelines (2014) 2013 ACC/AHA guideline on the treatment of blood cholesterol to reduce atherosclerotic cardiovascular risk in adults: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, 129(25 Suppl. 2): S1–S45.
- Takagi H., Niwa M., Mizuno Y. et al. (2014) Effects of rosuvastatin versus atorvastatin on small dense low-density lipoprotein: a meta-analysis of randomized trials. Heart Vessels, 29(3): 287–299.
- Tsimikas S., Viney N.J., Hughes S.G. et al. (2015) Antisense therapy targeting apolipoprotein(a): a randomised, double-blind, placebo-controlled phase 1 study. Lancet, 386(10002): 1472–1483.
- Weng T.C., Yang Y.H., Lin S.J., Tai S.H. (2010) A systematic review and meta-analysis on the therapeutic equivalence of statins. J. Clin. Pharm. Ther., 35(2): 139–151.