Aim — to analyze various aspects’ effect (conventional risk factors of coronary artery disease, anatomical features of coronary lesion, technical aspects of percutaneous coronary interventions, platelet aggregation, lipid profile, genetic factors regulating lipid metabolism) on long-term outcomes of percutaneous coronary interventions (PCI). Material and methods. There were 84 CAD patients who underwent elective coronary stenting. Two groups were analyzed depending on achievement of endpoints (recurrent angina after PCI, myocardial infarction after PCI, cardiovascular death). These events had angiographic confirmation including stent restenosis, further coronary lesion outside stenting area, thrombosis of stent. Group 1 (n=28) — patients with achieved endpoints (recurrent angina after PCI and/or myocardial infarction after PCI and/or cardiovascular death). Group 2 (n=56) — patients without adverse cardiovascular events after PCI within follow-up (6.15±0.2 years on the average). Results. Relationship of 4 polymorphisms of LPL gene with development of adverse cardiovascular events after PCI was identified: 1) LPL rs285. Allele T: OR=2.68; 95% CI 1.38—5.21. Genotype TT: OR=2.98; 95% CI 1.07—8.26. 2) LPL rs328 (S447X). Allele G: OR=6.06; 95% CI 1.54—23.8. Genotype CG: OR=7.07; 95% CI 1.7—29.3. 3) LPL rs2083637. Allele G: OR=2.45; 95% CI 1.2—5.01. 4) LPL rs10096633. Allele T: OR=7.13; 95% CI 2.42—21.0. Genotype CT: OR=5.67; 95% CI 1.71—18.8. There was no correlation of other polymorphic markers with adverse cardiovascular events after PCI. Following predictors of mid- and long-term adverse cardiovascular events after PCI were determined: antiplatelet therapy followed by insufficient suppression of platelet aggregation (χ2= 6.7; p=0.01); statin therapy without target levels of lipid contents (χ2=6.46; p=0.04); variant allele LPL rs285 (T) (χ2=10,0; p=0,01), genotype TT (χ2=5.55; p=0.05); variant allele LPL rs328 (G) (χ2=8.2; p=0.01), genotype CG (χ2=8.8; p=0.01); variant allele LPL rs2083637 (G) (χ2=30.6; p=0.007), genotypes GG and AG (χ2=6.2; p=0.04); variant allele LPL rs10096633 (T) (χ2=15.7; p=0.01), genotypes of CT and TT (χ2=13.3; p=0.01). Conclusion. Identification of patients carrying polymorphic alleles (genes regulating lipid metabolism) and advanced risk of adverse cardiovascular events after PCI may be later used to create individual strategy of lipid-lowering therapy. The last can include higher doses of statins and/or dual therapy (statin+fibrate, statin+nicotinic acid, new class of lipid-lowering drugs — monoclonal IgG2 inhibiting PCSK9) to prevent long-term cardiac complications after PCI.