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Objective: to study the association of C3256T, G13 513A, G14 846A, and G12 315A mutations in the mitochondrial genome with the presence and degree of coronary and carotid atherosclerotic lesions.Subjects and methods. The investigation enrolled 193 patients (mean age 54.6 ± 9.5 years), including 154 men, who had undergone coronary angiography. A study group consisted of 130 patients with coronary atherosclerosis. A control group comprised 63 patients without this disease. Genetic analysis consisted of 3 steps: 1) isolation of genomic deoxyribonucleic acid from whole blood leukocytes by phenol-chloroform extraction; 2) amplification of polymorphic sites in the examined mitochondrial deoxyribonucleic acid genes by polymerase chain reaction; 3) pyrosequencingfor the detection of nucleotide sequencing and the determination of the level of heteroplasmy of the examined mutations.Results. The level of heteroplasmy of G13 513A and C3256T mutations was statistically significantly higher in the patients with coronary atherosclerosis than in those without this condition (p = 0.03 and p = 0.01, respectively) whereas that of G12 315A mutation was significantly higher in the persons without coronary atherosclerosis (p = 0.004). The level of heteroplasmy of G14 846A mutation was greater in people over 45 years of age. No association was found between mutations in the mitochondrial genome and cardiovascular risk factors, such as smoking, hypertension, poor family history, and obesity. There was a direct relationship of hyperlipidemy to C3256T mutation (r = 0.18; р = 0.01) and its inverse relationship to G12 315A mutation (r = –0.2; р = 0.005), There was a positive correlation between G14 846A mutationand lipoprotein (a) levels. There was also a positive correlation between carotid atherosclerosis with С3256Т (r = 0.49; p = 0.0001)and G14 846A (r = 0.48; p = 0.0001) mutations. G12 315A mutation showed a negative correlation with carotid atherosclerosis (r = –0.32; p = 0.01). Conclusion. The case-control study gave proof to the association between the level of heteroplasmy of С3256T, G13 513A, G14 846A, and G12 315A mutations in the mitochondrial genome and coronary and carotid atherosclerosis. Measurement of the heteroplasmy of С3256T, G13 513A and G14 846A mutations in the mitochondrial gene may be proposed as potential genetic markers to improve the diagnosis of a preposition to coronary and carotid atherosclerosis.

Objective: to study an association of high lipoprotein(a) [Lp(a)] levels with the development of restenosis and the progression of coronaryatherosclerosis after percutaneous coronary interventions (PCI) in patients with chronic coronary heart disease (CHD).Subjects and methods. From 502 enrolled patients (mean age 54.7 ± 8.9 years), 92 underwent routine percutaneous transluminal coronary angioplasty (PTCA), 270 had PTCA with the bare metal stent (BMS) being implantation, 140 had PTCA using drug-eluting stents (DES). Functionalclasses III and IV angina have been registered in 337 (67 %) patients; history of one myocardial infarction (MI) was noted in 234 (47 %) cases, 171 (34 %) had experienced 2 or more MIs. Blood samples for lipid and Lp(a) measurements were taken in all the patients. Restenosis was defined as at least 50 % lumen narrowing of the coronary artery segment after angioplasty. Coronary atherosclerosis progression was established in cases of the new occlusion occurring, as well as identifying a 10 % decrease in lumen diameter in comparison with baseline angiograms.Results. Repeated coronary angiography revealed the signs of restenosis in 103 of 243 patients. Dividing patients into 3 groups according to the type of intervention demonstrated that the level of Lp(a) (median 25–75 % quartiles) was significantly higher in the restenosis group after implantation of BMS (33; 11–62 and 16; 6–39 mg/dl, respectively; p = 0.014) versus those who had undergone DES implantation (23; 10–30 and 20; 6–60 mg/dl; p = 0.7) or balloon angioplasty (17; 4–48 and 9; 4–36 mg/dl; p = 0.3). Patients with progression of coronary atherosclerosis had difference only in Lp(a) levels compared to the group without progression (36; 13–62 versus 12; 4–26 mg/dl, p < 0,001.Conclusion. During the first year after elective PCI Lp(a) concentration determined the severity of coronary atherosclerosis in non-culprit lesionsand associated with the risk of in-stent restenosis after BMS, independly of conventional risk factors.

Mitochondria are not only the major producers of adenosine triphosphate, but also an endogenous source of reactive oxygen species. Mitochondrialdysfunction plays a key role in the trigger and progression of atherosclerotic lesion. Impaired function in the mitochondria due to their elevated level of oxidized oxygen species, the accumulation of mitochondrial DNA damages, and the exhaustion of respiratory chains induces dysfunction and apoptosis in the endothelial cells; activation of matrix metalloproteinases; growth of vascular smooth muscle cells and their migration into the intima; expression of adhesion molecules, and oxidation of low-density lipoproteins. Mitochondrial dysfunction may be an important unifying mechanism that accounts for the atherogenic effect of major cardiovascular risk factors. Small clinical pilot studies have shown an association of different mitochondrial genome mutations with atherosclerotic lesion in the artery. Taking into account the available data on the possible role of mitochondria in atherogenesis, novel drugs are now being designed to affect mitochondrial function.