[Lipolysis in very low density lipoproteins - locus minoris resistentiae - in the pathogenesis of hypertriglyceridemia. Positive effects of diet, polyenic fatty acids, statins and fibrates.]

Inhibition of hydrolysis of palmitic and oleic triglycedires (TG) in very low density lipoproteins (VLDL), slow formation of active apoВ-100 conformation, blockade of апоЕ/В-100 ligand formation in VLDL and their reduced uptake by insulin-dependent cells cause hypertriglyceridemia (HTG). Palmitic and oleic VLDL (>80% total VLDL) are not converted in low density lipoproteins (LDL). Atherosclerosis is not an alimentary deficiency of polyenic fatty acids (PFA), but results from low in vivo bioavailability of PFA in LDL against the background of high dietary palmitic FA and palmitic LDL. Plasma PFA content and cellular PFA deficiency are as high as LDL cholesterol (CL). Primary prevention of atherosclerosis should be based on a decrease in dietary content of palmitic saturated FA, trans FA and a moderate increase in PFA. It seems highly unlikely that the xeobiotics statins, fibrates and probucol produce pleiotropic biological effects in vivo. These effects are brought about by phylogenetically early humoral mediators eicosanoids: prostacyclins, prostaglandins, thromboxanes, leukotrienes, and resolvins. It is reasonable to suggest that all preparations which act according to the same algorithm activate TG hydrolysis in VLDL and normalize cellular uptake of PFA in linoleic and linolenic LDL via apoВ-100 endocytosis. Atherosclerosis is a syndrome of cellular deficiency of essential polyenic FA.

[Giant Aneurysms in Coronary Arteries of a Young Woman].

Coronary arteries aneurysms with their thrombotic occlusion are known to be detected in young patients who have suffered Kawasaki disease in childhood. The other vascular beds are usually not involved. In the literature one can find not enough information regarding diagnostics of this pathology, as well as no specific treatment algorithm. We present here a clinical case of re-emergence of giant aneurysms of coronary arteries in the young female patient with subsequent immuno-histological confirmation of previous Kawasaki disease.

The association of lipoprotein(a) and apolipoprotein(a) phenotypes with peripheral artery disease.

AIM: Lipoprotein(a) [Lp(a)] is an independent risk factor of coronary heart disease (CHD) and myocardial infarction. Data about the role of Lp(a) in the development of peripheral artery disease (PAD) is controversial and uncertain. The aim of the study was to evaluate the association between Lp(a), apolipoprotein(a) [apo(a)] phenotypes and PAD. MATERIALS AND METHODS: The study included 998 patients (707 male and 291 female, average age 60±12). The patients were divided into 4 groups depending on the presence or absence PAD and CHD: group I (n=188, PAD+CHD+), group II (n=78, PAD+CHD-), group III (n=407, PAD-CHD+), group IV (n=325, PAD-CHD-). RESULTS: The level of Lp(a) was significantly higher in groups I, II, III in comparison with patients of control group (group IV): 34 [15; 80], 30 [10; 49], 22 [8; 60] mg/dl vs. 15 [6; 35] mg/dl respectively, p<0.01 in all cases. Lp(a) level was higher in the group I than in the other groups (p<0.05). The prevalence of elevated Lp(a) level (≥ 30 mg/dl) was significantly higher in groups I, II, III than in control group: 54%, 50%, 43% respectively vs. 30%, p<0.01 in all cases. The prevalence of Lp(a) ≥ 30 mg/dl was more frequent in the group with PAD and CHD than in the group with CHD and without PAD (p=0.02). The odds ratio (OR) of PAD in the presence of elevated Lp(a) level was 1.9 (95%CI, 1.4-2.5, p<0.01). Low molecular weight (LMW) apo(a) phenotype was met more frequently in groups I, II, III compared to group IV: 46%, 56%, 52% respectively vs. 28%, p<0.01. LMW apo(a) in the patients without CHD was associated with PAD (OR 3.3; 95% CI, 1.6-6.8, p<0.01), and there was no association with the patients with CHD. In logistic regression analysis adjusted for age, sex, hypertension, obesity, smoking, diabetes, LDL-C, Lp(a) and LMW apo(a) phenotype were independent predictors of PAD when included separately. CONCLUSION: Elevated level of Lp(a) and LMW apo(a) phenotype are independent risk factors of PAD. The level of Lp(a) in the patients with PAD and CHD was higher than in the case of isolated lesion of each vascular pool. Higher level of Lp(a) is associated with more severe atherosclerosis involving more than one vascular pools.

[Recommendations of the European Society of Cardiology and the European Atherosclerosis Society on Cardiovascular Disease Prevention and Management of Dyslipidemias. for the Diagnosis of Atherosclerosis and Dyslipidemia Treatment (2016): Basic S.G.]

This review summarizes the main provisions of the new, issued in 2016, recommendations of the European Society of Cardiology and Atherosclerosis Society in cooperation with the European Association on Cardiovascular Prevention and Rehabilitation on Cardiovascular disease prevention and Management of dyslipidemia. In these recommendations, the following trends can be traced distinctly: priority in primary prevention is given to non-drug methods of influence; targets of hypolipidemic therapy are identified not only for low density lipoprotein (LDL) cholesterol (CH), but also for non-high density lipoprotein (HDL) CH, especially in cases of concomitant hypertriglyceridemia. In the field of therapy, in which statins remain the main tool of correction of hyperlipidemia, it is recommended to more widely resort to the use of combination therapy, especially in cases of familial hypercholesterolemia or intolerance to statins; introduction of a new class of drugs- inhibitors of proprotein convertase subtilisin/kexin type 9 makes it possible to further reduce the level of LDLCH, lipoprotein(a) more than 60%. Regarding the wider application of these drugs there are issues related to the relatively limited experience of their use and the lack of data on long-term results and the incidence of side effects. Much attention is paid to more active correction of dyslipidemia in elderly patients, patients with chronic renal failure, diabetes, and several other diseases. The emergence of new European recommendations will undoubtedly serve as a stimulus to the revision of the Russian recommendations, which remain unchanged from 2012.

[The physical chemical and biological features of triglycerides. The cell absorption of functionally different palmitic+oleic lipoproteins of very low and density and linoleic+linolenic lipoproteins of low density.]

The earlier insulin-independent low-density lipoproteins and more late insulin-dependent very low-density lipoproteins implement different functions at the stages of phylogenesis. The disorder of biological function of trophology, alteration of fatty acids in triglycerides, prevalence of palmitic very low-density lipoproteins over oleic very low-density lipoproteins supply mitochondria of cells with non-optimal substrate - palmitic saturated fatty acid for gaining energy, ATP synthesis. Physiologically, cells implement oleic alternative of fatty acids metabolism, oxidizing mainly ω-9 endogenous oleic mono-unsaturated fatty acid. The pathology of low density lipoproteins is primary deficiency of poly-unsaturated fatty acids in cells, atherosclerosis and atheromotosis of intima of arteries of elastic type with development of dense plaques from poly-unsaturated fatty acids in the form of polyethers of cholesterol. The pathology of very low-density lipoproteins includes: a) syndrome of resistance to insulin; b) pathology of phylogenetically earlier insulin-independent visceral fatty tissue - metabolic syndrome; c) pathology of phylogenetically later insulin-dependent subcutaneous adipocytes - obesity; d) secondary atherosclerosis, under cumulation of palmitic low-density lipoproteins in blood with development of atherothrombosis of intima of arteries, soft plaques rich with triglycerides. As for the prevention of disorders of transfer of fatty acids to very low-density lipoproteins and low-density lipoproteins is common in many ways - minimization of aphysiological effect of surplus amount of food, biological function of diet. The prevention at the level of population includes: a) maximal limitation of content of palmitic saturated fatty acid in food; b) moderate increasing of polysaturated fatty acids, ω-3 poly-saturated fatty acids predominantly; c) increasing of physical activity. The pharmaceuticals are not provided by biology in primary prevention of metabolic pandemics under aphysiological impact of environment factors.

[The individual fatty acids of blood plasma: biological role of substrates, parameters of quantity and quality, diagnostic of atherosclerosis and atheromotosis.]

The atherosclerosis and atheromotosis are supposed to be, according to phylogenetic theory of general pathology, two etiologically different aphysiological processes, unified by community of pathogenesis. The atherosclerosis is a derangement of biological function of trophology (feeding), biological reaction of exotrophy (external feeding) and biological function of adaptation, biological reaction of compensation in response to deficiency of ῳ-3 and ῳ-6 polyenoic fatty acids. In case of deficiency of polyenoic fatty acids in cells and during synthesis of eicosanoids of group I from unsaturated endogenous ῳ-6 С20: 3 digomo-γ-linoleic unsaturated fatty acid, atherosclerosis is developed, a complex metabolism disorder in vivo. The atheromotosis is a derangement of biological function of endoecology, biological reactions of inflammation and inherent immunity. This incomplete utilization in intima of arteries of non-ligand palmitic lipoproteins of very low → low density under effect not of polyfunctional resident macrophage but monocytes of hematogenic origin without expression of acid hydrolase of polyenoic ethers of cholesterol. In intima, in area of cumulation of endogenous phlogogens (initiator of inflammation) from the pool of intra-vascular medium, polyenoic unsaturated fatty acids are cumulated that were not absorbed by cells in structure of ligand low density palmitic lipoproteins using apoB-100- endocytosis. The pathogenic factor of atherosclerosis - derangement of biological function of trophology. biological function of exotrophy under alimentary deficiency of in vivo of ῳ-3 and ῳ-6 polyenoic fatty acids with physiological parameters of feeding. The pathogenic factor of atheromotosis - phylogenetically herbivorous (carnivorous) human misusing of animal (meat) food, palmitic unsaturated fatty acids, development by hepatocytes of a large number of palmitic triglycerides and lipoproteins of very low density of the same name. The late in phylogenesis insulin-dependent lipoproteins of very low density transfer palmitic lipoproteins of very low density to cells slowly. The cells absorb them also slowly. The cumulation of non-ligand palmitic lipoproteins of very low density → low density in blood competitively blocks physiological absorption of polyenoic unsaturated fatty acids by cells in structure of physiological palmitic lipoproteins of low density. The atherosclerosis occurs blood flow and atheromotosis in intima of arteries of elastic type.

[The integrated etiology and separate pathogenesis of atherosclerosis and atheromatosis. The differences of fatty acids transfer in lipoproteins of herbivorous and carnivorous animals.]

According phylogenetic theory of general pathology, overconsumption of meat food by herbivorous animals always results in atherosclerosis and atheromatosis of intima of arteries. The etiological factors of atherosclerosis, atheromatosis in vivo: a) absorption by cells of polyene fatty acids in anoB-100 lipoproteins of low density; b) impossibility of converting exogenous palmitic saturated fatty acids into mono-unsaturated oleic fatty acid; c) monocytes-macrophages in intima inactively hydrolyze polyene fatty acids esterified by alcohol cholesterol. The disorder of biological function of trophology (nutrition), biological reaction of exotrophy (external nutrition) and aphysiologically high content of palmitic unsaturated fatty acids and alcohol cholesterol in food become a pathogenic factors. The key stage of pathogenesis is formation in blood of non-ligand palmitic lipoproteins of very low density. At that: a) how to utilize in vivo non-ligand palmitic lipoproteins of very low density; it is possible under activation of biological function of endoecology, biological reaction of inflammation, formation of atheromatosis of intima of arteries and b) how to prolong function to cells at impossibility of of absorbing from inter-cellular medium polyene fatty acids; this is a foundation of atherosclerosis, disorders of biological function of adaptation, biological reaction of compensation. The primary prevention of myocardium infarction requires elimination of consumption of surplus amount of animal food. At low content of palmitic saturated fatty acids in food insulin forms optimal oleic alternative of metabolism of fatty acids supporting high "kinetic parameters" of organism and effective synthesis of ATP. According single pathogenesis of atherosclerosis and atheromatosis it is necessary to prevent development of non-ligand palmitic lipoproteins of very low density in blood. Without them no development of both atherosclerosis and atheromatosis is possible.

[Vasorenal Hypertension and Primarily Contracted Kidney in a Man Aged 44 years: Is Invasive Intervention Needed?]

Presentation of a clinical case of vasorenal hypertension in a patient with chronic renal artery occlusion and primarily contracted kidney is accompanied by discussion of current recommendations concerning indications to invasive intervention in patients with vasorenal arterial hypertension.

[Degenerative Aortic Stenosis: Modern View on Development, Course, and Management].

Degenerative aortic stenosis is an acquired heart defect manifesting as progressive thickening and calcification of leaflets of originally normal tricuspid or congenital bicuspid aortic valve with development of orifice narrowing, left ventricular hypertrophy, and high risk of cardiovascular complications. In this review we present modern concepts of formation and progression of degenerative aortic stenosis and discuss optimal methods of management of this disease.

[The evaluation of unsaturation of blood lipids using methods of physical chemistry and clinical biochemistry. The insulin regulation of metabolism of fatty acids, number of double binds and cell absorption of glucose].

It is supposed that the main cause of insulin synthesis at late stages of phylogenesis became discrepancy between increase in vivo need in energy and physical chemical parameters of palmitic saturated fatty acid; its transportation to cells in composition of lipoproteins in optimal quantity (more than 15% of all fatty acids) became in vivo unfeasible. The biological role of insulin consists in supporting of insulin-dependent cells (skeletal miocytes in the first place) with substrates for gaining energy. The hormone transforms all palmitic saturated fatty acid endogenously synthesized from glucose into specific for animal cells rn-9 C18:1 oleic mono unsaturated fatty acid. The endogenous mono unsaturated fatty acid is oxidized by mitohondria with the highest constant of reaction velocity gaining for cells optimal quantity of biotransforming energy in the form of ATP. The insulin expresses in hepatocytes synthesis of oleic triglycerides and formation of oleic lipoproteins of very low density that only insulin-dependent cells absorb using apoE/B-100-endocytosis. The insulin expresses synthesis of Palmitoyl-KoA-elongase, stearyl-KoA-desaturase and glucose transporters 4, activates glucose absorption by cells with the purpose of synthesis endogenous oleic saturated fatty acid. The insulin substitutes in vivo ineffective palmitic alternative of metabolism of fatty acids for potentially more effective oleic metabolism of fatty acids. The insulin increases unsaturation of fatty acids and number of double binds in them. This can be established by direct titration of double binds by ozone on the basis of quantitative detection of fatty acids using technique of gas chromatography and calculating ratio C16:1/C16:0, C18:1/C18:0 and C18:1/C16:0. The diabetes mellitus is a disorder of metabolism of mono unsaturated fatty acid in the first place and only in the second place pathology of glucose absorption by cells.

[The oleic triglycerides of palm oil and palmitic triglycerides of creamy fat. The reaction of palmitoylation, potassium and magnesium palmitate, absorption of fatty acids by enterocytes and microbiota of large intestine].

The decreasing of content of animal, palmitic milk fat (butter) by means of its substitution with vegetable, oleic, palmy oil in food of adults optimal by its quantity is physically chemically and biologically substantiated. In oleic palmy oil higher content of oleic mono unsaturated fatty acid and oleic triglycerides than in creamy fat is established. The biologic availability of palmitic unsaturated palmitic acid in the form of free fatty acid is decreased at its absorption by enterocytes of small intestines is detected. There are no transforms of mono unsaturated acids in palmy oil in contrast with hydrogenated margarines. In palmy, oleic oil there is not enough of short-chained fatty acids (C4-C6) and it has no taste quality and it has low level of unsaturated fatty acids and factually it is lacking of ω-6 polyunsaturated fatty acids. However, it is compensated in case of availability offish and sea products in food. If adults, especially older ones, will refuse to consume creamy fat and decrease intake of products with high content of palmitic unsaturated fatty acid and palmitic triglycerides (beef, sour cream, fatty cheeses) it'll positively impact their health. The refusal from these products is a real step in prevention of metabolic pandemic (atherosclerosis and atheromatosis, metabolic syndrome, resistance to insulin, obesity). There are still large number of people who at optimal amount of food retain in vivo increased amount of exogenous, endogenously synthesized from glucose palmitic unsaturated fatty acid in the form of unesterified fatty acids (syndrome of resistance to insulin) and increased content of palmitic triglycerides.

[The positional specificity of individual triglycerides-substrates for lipase action. The oleic triglycerides of palm oil, palmitic triglycerides of milk, ions of calcium and magnesium.]

The counter-insulin effect of surplus of palmitic fatty acid in food is implemented under: a) formation in vivo of palmitic type of fatty acids metabolism with deficiency of substrate for ATP synthesis and permanent shortage of energy for accomplishment of biologic functions; b) compensatory activation of biologic function of adaptation, biologic reaction of compensation. The activation with catecholamines in visceral fatty cells of gland the hormone-dependent lipase which is not blocking insulin, increases content of unesterified fatty acids in blood plasma. Until in blood plasma the level of unesterified fatty acids is increased the cells phylogenetically justified stop absorption of glucose along with development of hyperglycemia and hypertriglyceridemia - insulin resistance syndrome. Thew increasing of content of triglycerides (alcohol glycerin) always increases cholesterol - low density lipoproteins; the highest numbers of cholesterol result in no increasing of triglycerides concentration in blood. All triglycerides of milk positionally are palmitic ones and all triglycerides of palm oil are oleic ones. The surplus of palmitic unesterified fatty acids in small intestine under hydrolysis of oleic triglycerides decreases bio-availability and absorption of ions of Ca++ and Mg++ by enterocytes. This occurrence is absent in case of hydrolysis of palmitic triglycerides of maternal milk in intestine since all released unesterified fatty acids are oleic ones. The position of fatty acids in the composition of triglyc erides is a functional characteristic of substrate under impact of positionally specific lipases in all biologic mediums.

[Mass spectrometry analysis of blood plasma lipidome as method of disease diagnostics, evuation of effectiveness and optimization of drug therapy].

A new method for the analysis of blood lipid based on direct mass spectrometry of lipophilic low molecular weight fraction of blood plasma has been considered. Such technique allows quantification of hundreds of various types of lipids and this changes existing concepts on diagnostics of lipid disorders and related diseases. The versatility and quickness of the method significantly simplify its wide use. This method is applicable for diagnostics of atherosclerosis, diabetes, cancer and other diseases. Detalization of plasma lipid composition at the molecular level by means of mass spectrometry allows to assess the effectiveness of therapy and to optimize the drug treatment of cardiovascular diseases by phospholipid preparations.

[Lipoprotein-associated phospholipase A2 serum levels in patients from different categories of cardiovascular risk].

AIM: To compare levels of lipoprotein-associated phospholipase A2 (Lp-PLA2) in blood serum of patients from different cardiovascular risk categories. MATERIAL AND METHODS: Patients from Moscow prospective study database (n = 519) were divided into 4 cardiovascular risk categories according to present clinical recommendations (low, moderate, high, very high). Measurement of Lp-PLA2 concentration (mass) was performed using PLAC Test ELISA Kit. Measurement of Lp-PLA2 activity was made using PLAC Test for Lp-PLA2 Activity. Blood serum levels of total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), lipoprotein (a) (Lp(a)), high sensitive C-reactive protein (hsCRP) and uric acid were also determined. RESULT: Preliminary analysis showed that associations between Lp-PLA2 mass and activity became more obvious in patients not treated with statins and patients without diabetes mellitus. So patients receiving statins and diabetics were excluded from final analysis. Lp-PLA2 mass and activity were lower in low cardiovascular risk category patients. There were no significant differences in Lp-PLA2 mass and activity between patients from moderate, high and very high risk categories. There was moderate correlation between Lp-PLA2 mass and Lp-PLA2 activity (r = 0.38, p < 0.00001). We did not find any correlation between Lp-PLA2 and hsCRP, Lp(a) levels, but detected moderate correlation between Lp-PLA2 mass and activity and TC, LDL-C. We also found a mild positive correlation between Lp-PLA2 mass and HDL-C levels. There was a positive correlation between Lp-PLA2 activity and TG, uric acid and negative correlation between Lp-PLA2 activity and HDL-C levels. CONCLUSION: In this group of nondiabetic patients not treated with statins both Lp-PLA2 activity and mass were similarly related to categories of cardiovascular risk.

[Hypolipidemic and pleiotropic effects of a combination of simvastatin and ezetimibe in patients with different types of hyperlipidemia].

The review considers trials dealing with the efficiency of combination hypolipidemic therapy with simvastatin and ezetimibe. Its synergistic potentiating effect can cause a considerable decrease in the level of total cholesterol, low-density lipoproteins, triglycerides, and C-reactive protein, which are important participants in the atherogenic process. This effect promotes the achievement of hypolipidemic therapeutic goals in many cases when this cannot be attained by high-dose statin monotherapy. The authors consider the results of trials of combination hypolipidemic therapy with simvastatin and ezetimibe performed as basic ones done in both previous and recent years.

[Influence of intensive hypolipidemic therapy on blood concentration of lipoprotein-associated phospholipase A2 in patients with ischemic heart disease].

AIM: To assess the impact of combined treatment with simvastatin and ezetimibe or treatment with simvastatin only on lipoprotein-associated phospholipase A2 in patients with ischemic heart disease. METHODS: One hundred patients with angiographically documented coronary atherosclerosis took part in the investigation. Lp-PLA2 mass and cholesterol fractions were determined at baseline and after 6 months of treatment. Lp-PLA2 mass was determined by enzyme immunoassay method, using two highly specific monoclonal antibodies. RESULTS: Combined treatment with ezetimibe and simvastatin led to significantly greater declines in Lp-PLA2 and cholesterol fractions compared with treatment only with simvastatin: Lp-PLA2 decreased by 46 vs 38%, total cholesterol by 35 vs 28%, LDL cholesterol by 50 vs 40%, respectively (p<0.05). Combination therapy with ezetimibe and simvastatin 20 and 40mg/day proved to be as effective as monotherapy with simvastatin 80 mg/day on the effect on Lp-PLA2 mass and cholesterol fractions (p<0.05). Lp-PLA2 correlated positively with total cholesterol (r=0.28) and LDL-C (r=0.33). CONCLUSIONS: Combined treatment led to greater reduction of total cholesterol and LDL-C, as well as significantly reduced level of Lp-PLA2 mass. The latter can be considered as target for suppression of inflammation and achievement of stabilization of atherosclerotic plaque.

[An experience of the use of a curative method of cardiac shock wave therapy in patients with ischemic heart disease].

Aim of the study was to assess effects of cardiac shock wave therapy (CSWT) in patients with coronary artery disease (CAD) with refractory stable angina pectoris. Seventeen CAD patients with refractory II-IV class angina (3 women and 14 men, mean age 67.4+/-8.6 years) received the course of 9 procedures of CSWT. All patients had I-III New York Heart Association (NYHA) class congestive heart failure. Before and after CSWT medical examination with life quality assessment by means of the Minnesota Living Questionnaire, echocardiography, veloergometry, myocardial perfusion imaging with single-photon emission computed tomography (SPECT) using 99M-Tc-methyl-iodine-benzyl-guanydin (MIBG) and Holter ECG monitoring was performed. The dynamics of pro-angiogenic factors (VEGF, HGF, FGF-) were also measured by ELISA, and of brain natriuretic peptide (Nt-proBNP) by the electrochemoluminescence method. Most patients (80%) had significant life quality (<0.01) and myocardial perfusion improvement. Episodes of angina pectoris and nitrate intake were more than twice decreased. There was a significant increase in exercise tolerance (p<0.01). Holter ECG monitoring showed decreasing of an average heart rate (p<0.02); no worsening of previous cardiac arrhythmias was observed. The significant (p<0.05) decreases in plasma Nt-proBNP and increases in VEGF concentration were revealed after CSWT. CSWT procedures were well tolerated. The results of our study confirm high effectiveness and safety of CSWT in complex treatment of patients with CAD, resistant angina pectoris, including patients after myocardial revascularization and with heart failure.

[Clinical role of lipoprotein-associated phospholipase A2].

Inflammation plays an important role in origin and progression of atheromatous plaque. Lipoprotein-associated phospholipase A2 (Lp-PLA2) is considered a biomarker of inflammation and a predictor of vascular events. Lp-PLA2 is an enzyme secreted by leukocytes and associated with circulating lipoproteins and macrophages in atherosclerotic plaques. Lp-PLA2 hydrolizes phospholipids of oxidized low density lipoproteins and generates two proinflammatory mediators, lysophosphatidylcholine and oxidized nonesterified fatty acids, which play a major role in the development of atherosclerotic lesions, myocardial infarction and ischemic stroke. Recently the first publications appeared about selective inhibitor of phospholipase A2 - darapladib as a novel therapeutic approach for the treatment of patients with coronary artery disease. However, first results need to be confirmed by ongoing large long-term randomized clinical trials.

[Trends in the risk factors and signs of subclinical atherosclerosis in subjects at low and moderate risk according to the SCORE scale in different medical management tactics: two-year follow-up results].

AIM: To comparatively analyze the following parameters of the subclinical manifestations of atherosclerosis: carotid intima-media thickness (IMT), the presence and number of carotid atherosclerotic plaques (ASP), ankle brachial pulse wave velocity (ABPWV) in patients from 2 (active and conventional observation) groups at low and moderate risks according to the SCORE scale in two-year outpatient practice. SUBJECTS AND METHODS: A screening could select 600 able-bodied persons (445 women and 155 men) aged 30 to 65 years at low and moderate risks (according to the SCORE scale without atherosclerosis-associated diseases who were divided into 2 groups: A) active observation (n =400) and B) conventional medical management tactics (n = 200). Five hundred and seven (85%) persons (339 in Group A and 168 in Group B) completed the study following 2 years. Carotid duplex scanning, computed sphygmography, and biochemical tests for blood lipid composition were performed. The delta index (%) calculated by the special formula, by subtracting the results during the first visit from those obtained 2 years later, was used to statistically analyze the time course of changes in the parameters under study. RESULTS: Delta IMT (%) statistically significantly increased in Group B men as compared to that in Group A men (p = 0.042). The delta parameter of total carotid stenosis, which reflected the percentage of the latter, proved to be high in both Group B women and men (p = 0.0001) and the persons with a larger number of ASP were statistically significantly more in Group B (p = 0.035). Delta ABPWV (%) was also greater in Group B (p = 0.001). CONCLUSION: Just after 2 years, the active medical observation tactics in patients at low and moderate risks (according to the SCORE scale) can result in a reduction in the rate of subclinical atherosclerosis progression in the carotid artery.