[Patent foramen ovale as the cause of recurrent embolic strokes. Case report].

А clinical case of a young patient with recurrent ischemic strokes is presented. The problems of diagnostic embolic strokes are discussed. We set out the algorithm for identifying patients, in whom patent foramen ovale is the most probable cause of embolic stroke. Detailed consideration of imaging diagnostic methods possibility is included. Hypothesis of probable source of cardioembolism from patent foramen ovale is presented. Recommendations for the secondary prevention of recurrent ischemic stroke, associated with patent foramen ovale, are provided. We also considered the issues of antithrombotic treatment.

Monomeric form of C-reactive protein in the assessment of the residual inflammatory cardiovascular risk in patients with subclinical carotid atherosclerosis.

Aim      To study the relationship between monomeric C-reactive protein (mCRP) and the progression of asymptomatic carotid atherosclerosis in patients with a moderate risk for cardiovascular diseases (CVD) as assessed with the SCORE model.Material and methods  The study included 80 men and women aged 53.1±5.8 years assigned to the category of a moderate risk for CVDs by the SCORE model with a low-density lipoprotein cholesterol (LDL-C) level of 2.7-4.8 mmol/l and asymptomatic, hemodynamically insignificant (<50% luminal narrowing) carotid atherosclerosis according to ultrasonic data. All patients were prescribed atorvastatin to achieve a LDL-C level <2.6 mmol/l. After 7 years of follow-up, ultrasonic examination of carotid arteries was performed, and concentrations of high-sensitivity C-reactive protein (hsCRP) and mCRP were measured.Results A concentration of LDL-C <2.6 mmol/l was achieved in all patients. The progression of atherosclerosis as determined by an increased number of atherosclerotic plaques (ASPs), was observed in 45 (56 %) patients. At 7 months of follow-up, concentrations of cCRP were higher in the group of patients with progressive carotid atherosclerosis, while the levels of hsCRP did not differ between the groups. Increased mCRP concentrations were associated with changes in variables of the "atherosclerotic load", including the number of ASPs, total ASP height, and the intima-media thickness (IMT). In patients with a median mCRP concentration of 5.2 [3.3; 7.1] µg/l and more, the increases in mean ACP number and total ASP height were considerably higher than in patients with mCRP concentrations lower than the median (3.9 and 2.7 times, respectively), whereas the odds ratio for the progression of asymptomatic carotid atherosclerosis was 5.5 (95 % confidence interval, CI: 2.1-14.6; p=0.001). ROC analysis showed that the concentration of hsCRP had no predictive value for prognosis of asymptomatic carotid atherosclerosis (p=0.16), while the area under the ROC curve (AUC) for mCRP was 0.75±0.056 (95 % CI: 0.64-0.86; p=0.001).Conclusion      According to the results of 7-year follow-up, the plasma concentration of mCRP was significantly higher in patients with an increased number of ASPs than in patients without this increase. An increased level of mCRP may indicate a higher inflammatory risk of CVD.

Endovascular repair of the aorti arch. / Éndovaskuliarnoe protezirovanie dugi aorty.

AIM: The study was aimed at assessing the in-hospital results of aortic arch endoprosthetic repair using different variants of endovascular supraaortic debranching. PATIENTS AND METHODS: The analysis included 27 patients subjected within the framework of aortic arch endoprosthetic repair to various types of supraaortic endobranching, including the technique of parallel prostheses and implantation of fenestrated stent grafts. We analysed the clinical and morphological status of patients prior to operation, peculiarities of the intervention (type of debranching and Ishimaru's classification zones in which the reconstruction was performed) and in-hospital results of treatment. RESULTS: The patients' mean age amounted to 66 years. The main nosology (70%) was an aortic aneurysm. Nearly in 30% of cases, the operation was performed emergently for acute aortic syndrome. The main causes of refusal from the traditional prosthetic repair included chronic kidney disease (22.5%), chronic obstructive pulmonary disease (11%), acute cerebral ischaemia within the previous 6 months (15%). The technical success rate of the operation was achieved in 100% of cases. The average duration of the intervention amounted to 226 min, with the mean blood loss equalling 355 ml. The majority of reconstructions were performed in zones 1 and 2 according to Ishimaru (59 and 33%, respectively), in 2 (7%) patients prosthetic repair was performed in zone 0. The total number of the aortic branches involved into reconstruction amounted to 45. Intervention-related complications included 3 (11%) cases of acute cerebral circulation impairment, 2 (7.4%) aortic branch occlusions, and 1 (3.7%) type II endoleak. The in-hospital and 30-day mortality rates amounted to 3.7 and 7.4%, respectively. CONCLUSION: Aortic arch endoprosthetic repair using supraaortic endobranching is considered to be an effective alternative method of treatment for patients with various pathology of the aortic arch and contraindications to traditional prosthetic repair involving artificial blood circulation.

Factors of Progression and Occurrence of Atherosclerosis in Rheumatoid Arthritis.

Aim      To determine in a prospective study factors of progressive atherosclerotic lesion of blood vessels in patients with rheumatoid arthritis (RA).Material and methods  This prospective study included 124 patients with RA and suspected ischemic heart disease (IHD) and 30 patients with IHD (comparison group) aged 58 [52; 63] years. On enrollment to the study and at 3 years of follow-up, all patients underwent clinical and instrumental examination according to European and Russian guidelines for diagnosis and treatment of stable IHD (2013), including coronography as indicated. For all RA patients of the comparison group, risk factors (RF) were evaluated, including arterial hypertension, smoking, excessive body weight, family history of cardiovascular diseases (CVD), diabetes mellitus, and dyslipidemia. The following laboratory data were evaluated: blood count; biochemistry, including total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides (TG), rheumatoid factor (RhF), cyclic citrullinated peptide antibodies, and high-sensitivity C-reactive protein (hsCRP). Proinflammatory cytokines, including interleukin (IL)-1ß, IL-6, and tumor necrosis factor-α (TNF- α), were measured in RA patients once, at 3 years of follow-up.Results Incidence of FRs for CVD was similar in RA patients and in the comparison group. Median RA duration before inclusion into the study was 11 years, and median DAS28 index score was 3.8. Incidence of dyslipidemia due to increased TC, LDL-C, and HDL-C was higher for RA patients at baseline. The LDL-C goal (<1.8 mmol/l) was achieved only in 3 (10 %) patients of the comparison group and 10 (8 %) RA patients. RA patients had higher levels of the inflammation indexes, hsCRP (0.75 mg/dl vs. 0.16 mg/dl; p<0.05) and erythrocyte sedimentation rate (ESR) (15 mm/h vs. 11.5 mm/h; p<0.05). In the RA group at baseline, atherosclerotic plaques with carotid artery (CTA) stenosis of 20% or more were found in 94 (77 %) patients; in 3 of them, CA stenosis was >50%. Patients with RA frequently had unchanged or slightly changed coronary arteries (CA) (47% of patients), and less frequently they had hemodynamically significant multi-arterial coronary atherosclerotic lesions (7 % vs. 57 % of patients in comparison group). At 37.5 months, 21 (23 %) of 94 RA patients had progressive atherosclerosis in CA and/or CTA; 12 (13 %) RA patients had only progressive CA atherosclerosis; 7 (8 %) had only progressive CTA atherosclerosis; and 2 (2 %) had simultaneous progression of CA and CTA atherosclerosis. Two groups of RA patients were formed, with the progression of atherosclerosis (n=21) and without the progression of atherosclerosis (n=69). RFs for the development/progression of atherosclerosis in RA patients included smoking, family history of CVD, and duration of the disease. Levels of lipids did not differ. Levels of proinflammatory cytokines (IL-1ß, IL-6, TNF-α) were higher in RA patients with progressive atherosclerosis. No effects of the anti-rheumatic therapy on the progression of atherosclerosis were observed.Conclusion      Progression of atherosclerosis in RA remains in disease with low and moderate activity during the anti-rheumatic and hypolipidemic treatment. The development of atherosclerosis in RA is determined by lipid, inflammatory, and immune disorders.

The severity of internal carotid artery stenosis is associated with the circulating Th17 level.

AIM: Immune and inflammatory reactions contribute to the progression of atherosclerosis. The walls of the different arteries and segments of the arteries have heterogeneous haemodynamic and histological features. We aimed to explore the relationship between the circulating T-cell subsets and the abundance of carotid atherosclerosis in different segments of carotid arteries. METHODS: 70 patients underwent ultrasound duplex scanning to determine the degree of stenosis of the common carotid artery (CCA), the CCA bifurcation or the internal carotid artery (ICA). The blood frequencies of T-, B-, NK-cells, regulatory T cells (Treg), activated T-helpers (Th), IL10-producing Th, Th1 and Th17, as well as blood levels of hsCRP, sCD25, IL10 and IL17a were assessed. RESULTS: The frequencies of Th17 were increased in patients with ICA stenosis >35% and >50% vs. patients with ICA stenosis <35%. Th17 blood level ≥0.55 % of lymphocytes was associated with more severe stenosis of ICA (OR 4.3 (1.0-17.6), p < 0.05 for ICA stenosis of 35-50% and 6.8 (1.3-35.0), p < 0.05 for ICA stenosis >50%). BMI positively correlated with the CCA bifurcation stenosis degree (r = 0.33, p < 0.05). CONCLUSION: The severity of ICA stenosis can be associated with the circulating Th17 level.

Rate of Complications at Early Removal of Compression Bandage After Transradial Coronary Angiography.

PURPOSE: to compare rates of access site complications at early (after 4 hours) and traditional (after 24 hours) removal of a compression bandage after diagnostic transradial (TR) coronary angiography (CA) in patients not receiving anticoagulants. MATERIALS AND METHODS: We included into this study 392 patients (mean age 63±8.7 years, 62.8% men) who underwent transradial coronary angiography. Patients were divided into 2 groups. In group 1 patients (n=221) compression bandage was removed from puncture site in 4 hours after procedure with subsequent control of radial artery patency using presence of pulse metric curve during ulnar artery compression (the reverse Barbeau test with pulse oximeter). In patients of group 2 (n=171) compression band was removed after 24 hours. In both groups control of radial artery patency was carried out after 24 hours using the reverse Barbeau test. Upon detection of radial artery occlusion (RAO) ultrasound imaging of the forearm arteries was performed. RESULTS: No RAO was detected in group 1 while in group 2 number of detected RAO was 15 (8.8%) (р<0.05). Rates of hematomas at puncture site were not significantly different. Puncture site bleeding after band removal requiring repeated banding occurred in 1 patient of group one (0.6%); no such cases were registered in group 2 (p>0.05). CONCLUSION: Compared with traditional method early removal of compression bandage after TR CA was associated with lower rate of RAO.

[Dynamics of asymptomatic atherosclerosis of carotid arteries depending on the achieved level of cholesterol in moderate-risk patients]. / Dinamika bessimptomnogo ateroskleroza sonnykh arterii v zavisimosti ot dostignutogo urovnia kholesterina u patsientov s umerennym riskom.

The study was aimed at assessing the dynamics of asymptomatic atherosclerosis of carotid arteries (CA) depending upon the achieved level of low-density lipoprotein cholesterol (LDLC) in patients with moderate total risk by the SCORE scale. We followed up a total of eighty-two 40-to-65-year-old patients with the LDLC level above 2.6 mmol/l, being at moderate total risk by the SCORE scale and having symptom-free atherosclerosis of the extracranial portion of brachiocephalic arteries (up to 50% narrowing of their lumen) as diagnosed by duplex scanning. The patients were randomly divided into two groups. Group One patients (n=41) received therapy with atorvastatin in order to achieve the LDLC level less than 1.8 mmol/l. Group Two patients (n=41) were treated in order to achieve the LDLC level below 2.6 mmol/l. At 12 months of follow up we compared the dynamics of carotid atherosclerosis (change in the number, total height, structure, echogenicity, as well as the state of the surface of atherosclerotic plaques, alteration of the thickness of the CA intima-media complex). Group Two patients were found to have an increase in the number and average sum of the heights of atherosclerotic plaques. An increase of the maximum thickness of the intima-media complex of the wall of the right and left CA was more pronounced as compared with that in Group One patients. Aggressive hypolipidemic therapy aimed at achieving the LDLC level below 1.8 mmol/l turned out to be more effective in slowing down the progression of asymptomatic carotid atherosclerosis in patients with moderate cardiovascular risk than therapy targeted at achieving the LDLC level below 2.6 mmol/l.

[Subpopulation Composition of CD4+ T-lymphocytes as Factor Contributing to the Progression of Atherosclerosis of Carotid Arteries].

AIM: to assess prognostic significance of blood content of regulatory and effector T-lymphocytes for progression of atherosclerosis (AS) of carotid arteries. MATERIAL AND METHODS: We enrolled in this study 33 men with various severity of carotid AS. Carotid artery duplex scan was done at admission and in 1 year after enrollment. AS progression was defined as appearance of novel stenosis in common or internal carotid artery or more or equal 5% increase of preexisting stenosis. Peripheral blood lymphocyte phenotyping was performed by direct immunofluorescence and flow cytometry at the enrollment. T-helpers (Th) 1 were identified as CD4+IFNgamma+ cells, Th2 - CD4+IL4+, activated T-cells (T-act) - D4+CD25lowCD127high, regulatory T-cells (T-reg) - D4+CD25highCD127 low and CD4+FoxP3+, Th17 - CD4+IL17a+ cells. RESULTS: Progression of carotid AS was observed in 18 patients. Basal values of Th17 were higher while ratio T-reg/Th17 was lower in patients with compared with those without AS progression. ROC-analysis showed high sensitivity and specificity of blood levels of Th17, T-act and T-reg/Th17 ratio for carotid AS progression during one year in patients with low density lipoprotein cholesterol (LDLCH) level below 3.5 mmol/l. CONCLUSION: The imbalance between circulating levels of regulatory T-cells and T-helpers 17 with the prevalence of proinflammatory T-helpers 17 may reflect a predisposition for carotid AS progression, what also refers to patients with relatively low LDLCH.

[Carotid Plaque Instability in Patients With Acute Coronary Syndrome as Assessed by Ultrasound Duplex Scanning].

AIM: to study carotid plaques structure in patients with acute coronary syndrome by ultrasound duplex scanning. MATERIALS AND METHODS: We included in this study143 patients with acute coronary syndrome (ACS) aged 32-83 years and 28 patients with documented coronary heart disease (CHD) aged 46-83 years. Duplex scanning of carotid arteries was carried out with Philips iU22 ultrasound system and L9-3 linear array transducer. Atherosclerotic plaques in CCA, CCA bifurcation, and ICA from right and left side were investigated. Off-line analysis of B-mode images and plaque gray scale median (GSM) was performed with computer semiautomated workstation MultiVox. RESULTS: 378 plaques of ACS and 59 plaques of CHD patients were studied. We assessed traditional (heterogenous structure, hypoechogenic component, irregular plaque surface) as well as additional (positive remodeling, "layered" structure of plaque, local calcification) criteria of plaque instability. In ACS compared with CHD group there were more plaques with hypoechogenic component (43.4 and 28.8%, p=0.0459), heterogenous structure (77.8 and 64.4%, p=0.0327), irregular surface including irregularities more than 2.0 mm (22.5 and 6.8%, p=0.0048, respectively). There was significant difference in "layered" structure (55.7 and 35.8%, p=0.0011) and insignificant difference in positive remodeling (16.3 and 7.5%, p=0.06, respectively). There were no differences of GSM value (53.1 and 57.2, p=0.24) and local calcification (23.2 and 24.5%, p=0.23, respectively). CONCLUSION: In our study ultrasound duplex scanning revealed that signs of plaque instability in carotid arteries in patients with ACS were more frequent than in patients with stable CHD. The newly introduced parameter "layered" structure of atherosclerotic plaque was found to be most significant.

Specific Lipoprotein(a) apheresis attenuates progression of carotid intima-media thickness in coronary heart disease patients with high lipoprotein(a) levels.

BACKGROUND: To date, there have been no studies evaluating the effect of isolated lipoprotein(a) (Lp(a)) lowering therapy on carotid atherosclerosis progression. METHODS: We enrolled 30 patients who had coronary heart disease (CHD) verified by angiography, Lp(a) level ≥50 mg/dL, and low density lipoprotein cholesterol (LDL-C) level ≤2.6 mmol/L (100 mg/dL) on chronic statin therapy. Subjects were allocated in a 1:1 ratio to receive apheresis treatment on a weekly basis with immunoadsorption columns ("Lp(a) Lipopak"(®), POCARD Ltd., Russia) added to atorvastatin, or atorvastatin monotherapy. The primary efficacy end-point was the change from baseline in the mean intima-media thickness (IMT) of the common carotid arteries. RESULTS: After one month run-in period with stable atorvastatin dose, LDL-C level was 2.3 ± 0.3 mmol/L and Lp(a) - 105 ± 37 mg/dL. As a result of acute effect of specific Lp(a) apheresis procedures, Lp(a) level decreased by an average of 73 ± 12% to a mean of 29 ± 16 mg/dL, and mean LDL-C decreased by 17 ± 3% to a mean of 1.8 ± 0.2 mmol/L. In the apheresis group, changes in carotid IMT at 9 and 18 months from baseline were -0.03 ± 0.09 mm (p = 0.05) and -0.07 ± 0.15 mm (p = 0.01), respectively. In the atorvastatin group no significant changes in lipid and lipoprotein parameters as well as in carotid IMT were received over 18-month period. Two years after study termination carotid IMT increased by an average of 0.02 ± 0.08 mm in apheresis group and by 0.06 ± 0.10 mm in the control group (p = 0.033). CONCLUSION: Isolated extracorporeal Lp(a) elimination over an 18 months period produced regression of carotid intima-media thickness in stable CHD patients with high Lp(a) levels. This effect was maintained for two years after the end of study. TRIAL REGISTRATION: Clinicaltrials.gov (NCT02133807).

[Structural and functional status of arteries in young and middle-aged men with ischemic heart disease].

Aim of the study was to determine whether structural and functional status of arteries differ between young and middle-aged men with ischemic heart disease (IHD). A total of 78 men aged 28 to 50 years were recruited in this study: 49 with angiographically proven obstructive atherosclerosis of coronary arteries, 29 without clinical manifestations of IHD (control group). Those with arterial hypertension, diabetes mellitus or marked hypercholesterolemia (LDL cholesterol more or equal 4.5 mmol/l) were excluded from the study. All patients underwent carotid ultrasound, endothelial function, and arterial stiffness measurements. Patients with IHD more often had multiple carotid plaques (86.7% vs 13.7%, p<0.001), and increased aortic pulse wave velocity (PWV) assessed by ultrasound duplex scanning (53.1% vs. 24.1%, p=0.02). Aortic PWV was related to the severity of coronary atherosclerosis. Presence of a carotid intima-media thickness more or equal 0.9 mm and abnormal flow-mediated dilatation (FMD) of the brachial artery was not significantly different between the groups.

[Comparative characteristics of the possibilities of imaging techniques (magnetic resonance imaging and 3D ultrasound study) in the qualitative estimation of atherosclerotic plaque volume].

OBJECTIVE: To estimate the possibilities of using three-dimensional ultrasound study (3D USS) in the diagnosis of the sizes and structure of an atherosclerotic plaque (ASP). MATERIAL AND METHODS: The data obtained by examination of 20 heterogeneous ASPs in the carotid artery wall, by applying 3D USS and magnetic resonance imaging (MRI), were compared. Intra- and interoperator reproducibilities were assessed by the Bland-Altman method; the volume of each plague was measured by two (contour and ellipse) methods. The contour method was used to estimate all plagues; the ellipse method was applied to 13 of the 20 plagues, which was due to the shape of ASPs that rarely had an ellipsoid shape. RESULTS: Intra- and interoperator reproducibilities in ASP volume estimation by 3D USS was as follows: with the use of contour and ellipse algorithms, the coefficient of variation was 7.72 and 3.77%, respectively; with these algorithms, the interoperator reproducibility was 8.18 and 6.21%, respectively; the derived values were not greater than those allowed for medical studies (10%). The coefficients of variations for MRI in the estimation of ASP sizes were significantly higher for inter- and intrareproducibilities (68.82 and 43.4%, respectively). CONCLUSIONS: The results of this investigation agree with thedata available in the literature and support that 3D USS is an effective diagnostic me-hod in evaluating the magnitude of an ather-sclerotic process.

[Nonspecific inflammation and structural changes in the arteries of hypertensive males at high and moderate risk for cardiovascular events].

AIM: To study relationships between nonspecific inflammation (NI) of the arterial wall and its structural changes in Stages I-II hypertensive disease (HD) males at moderate and high risks of cardiovascular events (CVE). SUBJECTS AND METHODS: Sixty hypertensive males aged 30 to 65 years (mean age 44 +/- 2 years), including 35 patients with grade 1 arterial hypertension (AH) and 25 with grade 2 AH at moderate and high risks of CVE, were examined. The concentrations of C-reactive protein (CRP) and methylglyoxal (MG) were measured. Pulse wave propagation velocity (PWPV) and ankle brachial index (ABI) were studied. Normal PWPV values were calculated in terms of gender and age features. RESULTS: The examined HD group showed a positive correlation of PWPV with systolic blood pressure over 24 hours (r=0.39; p < 0.02) and age (r = 0.47; p < 0.01). In smoking and nonsmoking hypertensive men, PWPV differences failed to achieve statistical significance (14.05 +/- 0.53 and 13.07 +/- 0.38 m/sec, respectively). PWPW was found to be correlated with CRP values weakly (r = 0.31; p = 0.07) and with MG levels moderately (r = 0.62; p < 0.01); there were also positive relationships of ABI to the levels of CRP (r = 0.50; p < 0.01) and MG (r = 0.46; p < 0.05). There was a positive correlation between CRP and MG levels (r = 0.45; p = 0.01). CONCLUSION: In middle-aged men with grades 1-2 AH at moderate and high risks of CVE, NI processes are not only related to MG metabolism, but also they have a substantial effect on the elastic properties of the wall of predominantly muscle-elastic type arteries, which validates the hypothesis of the involvement of NI processes in the course of HD.

[The biological reaction of inflammation, methylglyoxal of blood plasma, functional and structural alterations in elastic type arteries at the early stage of hypertension disease].

The article deals with studying of the relationship between biologic reaction of inflammation with glycosylation reaction and content of methylglyoxal in blood serum. The positive correlation between pulse wave velocity and content of methylglyoxal, C-reactive protein in intercellular medium and malleolar brachial index value was established. This data matches the experimental results concerning involvement of biological reaction of inflammation into structural changes of elastic type arteries under hypertension disease, formation of arteries' rigidity and increase of pulse wave velocity. The arterial blood pressure is a biological reaction of hydrodynamic pressure which is used in vivo by several biological functions: biological function of homeostasis, function of endoecology, biological function of adaptation and function of locomotion. The biological reaction of hydrodynamic (hydraulic) pressure is a mode of compensation of derangement of several biological functions which results in the very high rate of hypertension disease in population. As a matter of fact, hypertension disease is a syndrome of lingering pathological compensation by higher arterial blood pressure of the biological functions derangements occurring in the distal section at the level of paracrine cenoses of cells. The arterial blood pressure is a kind of in vivo integral indicator of deranged metabolism. The essential hypertension disease pathogenically is a result of the derangement of three biological functions: biological function of homeostasis, biological function of trophology - nutrition (biological reaction of external feeding - exotrophia) and biological function of endoecology. In case of "littering" of intercellular medium in vivo with nonspecific endogenic flogogens a phylogenetically earlier activation of biological reactions of excretion, inflammation and hydrodynamic arterial blood pressure occur. In case of derangement of biological function of homeostasis, decreasing of perfusion even in single paracrine cenoses and derangement of biological function of endoecology ("purity" of intercellular medium) the only response always will be the increase of arterial blood pressure.

[Pleiotropic effects of nicotinic acid therapy in men with coronary heart disease and elevated lipoprotein(a) levels].

PURPOSE: To assess effects of niacin on risk factors of atherosclerosis in men with coronary heart disease (CHD) and high lipoprotein(a) [Lp(a)] levels. MATERIAL AND METHODS: Sixty men (mean age 54+/-6 years) with angiographic evidence of CHD were randomized into two groups. Active group (n=30) received extended release nicotinic acid 1500 mg, control group consisted of remaining 30 patients. All patients received basic therapy with atorvastatin 10-40 mg qd. Blood samples were collected for total cholesterol (TC), triglycerides (TG), high density lipoprotein cholesterol (HDL-C), Lp(a), lipoprotein-associated phospholipase A2 (Lp-PL-2), high-sensitivity C-reactive protein (hsCRP), complex of tissue-type plasminogen activator with plasminogen activator inhibitor type 1 (tPA/PAI-1). Carotid intima media thickness (CIMT) was measured at baseline and after 6-months therapy. RESULTS: There was no statistically significant difference between the groups in the clinical and biochemical characteristics. During the study lipid profile data were within the target levels. In the active group median percent decrease of Lp(a) level was 23% (from 84+/-40 to 67+/-25 mg/dl after 6 weeks and up to 65+/-37 mg/dl after 6 months of treatment, p<0.01); LDL-C, TG, tPA/PAI-1, and Lp-PL-2 mass levels decreased by 25, 20, 25, and 32%, respectively; HDL-C increased by 16% (p<0.05 vs baseline, respectively). Nicotinic acid treatment produced statistically significant reduction nicotinic acid of the mean CIMT (right: 0.83+/-0.16 vs 0.77+/-0.17 mm, p<0.05; left: 0.88+/-0.21 vs 0.82+/-0.17, p<0.05). In control group no changes of CIMT or blood tests were observed. CONCLUSION: In men with CHD and Lp(a) excess of addition to atorvastatin results in regression of CIMT on an average of 0.06 mm in 6 months. Such rapid and significant effect on the arterial wall structure can be attributed to the complex influence of nicotinic acid on Lp(a), lipids, Lp-PL-2 and thrombogenic factors. This is the first study providing the evidence of using Lp(a) as one of therapeutic targets in patients with high Lp(a) levels for achieving beneficial effect on a surrogate marker of atherosclerosis.

[Circulating endothelial progenitor cells and vascular endothelial dysfunction].

Endothelial progenitor cells (EOCs) play a key role in reendothelization of injured blood vessels and in endogenous neovascularization of ischemic tissues. In the presented article, the mechanisms of endothelial function impairment and the role of EPCs in their correction are discussed. The objective of our study was to investigate the number of CD34+ cells in patients with different forms of ischemic heart disease (IHD) and association of this parameter with endothelial dysfunction. We quantified the numbers of CD34+ cells by flow cytometry, measured the brachial artery flow-mediated vasodilatation (FMD) and the common carotid artery intima-media thickness (IMT) by ultrasonography in 28 patients with ST-segment elevation acute coronary syndromes (ACS), in 33 patients with stable angina (SA) and in 17 subjects without IHD (control group). The level of CD34+ cells was lower in both groups of IHD, especially in patientes with ACS, and was associated with endothelial dysfunction. We suppose that CD34+ cells contribute to reparation of injured endothelium and the reduction of their numbers in peripheral blood indicates endothelial state.

[The study of peculiarities of immunotropic action of statins in chronic heart failure of various etiology].

AIM: To study features of statin therapy in patients with heart failure (HF) of different etiology on immune system. MATERIAL AND METHODS: The basic markers of immune activation in 43 patients with chronic heart disease (CHD) and HF in New York Heart Association (NYHA) class I to IV were studied. Mine age was 48 +/- 8 years (from 33 to 64 years). 43 patients with dilated cardiomyopathy (DCM) and HF were also observed. Mine age was 43 +/- 10 years (from 22 to 61 years). Parameters of systolic and diastolic left ventricle (LV) function were measured. Also non invasive methods for evaluation of endothelial function were used. Concentrations of hsCRP, IgG, IgA, IgM were measured using commercially available kits. IL 6, IL 8, sIL 2R, IL 18, IL 10, IFN Y, endothelin levels were measured using enzyme linked immunosorbent assay method. RESULTS: Statin therapy has immunomodulation effect in patients with heart failure any etiology. This effect depends on etiology of HF. In CHD patients the decreasing of IFN Y, IL 8, sIL 2R, hsCRP and increasing of IL 18, IL 6 levels were observed. In DCM patients the decreasing of IL 8, IL 18, sIL 2R and increasing of IL 10 were observed. There was significant clinical improving in patients with DCM and HF after statin therapy. But there were no changes of endothelial function in patients with CHD and DCM. There were no changes of LV function in patients with CHD. So statin therapy may reduce level of proinflammatory mediators but not fully control inflammation process in patients with HF of different etiology.

[Randomized FARVATER study. Part 2. Effect of atorvastatin on endothelial function, distensibility and stiffness of vascular wall].

AIM: To elucidate effect of two doses of atorvastatin (10 and 20 mg/day) on endothelial function, distensibility and stiffness of vascular wall. MATERIAL AND METHODS: Patients (n=50) with documented ischemic heart disease and hyperlipidemia were randomized to 10 or 20 mg/day of atorvastatin (Atoris, KRKA). Endothelial function and common carotid artery wall distensibility and stiffness were assessed at baseline and after 12 and 24 weeks of treatment. RESULTS: Administration of both 10 and 20 mg/day doses of atorvastatin for 6 weeks was associated with significant lowering of total cholesterol (CH), triglycerides (TG) and low density lipoprotein (LDL) CH (24.5, 18.4, 34.9% and 29.1, 28.2, 40.9%, respectively). After 24 weeks LDL CH lowering from baseline reached 34.9 and 43.9% (p<0.001) and that of TG - 22 and 15%, in 10 and 20 mg/day groups, respectively. There were no significant differences between 10 and 20 mg/day groups in baseline values of endothelium dependent vasodilation (EDV), carotid artery distensibility and stiffness (7.28 and 6.64%, 21.60 and 20.15, 8.04 and 9.19 U, in 10 and 20 mg/day groups, respectively). After 3 months of treatment there occurred significant 38.4% (10 mg/day) and 45.4% (20 mg/day) increases of EDV. Significant 27.6% (10 mg/day) and 28.8% (20 mg/day) enhancement of vascular distensibility was noted after 24 weeks. Vascular wall stiffness decreased 33.4% (p=0.008) and 31.3% (p=0.002) in 10 and 20 mg/day groups, respectively.

[Randomized FARVATER Study. Part 1. Effect of 10 and 20 mg/day atorvastatin on levels of lipids, C-reactive protein, and fibrinogen in patients with ischemic heart disease and hyperlipidemia].

Main aim of the clinical study FARVATER was comparison of effects of 10 and 20 mg/day of atorvastatin on levels of lipids, high-sensitivity C-reactive protein (CRP), fibrinogen (F), and structural-functional state of vascular wall in patients with documented and primary hyperlipidemia (HLP). Fifty patients (mean age 60.8 years) with documented ischemic heart disease and HLP were randomized to continuous administration of 10 and 20 mg/day atorvastatin for 24 weeks. Initial levels of total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDLCH), high density lipoprotein cholesterol (HDL CH), CRP and F were 6.22, 1.86, 4.15, 1.24 mmol/l, 1.46 and 2.93 g/l, respectively. After 6 weeks lowering of TCH, TG and LDLCH was significant both in 10 (24.5, 18.4, and 34.9%, respectively) and 20 mg (29.1, 28.2, and 40.9%, respectively) groups. After 24 weeks TG levels decreased by 22 and 15% in 10 and 20 mg subgroups, respectively. Changes of HDLCH (+11 and +12% in patients treated with 10 and 20 mg, respectively) were not significant. There were no significant changes of CRP and F levels. Seven side effects (4%) were registered during 24 weeks; 2 were related to study drug (allergy and symptomless elevation of creatine kinase).

[Successful midodrin treatment for vasovagal syncopes accompanied by asystole]. / Uspechnoe lechenie midodrinom vazovagal'nykh obmorokov, protekaiushchikh s asistoliei.

Vasovagal syncopes (WS) are fainting fits whose manifestations are systemic vasodilation and bradycardia. The development of WS is frequently accompanied by short-term cardiac arrest. Recent data show that implantation of a cardiac pacemaker fails to prevent the development of fainting fits in these patients. On the basis of the pathogenesis of WS, the use of alpha-adrenomimetic midodrine is justifiable. The presented case demonstrates the successful use of the agent in the treatment of vasovagal syncope accompanied by asystole.