[Cardiovascular diseases and mannose-binding lectin].

The role of innate immunity factors in the pathogens of ACS is not well studied, although there is evidence in the literature about their impact on the course of cardiovascular diseases. Mannose-binding lectin (MBL)--one of the key factors of the humoral innate immune system that activates one of complement activation pathways. The literature suggests an ambiguous, complex role of MBL, which can in different clinical situations either improve the prognosis of patients, or be a risk factor for complications. MBL could potentially be relevant to all main links in the pathogenesis of coronary artery disease and myocardial infarction: inflammation, thrombosis, apoptosis, and so on. At different stages of atherogenesis, including the formation and destabilization of the atherosclerotic plaque, thrombosis, MBL may have a significant impact. The review analyzes currently available literature on the impact of MBL on atherosclerosis, ischemic heart disease and acute coronary syndrome. Moreover, in the review there is data on the role of MBL in physiological reactions in innate immunity, gene structure of MBL2 and possible mutations leading to deficiency of MBL in blood, and the role of MBL in the pathogenesis of various diseases.

[Level of mannose-binding lectin and phagocytic activity of leukocytes in patients with acute coronary syndrome].

UNLABELLED: Mannose-binding lectin (MBL) is a key component of innate immunity that starts one of the ways of complement activation. Factors of neutrophil activation are cell factors of innate and acquired immunity. AIM: to study MBL levels and factors of neutrophil activation in patients with acute coronary syndrome (ACS). METHODS: A total of 45 patients with ST elevation (STE) ACS and non ST-elevation (NSTE) ACS were enrolled in the study, 15 persons were age-matched controls. RESULTS. Compared with control group MBL level was higher in patients with ACS (52.7 vs 127.2 hg/ml, respectively, p = 0.07), and significantly higher in patients with NSTE ACS (52.7 vs. 164.7 hg/ml, p = 0.03). There was no difference between MBL levels in STE ACS and NSTE ACS patients. Patients with inferior myocardial infarction (MI) had significantly higher MBL level than those with anterior MI (182.8 -92.7 hg/ml, p = 0.02). Patients with concomitant diabetes had statistically higher MBL level than patients without diabetes (225 vs 100 hg/ml, OR 2.25, p = 0.03). MBL level was lower in patients with low (<40%) ejection fraction - 92.7 vs 148.9 hg/ml in patients with EF > or = 40% (p = 0.19). No difference of neutrophil activation factors between ACS patients and controls was found (phagocytic activity of neutrophils 74.5 vs 74.3%, phagocytic number 3.34 vs 4.36, phagocytic reserve 88 vs 85.5 in ACS and control group, respectively). CONCLUSION: Elevated innate immunity factor (MBL) level was associated with ACS, especially in patients with diabetes mellitus. No association between cell immunity factors with ACS was found.

[Invasive methods of detection of unstable atherosclerotic plaques in coronary arteries].

In most cases direct cause of acute coronary syndrome and sudden death is an intracoronary thrombus formed on a surface of unstable atherosclerotic plaque (UAP). The following are main characteristics of UAP: active inflammation; large lipid rich nucleus occupying a 40% of plaque volume; thin (< 65 mm) fibrous cap; erosions of intima over plaque; tear of plaque cap; superficially located calcium nodules; intraplaque hemorrhage. Visualization of UAP in coronary arteries is a very important direction in diagnostics. During recent years both invasive and noninvasive methods of detection of UAP have been actively developed. In this review we present main invasive techniques used for detection of UAP: intravascular ultrasound study with virtual histology; optical coherent tomography; near-infrared spectroscopy; thermography; intravascular magnetic resonance imaging; direct visualization by angioscopy. In the review we have covered main advantages and limitations of each invasive method of UAP detection and delineated perspectives of development of this direction.

[Factors influencing platelet aggregation in patients with acute coronary syndrome].

AIM: To study factors influencing platelet aggregation in patients with acute coronary syndrome (ACS). SUBJECTS AND METHODS: The investigation enrolled 147 patients with ACS. Their blood was sampled on days 1, 3-5, and 8-12 days after the onset of ACS. All the patients received acetylsalicylic acid (ASA) 300 mg on day 1, then 100 mg/day and clopidogrel 300-600 mg on day 1, then 75-150 mg/day. Platelet aggregation was analyzed in 65 patients on day 1 after ASA intake, but prior to clopidogrel therapy. The aggregation was induced by 5 and 20 pmol of ADP. RESULTS: With the use of clopidogrel 75 mg/day on day 3-5, platelet aggregation was reduced by 2.1 and 1.7 times for 5 and 20 µmol of ADP, respectively, as compared to day 1 (ASA without clopidogrel) and remained unchanged on days 8-12. Increasing the dose of clopidogrel up to 150 mg/day potentiated its antiaggregatory effect. On day 1 (ASA without clopidogrel), there was a direct correlation between platelet aggregation levels and mean platelet volume (MPV) (correlation coefficients (r), 0.526 (p < 0.001) and 0.368 (p = 0.015) for 5 and 20 µmol of ADP, and between platelet aggregation levels and glycoprotein (GP) IIb-IIIa (r = 0.387; p = 0.002 and r = 0.411 (p < 0.001) for 5 and 20 µmol of ADP. No similar correlations were found on days 3-5 and 8-12 of administration of ASA and clopidogrel. The genetic polymorphism of GP lIb-Illa (GP Ila Leu33Pro) was not noted to affect platelet aggregation. Examining the effects of genetic variations in cytochrome P450 isoform CYP2C19 (a clopidogrel metabolizer) revealed the enhanced aggregation stimulated with 20 µmol of ADP in the carriers of slowly clopidogrel-metabolizing haplotype of CYP2C19 (differences were found on days 3-5 as compared to rapidly and routinely metabolizing haplotypes). CONCLUSION: In the patients with ACS, platelet aggregation is influenced by MPV, GP IIb-IIIa levels, and CYP2C19 polymorphism and is not by GP IIb-IIIa polymorphism.

[The role of multispiral computed tomography in assessment of viability of the myocardium and prognostication of left ventricular remodeling in patients with ST-elevation myocardial infarction].

Aim of the study was to assess perfusion defect and viability of the myocardium by the method of multispiral computed tomography (MSCT) in patients with ST-elevation acute myocardial infarction (AMI) and to assess their prognostic role in development of remodeling of the left ventricle (LV). We included into the study 117 patients with AMI. MSCT with intravenous contrast enhancement was carried out on days 3-4 and at 12 months after AMI. In the arterial phase we estimated volume of myocardial perfusion defect, LV end diastolic and end systolic volumes (LVEDV and LVESV), and LV ejection fraction (EF). Three types of myocardial opacification were distinguished on tomograms in delayed phase of MSCT: type I - subendocardial residual defect (RD), type II - transmural RD, type III - transmural delayed hyper enhancement (DE). Patients were divided in 3 groups: (1) with subendocardial RD (n=63), (2) with transmural RD (n=28), (3) with transmural DE (n=26). Development of LV remodeling was registered if at repeat MSCT LVEDV increased more or equal 20% from baseline. In patients with signs of viable myocardium (group 1) volume of perfusion defect was substantially smaller than in patients with nonviable myocardium (groups 2 and 3): 1cm3 (0.4-2.4) vs. 7.3 cm3 (5.3-10.0) and 6.3 cm3 (5.0-15.0), respectively, p<0.001. Compared with groups 2 and 3 patients of group 1 more often were female (p=0.04), had inferior MI (p<0.001), and spontaneous reperfusion (p<0.001). After 12 months LV remodeling was registered in 19.3% of patients, all had signs of nonviable myocardium in more or equal 3 LV segments. In patients with perfusion defect more or equal 10 cm3 probability of development of LV remodeling exceeded 50%. Disturbances of perfusion abnormalities and number of nonviable LV segments were main predictors of LV remodeling.

[Endovascular closure of the left atrial appendage in patients with atrial fibrillation: review of modern data and own experience of application].

Atrial fibrillation (AF) is the most often disturbance of cardiac rhythm met in clinical practice. Long term therapy with anticoagulants is used for prevention of thrombi formation in left atrial appendage and consequent thromboembolism. However some patients have contraindications to this therapy. This article contains consideration of various alternative methods of prevention of thromboembolic complications in particular those 2 which are most widely used at present - percutaneous transcatheter isolation of left atrial appendage with Amplatzer Cardiac Plug () or Watchman Device. We present also data on own experience of the use of the ACP device.

[Comparison of characteristics of atherosclerotic plaques in patients with acute coronary syndrome and stable ischemic heart disease: data of multispiral computed tomography].

AIM: To elucidate possibilities of multispiral computed tomography (MSCT) for assessment of morphology of atherosclerotic plaques in coronary arteries of patients with acute coronary syndrome (ACS) or stable ischemic heart disease (SIHD). MATERIAL AND METHODS: Assessment of internal relief of coronary arteries and composition of atherosclerotic plaques was carried out in 85 patients with ACS and 41 patients with SIHD. MSCT was performed with the use of computed tomograph. Visual assessment included determination of plaque type (calcified, soft, and heterogeneous) and contour (regular, irregular). Quantitative assessment included determination of plaque density and index of remodeling. RESULTS: Among patients with ACS we found 194 plaques (60--soft, 72--heterogeneous, and 62--calcified). Plaques in symptom related compared with non-symptom related arteries had higher index of remodeling (1.4 +/- 0.3 and 1.2 +/- 0.2, respectively, p < 0.0001), and more frequently had irregular contour (60.0 and 12.8%, respectively, p < 0.0005). Soft plaques and plaques with irregular contour prevailed in ACS group (68.0%) while calcified plaques were more frequent in SIHD group (66.4%). Plaques with irregular contour were more frequent and index of remodeling was higher in ACS compared with SIHD group (33.5 vs 7.2%, p < 0.0005, and 1.3 +/- 0.2 vs 1.0 +/- 0.2, p < 0.001, respectively). CONCLUSION: According to MSCT data main characteristics of atherosclerotic plaques in patients with ACS were low density and inclusions of microcalcinates. Specific features of plaques in symptom related arteries were irregular contour and positive remodeling index.

[Value of allele gene polymorphism of the inflammation system for prognosis of patients with myocardial infarction].

In recent years levels of a number of inflammatory markers namely C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor (TNF) etc. are measured for the purpose of postinfarction risk evaluation. Dynamics of inflammatory markers concentrations can reflect processes occurring in atherosclerotic plaque and coronary arteries. Concentrations of inflammatory markers depend particularly on genetic factors affecting transcription levels of individual genes. This data suggest that genotypes which determine increased inflammatory markers levels in blood can increase risk of unfavorable events after myocardial infarction. STUDY PURPOSES: Analysis of influence of allelic polymorphisms C1444T of CRP gene (rs1130864), G(-174)A of IL6 gene (rs1800795), A(-308)G of TNF gene (rs1800629), G252A of LTA gene (rs909253), (-509) of TGFB1 gene (rsl800469) and delta32 (w/d) of CCR5 gene (rs333) on development of cardiac unfavorable events in Russian patients with MI during two years follow-up. 211 Russian patients were included (52.3+/-10.3 years), 160 men (50.1+/-10.6 years) and 51 women (55.2+/-10.1 years). After two years of follow-up patients were examined in hospital, or telephon call occurred for determination of patient's condition or end point assessment. The end points were cardiac death, recurrent MI, recurrent hospitalization with unstable angina or stroke, CABG or PTCA performing. The genotyping was performed by methods based on polymerase chain reaction (PCR): PCR-SSP and PCR-RFLP. Analysis revealed association of allele T (p=0.036, OR=1.6, 95%CI: 1.052.6) and of allele T carriage (genotypes CT+TT) (p=0.046, OR=1.9, 95%CI: 1.053.6) of polymorphism C1444T of CRP gene with unfavorable events development. Analysis of survival rate by Kaplan-Meier estimation showed that cumulative part of patients without unfavorable events was significantly lower among allele T carriers than among carriers of genotype C/C of polymorphism C1444T CRP. Allele A of polymorphism A252G of LTA gene was also associated with unfavorable events risk (p=0.034, OR=1.96, 95%CI: 1.073.06). There was no association of polymorphisms delta 32 (w/d) of CCR5 gene, A(-308)G of TNF gene, G(-174)C of IL-6 gene, C(-509)T of TGFB1 gene with unfavorable events development.

[Platelet aggregation upon acetylsalicylic acid and clopidogrel treatment and glycoprotein IIb/IIIa content in patients with acute coronary syndrome].

Interaction between aggregating activity of platelets and glycoprotein (GP) IIb/IIIa (fibrinogen receptor) content on their surface was investigated in patients with acute coronary syndrome (ACS). Eighty nine ACS patients were included into the study - 69 with and 20 without elevation of ST segment. Blood was collected within the first hour of admission to the clinic (1 day), and then at 3-5 and 8-12 days. All patients received standard antiaggregant therapy - acetylsalicylic acid - ASA (thromboxane A2 synthesis inhibitor) and clopidogrel (ADP receptor antagonist). Platelet aggregation was analyzed at the first time point when patients had already taken ASA but not clopidogrel, and then (3-5 and 8- 12 days) upon combined therapy with both preparations. Aggregation was induced by 5 and 20 uM ADP and measured by turbidimetric method. In comparison with the initial level (1 day, ASA) at days 3-5, i.e. after development of clopidogrel effect, platelet aggregation was decreased by 54 and 40% upon its stimulation with 5 and 20 uM ADP, and was not further changed at days 8-12. GP IIb/IIIa content on platelet surface was determined by binding of 125I-labelled monoclonal antibody CRC64. GP IIb/IIIa number varied from 31100 to 73000 per platelet with the mean level of 48500 +/- 8400 (mean +/- standard deviation). No differences were detected between mean GP IIb/IIIa number at 1, 3-5 and 8-12 days after ACS onset. Upon repeat GP IIb/IIIa measurement coefficient of variation was 6.1% demonstrating the stability of this parameter in each patient. Positive correlation between platelet aggregation and GP IIb/IIIa content was detected at the first day - correlation coefficients (r) 0.425 and 0.470 for 5 and 20 uM ADP (n=57, p<0.001). However positive association between these parameters was not revealed at 3-5 and 8-12 days, when patients received not only ASA but clopidogrel as well (r from -0.054 to -0.237, p>0.05). These results indicates that variations of GP IIb/IIIa content affect platelet aggregating activity within first hours of ACS upon ASA treatment. However after saturation with clopidogrel this factor has no significant influence on platelet aggregation, at least on aggregation induced by ADP which receptor is the target of this antiaggregant. Under such conditions aggregation parameters are presumably influenced first of all by individual characteristics of clopidogrel pharmacokinetics.

[One-stage PCI of left main stenosis and infarct-related left main major branches in STEMI patients].

AIMS: to determine immediate and long-term results, safety and efficacy of one-stage PCI of LMCA and infarct-related LAD or CxA in STEMI. METHODS: 81 patients with STEMI treated with one-stage PCI of LMCA and infarct-related LAD or CxA were included into the study. LAD was infarct-related in 53 (65.4%) patients, circumflex (CxA) involved in 28 (34.6%) cases. Distal LMCA lesion was in 45 patients (55.6%). RESULTS: All patients were treated with drug-eluting stents. Radial access was used in 66 (81.4%) cases, in 38 (46.9%) patients intra-aortic balloon contrapulsation supported the procedure. IVUS was performed in 19 (23.4%) patients. Mortality during the procedure was 2.5% (2 patients with cardiogenic shock owing to infarct-related LAD). All other cases were technically successful. Two more patients died during the hospitalization, so short-term mortality was 4.9%. Angina symptoms persisted in 27 patients (33.3%) and were due to lesions in other coronary arteries. In these cases, the second PCI was performed. The mean follow-up period was 32-39 months. During follow-up 7 patients (8.6%) died due to various reasons. Target lesion revascularization was performed in 10 (12.3%) patients, including 3 repeated PCI of LMCA. Repeated revascularization due to atherosclerosis progression in other segments was done in 11 (13.5%) patients. MACCE-free survival was 60.7%. CONCLUSIONS: one-stage PCI of LMCA and infarct-related LAD or CxA seems to be effective and safe treatment in patients with STEMI but larger studies with prolonged follow-up are needed.

[Complex analsis of association of inflammation genes with myocardial infarction].

Carriage frequencies of alleles and genotypes of functionally important polymorphous loci of some inflammation genes: proinflammatory cytokines genes IL-6, LTA and TNF, anti-inflammatory cytokine gene TGFB1 and CC chemokine receptor 5 gene CCR5 were analyzed in the patients with myocardial infarction (MI) of Russian ethnic descent (199 cases) and in the control group of the same ethnic descent (142 controls). Complex analysis using APSampler algorithm revealed MI association with carriage of all polymorphous variants studied, as individual risk factors (insertion/deletion polymorphism of CCR5 and SNP G252A LTA) or only in combination with other alleles/genotypes. Carriage of bi- or triallelic combinations was associated with MI more significantly than carriage of any their subsets: single alleles or allele pairs. Protective triallelic combination d*CCR5 + 252G*LTA(+) -174C*Ll-6 was found to be most significant (p = 0.0006, OR = 0.23, CI = 0.090-0.56). Separate analysis of genetic susceptibility to MI for men and women displayed sexual dimorphism for CCR5 gene.

[Peculiarities of dynamics and prognostic value of NT-proBNP level in different variants of treatment of patients with acute coronary syndrome].

UNLABELLED: Aim of the study was to assess dynamics of NT proBNP in ACS as well as to analyze effect of different methods of treatment on the level of the parameter and its prognostic value. MATERIAL AND METHODS: Patients aged 30-70 years were included into the study: 52 patients with ST segment elevation ACS (STEACS), 61 patients with non ST-segment elevation ACS (NSTEACS). Control group comprised 20 people of the same age without ischemic heart disease. In all patients serum was taken for subsequent measurement of NT proBNP at admission, on day 3 of hospitalization, and before discharge (days 7-10). RESULTS: In ACS baseline NT proBNP concentration was significantly higher than in stable angina and in control group. During period of hospitalization NT proBNP level rose in the group of patients with STEACS and fell in the group of patients with NSTEACS. After early restoration of coronary blood flow (less than 4 hours after onset on the pain syndrome) in patients with STEACS dysfunction of the left ventricular myocardium was less pronounced (NT proBNP level was lower). High level of NT proBNP was an unfavorable prognostic factor in ACS irrespective of the selected tactics of treatment.

[Polymorphism C1444T of C-reactive protein gene and C-reactive protein concentration in blood serum of healthy people and patients with myocardial infarction].

UNLABELLED: CRP level is a risk factor of development of ischemic heart disease (IHD) and acute myocardial infarction (MI) in healthy people, while in patients with cardiovascular diseases it is a marker of unfavorable prognosis. It has been shown in recent investigations that individual variations of plasma CRP levels to a great extent are genetically determined. These data constitute a basis for the study of associations of polymorphic variants of the CRP gene with risk of MI in healthy people as well as with unfavorable prognosis in IHD patients. MATERIAL AND METHODS: We included into the study 232 Russian patients aged 52.3 +/- 10.3 years, 175 men (50.1 +/- 10.6 years) and 57 women (55.2 +/- 10.1 years). Control group comprised 159 Russians without history of cardiovascular diseases and other serious severe concomitant diseases (age 60.5 +/- 14 years), 76 men (age 57.3 +/- 13.9 years ) and 83 women (age 63.1 +/- 14 years). CRP concentration was measured initially (at the moment of hospitalization), on days 3, at discharge, in 1 and 6 months, 1 year after onset of infarction. For genomic typing of C1444T polymorphism of CRP gene we used restriction fragment length analysis of products of polymerase chain reaction (PCR). RESULTS: Distribution of genotypes of C1444T polymorphism of CRP gene: C/C 51.8%, C/T 35.8%, T/T 12.4% in patients with MI; C/C 55.2%, C/T 40.2%, T/T 4.6% in control group. We found significant difference (p = 0.006, relative risk [RR] 0.3, 95% confidence interval [CI] 0.15-0.74) in frequency of carriers of C1444 allele (sum of C/C and C/T genotypes), which was higher in control group. Correspondingly in the group of patients with MI T/T genotype was met significantly more frequently than in control (p = 0.006, RR 3.0, 95% CI 1.3-6.5), and can be looked upon as risk factor of MI. We found no relation between carriage of CRP alleles/genotypes of CRP and one year prognosis in patients with MI. Analysis of association of the C1444T polymorphism with CRP concentration revealed significant relationship between T/T genotype and higher CRP level.

[The clinical value of determination of natriuretic peptides in acute coronary syndrome].

The production and release of natriuretic peptides (NPs) into the bloodstream are stimulated by increased left ventricular wall tension during volume overload. In ischemia, NPs are secreted by myocardial cells in response to stress or overload, particularly in the development of myocardial systolic dysfunction. The review details the time course of changes in amino acid N-terminal proBNP in acute coronary syndrome (ACS) with and without ST-segment elevation and discusses the role of the index in defining the tactics of treatment and prognosis in patients with ACS.

[Clopidogrel resistance in patients with acute coronary syndrome].

AIM: to reveal the frequency of clopidogrel resistance in patients with acute coronary syndrome (ACS) and its impact on prognosis in these patients. SUBJECTS AND METHODS: Seventy-five clopidogrel-treated patients with ACS were followed up. Optical aggregometry was conducted using ADP 20 micromol. The resistance criteria were baseline platelet aggregation, platelet aggregation on day 7, % < 10%. Inflammatory markers (IL-6, IL-10, and C-reactive protein) were determined. Genetic polymorphisms (the IIIa subunit gene--Leu33Pro, the receptor P2Y(12) C18T and G36T gene, and the CYP3*A4(A-293G) gene) were studied. RESULTS: According to the accepted resistance criteria, 54 (72%) patients were sensitive to clopidogrel and 21 (28%) were resistant to the agent. The resistance was revealed in 7 (23%) of the patients with ECG ST-segment elevation and in 14 (31%) of those with ST-segment elevation. Before admission to the clinic, the unresponsive patients had significantly more frequently received the loading clopidogrel dose of 300 mg while that latter was 600 mg in the responsive patients. As compared with the responsive patients, the unresponsive ones showed a significantly lower baseline antibody level that was increased on day 7. The clopidogrel resistance determined by this criterion had no impact on prognosis. On dividing the patients by aggregation quartile values, poor manifestations insignificantly more frequently occurred in the third and fourth quartiles. No clear correlation was found between the occurrence of clopidogrel resistance and the activation of an inflammatory process. The monozygous variant of the receptor P2Y(12) CT18T gene was insignificantly more frequently encountered in the unresponsive patients. CONCLUSION: The laboratory phenomenon of clopidogrel resistance exists. Large multicenter studies of this issue are needed to identify simple and least expensive resistance methods and clear diagnostic criteria that enable the findings to be compared.

[Broken heart syndrome or Takotsubo cardiomyopathy. (Literature review and clinical observations)].

Takotsubo cardiomyopathy is an acute cardiac syndrome that mimics ST segment elevation myocardial infarction. It is characterized by transient local contractility disturbances as akinesis of the apical and middle segments of the left ventricle concurrent with hyperkinesis of its basal portions in the absence of significant coronary artery changes. A description of 2 clinical cases and a review of literature on this rare myocardial disease are given.

[An experience of the use of stem cells in the treatment of patients with myocardial infarction and low ejection fraction].

We present our own experience of assessment of effect of cell therapy on functional state of the myocardium in patients with lowered contractile capacity of the left ventricular myocardium. Intracoronary administration of stem cells in acute myocardial infarction is a safe method of treatment. It does not cause additional damage of the myocardium and does not provoke appearance of malignant arrhythmia. Cell therapy does not affect global left ventricular function. Data we have obtained demonstrate tendency to improvement of myocardial contractile function in dynamics in the majority of studied patients, including patients of the comparison group. This most probably indicates that the given process has been caused by restoration of blood flow to surviving cardiomyocytes after transluminal coronary angioplasty and improvement of function. Confirmation of participation of administered cells in myocardial contraction and improvement of perfusion requires further clinical investigations.

[Spontaneous reperfusion of the infarct-related artery in patients with ST elevated myocardial infarction].

AIM: To characterize a clinical course of ST elevation myocardial infarction (STEMI) and spontaneous reperfusion of the coronary arteries (SR) as well as in patients after reperfusion thrombolytic therapy (TLT) and/or transluminal balloon coronary angioplasty (TBCA); to compare effectiveness of different approaches to treatment of SR patients: conservative--early medication and active--TBCA on the first postmyocardial 24 hours. MATERIAL AND METHODS: We studied 479 patients admitted to hospital not later than 6 hours since STEMI onset and either having SR (n = 49) or treated using active methods of coronary circulation restoration--prehospital thrombolysis (n = 127), thrombolysis after hospitalization (n = 127), primary TBCA (n = 60) and TBCA after initiation of TLT (n = 116). We made a more detailed analysis on the sample of 149 SR patients. RESULTS: SR was diagnosed in 10.2% cases with STEMI and occurred much earlier than recovery of coronary circulation due to TLT and/or TBCA. Patients with SR developed Q-MI, right ventricular infarction, cardiac failure and atrioventricular block less frequently. They had the lowest peak activity of creatin phosphokinase and a higher left ventricular ejection fraction versus patients without SR (50.7 +/- 6.8 and 45.4 +/- 6.6%, respectively; p < 0.05). As shown by coronaroangiography, SR patients had no "no reflow" phenomenon (0% and 17%, respectively). Active policy of SR patients treatment had no significant advantages over conservative treatment. CONCLUSION: Early SR had more favourable course of MI, less mass of the affected myocardium and better contractile function of the left ventricle. The conservative policy of STEMI treatment in the presence of SR is more effective than the active one if a due control over the patients' condition is provided.

[Comparative dynamics of markers of inflammation and NT-proBNP in different variants of treatment of patients with ACS].

STUDY AIM - assessment of dynamics of markers of inflammation (CRP, Il-6, Il-10, TNFa, CD40L, fibrinogen) and N - N in acute coronary syndrome (ACS) as well as analysis of effect of various methods of treatment on level of these parameters. Patient aged 30 - 70 years were included in the study: 52 patients with ACS with ST-segment elevation (STEACS) and 61 - without ST-segment elevation (NSTEACS). Initial level of markers of inflammation (Il-6, CRP) in STEACS was lower than in NSTEACS. Initial level of antiinflammatory Il-10 was significantly higher in patients in the STEACS group (72.6 +/- 39.1 and 6.6+4.2 pg/ml, < 0.01). At admission the highest values of N - N were noted in the group of NSTEACS (761.5 pg/ml compared with 451.1 pg/ml in STEACS, =0.04). During period of hospitalization elevation of N - N occurred in the group of STEACS while its lowering occurred in the group of NSTEACS. In STEACS patients with early restored coronary blood flow dysfunction of the myocardium was less pronounced (lower level of N - N ). In patients with NSTEACS during period of hospitalization levels of CRP, Il-6 fibrinogen lowered. In invasively treated patients with NSTEACS levels of CRP and fibrinogen lowered to a greater extent than in conservatively treated.

[The role of multidetector computed tomography in detection of myocardial infarction].

UNLABELLED: The aim of the study was to assess the diagnostic value of multidetector computed tomography (MDCT) in detection of myocardial infarction (MI) in acute and chromic stages. MATERIAL AND METHODS: 49 patients with suspected MI were included in the study. In 44 patients the diagnosis of acute MI had been confirmed according to standard criteria. Contrast-enhanced MDCT of the heart and vessels was performed with 4-row MDCT scanner. RESULTS: MDCT detected areas of MI in 39 of 44 patients with proven MI. In 66,7% of cases they were transmural and in 33,3% -- subendocardial. In arterial phase the density of infarcted area was significantly lower than in normal myocardium (mean, 32,6 +/- 3,7 HU versus 101,9 +/- 3,7 HU, correspondingly, p < 0,0001). Mean values of myocardial density in the area of the MI did not change during follow-up (32,6 +/- 3,7 HU vs 41,3 +/- 4,5 HU, ns). In comparison to SPECT, sensitivity and specificity of MDCT in detection of transmural MI were 96,9% and 100%. corr. In the whole group of patients, taking results of troponin test as a gold standard, the sensitivity of MDCT in detection of Q-MI and non-Q MI were 89,1% and 93,5%, correspondingly. CONCLUSION: Cardiac MDCT can reliably detect and localize areas of acute and chronic MI. Contrary to SPECT, it also gives information about stenosis and occlusions in the coronary arteries.