Search

Aim      This retrospective cohort study focused on evaluating the incidence of contrast-induced nephropathy (CIN) associated with administration of an atorvastatin loading dose (80 mg) prior to invasive coronary angiography (CAG) in patients with ST-segment elevation myocardial infarction (STEMI).Material and methods  This retrospective cohort study included 386 patients with STEMI. The patients were divided into two groups: intervention group (n=118) and control group (n=268). Patients in the intervention group, at the stage of admission to the catheterization laboratory, were administered a loading dose of atorvastatin (80 mg, p.o.) immediately before access (introducer placement). The endpoints were development of CIN, which was determined by increased serum creatinine 48 h following the intervention by at least 25% (or 44 µmol/l) of baseline value. In addition, in-hospital mortality and incidence of CIN resolution were assessed. To adjust the groups for dissimilar characteristics, a "pseudorandomization" method was used by comparing propensity scores.Results The incidence of CIN was significantly lower in the intervention group than in the control group (10.5 % vs. 24.4 %; p=0.016) with the odds for the CIN development lower than in the control group (odds ratio (OR) 0.36; 95 % confidence interval (CI), 0.16-0.85). Creatinine concentrations returned to the baseline value in 7 days more frequently than in the control group (66.3 % vs. 50.6 %, respectively; OR, 1.92; 95 % CI, 1.04-3.56; p=0.037). In-hospital mortality was higher in the control group but did not differ significantly between the groups.Conclusion      ~Administration of atorvastatin 80 mg to STEMI patients immediately before CAG was associated with a reduced risk of CIN and a higher likelihood of serum creatinine returning to the values at admission by day 7.

Aim      To determine predictors of acute kidney injury (AKI) related with surgeries for correction of acquired valvular heart disease (HD) and to evaluate the incidence of in-hospital complications in patients with postoperative AKI.Material and methods  This study included 62 patients after surgery for correction of acquired valvular HD (mean age, 61±10.9 years) with a disease duration of 11±5.3 years. NYHA functional class (FC) 1 chronic heart failure (CHF) was observed in 1.6 % of patients, FC 2 in 64.5 %, and FC 3 in 33.9 %.17.7% of patients had chronic kidney disease (CKD). Coronary lesions of ≥50 % of vascular lumen were detected in 27.4 % of patients. Surgical correction of mitral valvular disease was performed in 32 cases, aortic valvular disease in 36 cases, tricuspid valvular disease in 8 cases, and combined operations for correction of valvular disease and coronary bypass in 8 cases. Creatinine concentrations were measured according to the Jaffe method; glomerular filtration rate (GFR) was estimated with the CKD-EPI equation. AKI was diagnosed based on KDIGO (2012) criteria.Results The AKI incidence related with surgeries for correction of valvular HD was 16.1 % (8.1 % of patients had stage 1 AKI, 3.2 % had stage 2 AKI, and 4.8 % had stage 3 AKI), and 3.2% required kidney replacement therapy. AKI was associated with the presence of CKD at baseline (р=0.044), development of hemopericardium requiring drainage (р=0.012), more pronounced coronary lesions (in the AKI group: stenoses from 50 to 70 % in 20% of patients, from 70 to 90 % in 30 % of patients, and ≥90 % in 0 %; without AKI: from 50 to 70 % in 13.4 % of patients, from 70 to 90 % in 3.8 %, and ≥90 % in 5.8 % of patients, respectively; р=0.032). Probability of postoperative AKI significantly increased with the development of hemopericardium requiring drainage. Patients with postoperative AKI compared to persons without AKI had higher mortality (20 % and 0 %; р=0.001), greater incidence of decompensated CHF (40 and 9.6 %; р=0.012) and hemopericardium requiring drainage (30 and 1.9 %; р=0.012).Conclusion      The development of postoperative AKI is associated with CKD at baseline, more pronounced coronary injury, and hemopericardium requiring drainage.

Aim: Evaluation of the frequency hospital cardiovascular events in groups of patients with stable angina who underwent percutaneous coronary interventions (PCI) with stenting of the arteries before coronary bypass surgery, or who did not have previous myocardial revascularization., Materials and Methods: The 120 patients with stable angina who underwent routine coronary artery bypass grafting were examined. Group composition: Men 80.8%, age 587.6, duration of coronary heart disease 65.7 years, history of myocardial infarction (MI) 77.5%. Arterial hypertension was present in 92.5%, diabetes mellitus in 12.5% of patients. Multivessel coronary artery disease in 72.5% of patients. 28 (23.4%) patients had previously undergone PCI with stenting of the coronary arteries. The period from PCI to coronary bypass surgery was 2032.6 months. Coronary bypass surgery on-pump was performed in 88.3%, coronary bypass surgery on off-pump in 11.7%. The number of distal anastomoses ranged from 1 to 4., Results: There were no differences in clinical and angiographic indicators, pharmacotherapy, and operation characteristics between the groups of patients who were subjected to or did not have PCI before coronary bypass surgery. There were no differences between the analyzed groups of patients in the frequency of cardiac death (0 and 1.1%, p=0.58), non-fatal MI (3.6% and 9.8%, p=0.29), stroke (0 and 1.1%, p=0.58), acute heart failure (11.7% and 34.8%, p=0.06), the number of patients with paroxysms of atrial fibrillation (28.6% and 17.4%, p=0.94), the proportion of patients with resternotomies (3.6% and 3.3%, p=0.94) and gastrointestinal bleeding (3.6% and 4.3%, p=0.86)., Conclusion: PCI with coronary artery stenting, prior to coronary bypass surgery, does not affect the frequency of post-operative hospital cardiovascular and hemorrhagic complications.

Aim: To assess the prevalence and prognostic value of AKI in patients with acute decompensation of chronic heart failure (ADCHF) with a reduced ejection fraction (HFrEF) and with preserved ejection fraction (HFpEF) or acute coronary syndrome (ACS), to identify predictors of AKI., Materials and Methods: In a prospective study included 863 patients, of which 141 with ADCHF, 446 - non-ST-elevation acute coronary syndromes (NSTE-ACS) and 276 - ST-segment elevation myocardial infarction (STEMI). AKI was diagnosed according to KDIGO recommendations. The end point was defined as death from cardiovascular causes., Result: During the follow-up from 1 to 37 months (median follow-up was 18 months) for patients with ADCHF in 24,8 % an endpoint was reported. For patients with ACS, the observation time ranged from 1 day to 14 months (median follow-up was 12 months), in 4,3 % - NSTE-ACS, 10,9 % - STEMI the end point was recorded. AKI developed in 14,8 % of patients with ADCHF HFpEF and 11,2 % ADCHF HFrEF, in 23,1 % - STEMI and 21,4 % - NSTE-ACS. AKI increases the risk of death from cardiovascular causes in patients with ADCHF HFrEF (OR 95 % 98,750 (11,158-873,976), р<0,001) and STEMI (OR 95 % 5,395 (2,451-11,878), p<0,001), but did not increase the risk of an endpoint occurrence in patients with ADCHF HFpEF (OR 95 % 1,875 (0,221-15,930), р=0,565) and NSTE-ACS (OR 95 % 1,199 (0,421-3,412), р=0,734). The multivariate analysis revealed risk factors for the development of AKI in patients with ADCHF HFrEF: high albuminuria (AU) from 30 mg / l (OR 95 % 5,763 (1,338-24,819), р=0,019), GFR<45 ml / min initially at admission to hospital (OR 95 % 76,593 (1,193-36,446), p=0,031), age>75 years (OR 15,933 (1,020-248,856), р=0,048). In patients with STEMI: age>75 years (OR 95 % 3,248 (1,476-7,146), p=0,003), female gender (OR 95 % 2,321 (1,190-4,526), p=0,013), acute heart failure (AHF) Killip IV (OR 95 % 10,334 (1,777-60,110), p=0,009). Risk factors for the development of AKI in patients with NSTE-ACS: age>75 years (OR 95 % 1,761 (1,051-2,949), р=0,032), PCI on RCA (OR 95 % 2,565 (1,193-5,517), р=0,016)., Conclusion: In patients with ADCHF HFrEF and STEMI development AKI is associated with a poor prognosis, but does not affect the prognosis of patients with ADCHF HFpEF and NSTE-ACS. AKI in patients with ADCHF HFrEF can be predicted using predictors: GFR<45 ml / min, AU more than 30 mg / l and age>75 years. In patients with STEMI, the predictors of AKI were age>75 years, female gender, AHF Killip IV, and in patients with NSTE-ACS age>75 years, PCI on RCA.

The literature review presents the characteristics of modern high - sensitivity tests for detection of Tn (hs - cTn) in the blood and the results of large studies on the diagnosis of non segment elevation myocardial infarction (nonSTEMI) using hs - cTn. The results of these studies served as the basis for the development of three - and one - hour diagnostic algorithms nonSTEMI, presented in the recommendations of the European Society of Cardiology 2012 and 2015 and also in fourth Universal Definition of Myocardial Infarction 2018.

Aim: To study clinical prognostic value of residual platelet activity in patients with acute coronary syndrome without ST segment elevation., Material and Methods: The study included 120 patients with acute coronary syndrome without ST segment elevation (NSTE ACS) with coronary artery stenting. Testing of residual reactivity of platelets in the subjects was carried out after loading doses of  aspirin and P2Y12-inhibitors.Patients were divided into two groups comparable in gender and age: with low residual reactivity of platelets (LRR), n=90 and with high residual reactivity of platelets (HRR), n=30. Between the groups a comparative assessment of clinical-laboratory and instrumental indicators, development of a combined end point (ischemic events) and bleeding during follow-up (16 ± 6 months)., Results: The group with HRR was initially heavier: patients with angina pectoris of functional class III, atrial fibrillation, myocardial infarction, was a higher risk on the GRACE (202,6±11 vs. 148,6±7, р=0,03),increased levels of Troponin T (70,0 vs. 45,5%, р=0,02), acute occlusion in the coronary arteries (66,6 vs. 42,4%, р=0,02).The combined endpoint was more often reported in patients with HRR (40 vs. 20,7%, р=0,04). Patients with ADP-aggregation of platelets in the range 0-1 Om had a greater risk of developing hemorrhagic events (17,1 vs. 2,1%, RR 8,05 CI: 1,1-59,9, р=0,01)., Conclusion: In patients with NSTE ACSHRR after loading doses of aspirin and P2Y12-inhibitor was associated with the development of repeated atherothrombotic events. Very low LRR was associated with the development of bleeding.

Aim: To assess frequency and prognostic value of contrast-induced acute kidney injury (CI-AKI) after percutaneous coronary intervention (PCI) in patients with ST-elevation myocardial infarction (STEMI)., Materials and Methods: We included in this prospective observational study 233 patients with STEMI. Duration of follow-up was 6 months. During this period, we traced development of CI-AKI with subsequent analysis of relation of CI-AKI to STEMI outcomes., Results: CI-AKI was registered in 29.6% of patients. Hospital mortality was 14.5 and 6.1% among patients with and without CI-AKI, respectively (p=0.037). Mortality from cardiovascular causes during the follow-up period was 17.4 and 7.3%, respectively (p=0.021). CI-AKI was associated with increase of risk of death during hospitalization (odds ratio 2.6, 95% confidence interval 1.033-6.592, p=0.042). The development of CI-AKI was associated with glomerular filtration rate.

In recent years, the issues of choice of an agent for dual antiplatelet therapy (DAPT) as well as timing of initiation and duration of DAPT in patients with acute coronary syndrome (ACS) have been actively discussed. In this article we present data of major randomized trials of clopidogrel and novel P2Y12 inhibitors - prasugrel, ticagrelor, cangrelor - assessing strategy of administration of antiaggregants in patients with ACS before coronary angiography / percutaneous coronary intervention. The article also contains analysis of differences between recommendations of the European Society of Cardiology and American College of Cardiology/American Heart Association on therapy with oral P2Y12 inhibitors in the management of patients with ACS.

Background: Despite the PCI in patients with ST-segment elevation myocardial infarction (STEMI) the development of acute heart failure (AHF) Killip ≥II is associated with a poor prognosis., Aim: To identify predictors of the development of AHF and the prognostic value of AHF in patients with STEMI after PCI., Materials and Methods: In a prospective study, which lasted 6 months, included 233 patients (average age of 62.1±10.89 years, 73.4% of men) admitted to the hospital due to the development of STEMI who underwent PCI. The endpoint was defined as the death from cardiovascular causes. Statistical processing of the results was carried out using the statistical packages of the programs "SPSS Statistics 17.0"., Result: During the follow-up observation from 1 day to 6 months (median follow-up of 5.2 months), 25 patients (10.7%) reported the onset of the endpoint, including 20 cases during the index hospitalization. AHF Killip ≥II during indexed hospitalization developed in 25 patients (10.7%). Independent predictors of Killip ≥II were: GFR.

The study was aimed at revealing the factors associated with renal dysfunction having developed after coronary artery bypass grafting (CABG) and assessing the in-hospital cardiovascular complications rate amongst patients with postoperative renal dysfunction. The study included a total of 99 patients presenting with stable angina pectoris and having indications for CABG. The mean age of the patients amounted to 57±7 years, with the average duration of coronary artery disease (CAD) of 6±5.7 years. A multi-vessel lesion of coronary arteries was revealed in 69.7% of patients, ≥ 50% stenosis of the trunk of the left coronary artery was diagnosed in a further 15.1%. CABG was performed in conditions of assisted circulation (AC) in 88.9% of patients and on the functioning heart in 11.1%. We implanted from 1 to 4 grafts to each patient. At admission, and then on the first and second postoperative days after CABG we determined blood serum creatinine and calculated the creatinine clearance (CrCl) according to the Cockcroft-Gault equation. A decrease in the CrCl < 60 ml/min was regarded as renal dysfunction. Assessing the cardiovascular complications rate we took into consideration cases of cardiac death, perioperative myocardial infarctions (POMI), severe acute cardiac insufficiency having required placement of a counterpulsator, and as well as the proportion of patients with paroxysmal atrial fibrillation. We also evaluated the frequency of repeat sternotomy. The incidence rate of transitory renal dysfunction following CABG amounted to 18.2%. The factors associated with a decrease in the CrCl < 60 ml/min after CABG were found to be as follows: age above - Me 62.5 (range 59-68) years, increased duration of AC above - Me 103 (range 88-133) min and prolonged time of aortic occlusion (AO) above - Me 53 (range 44-60) min, severe postoperative acute cardiac insufficiency, and re-sternotomy. The cumulative rate of in-hospital cardiovascular complications turned out to be significantly higher (55.6 versus 18.5%, p=0.001) amongst patients with postoperative renal dysfunction. We also revealed a substantially higher incidence rate of re-sternotomies in the cohort of patients with a CrCl < 60 ml/min after CABG (11.1 vs.1.2%, p=0.027). Hence, moderate transitory renal dysfunction appears to develop nearly in every fifth patient in the early period after CABG. The risk factors for the development of postoperative renal dysfunction include: age, increased duration of the period of artificial circulation (AC) and time of aortic occlusion (AO), severe acute postoperative cardiac insufficiency, and re-sternotomy. Even moderately pronounced transitory renal dysfunction after CABG is associated with an unfavourable prognosis of in-hospital cardiovascular complications.

The GRACE prognostic scale appeared ineffective for prognostication of deaths and sum of deaths and myocardial infarctions (MI) during hospitalization and demonstrated moderate level of prognostic value during 6 months of observation. TIMI model gave similar result relative to prediction of death/MI/refractory ischemia during 14 days and 12 months of observation. PURSUIT risk model showed very good level of prognostic significance during 30 days and 12 months of observation. Comparison of GRACE and PURSUIT models relative to all cause death and composite of death and MI showed that PURSUITd scale had better accuracy of predictions.

The aim of this work was to investigate prognostic value of creatine kinase MB-fraction and troponin T increase in patients after coronary bypass grafting (during 3-year prospective observation). Parameters were studied in 6, 12, 48 and 72 hours after surgical myocardial revascularization. It was revealed that increase of myocardial necrosis markers is associated with significant more frequent development of cardiovascular complications during 3-year prospective observation.

Aim: To study the prognostic value of therapy-induced changes in plasma NT-proBNP levels in patients with left ventricular (LV) systolic dysfunction., Subjects and Methods: The study covered 84 patients aged 23 to 70 years (mean 54 +/- 8.1 years) with LV systolic dysfunction (an ejection fraction of < 40%). Plasma NT-proBNP levels were determined in all the patients at baseline and 3 months later to evaluate the efficiency of therapy for heart failure (HF). The median follow-up was 18 months. The follow-up recorded the following outcomes (end points): death from decompensated HF and unplanned hospital admissions for progressive HF symptoms., Results: The baseline and therapy high plasma levels of NT-proBNP (more than 3000 pg/ml) were associated with worsening prognosis. The therapy-induced decrease in NT-proBNP levels was associated with more favorable prognosis., Conclusion: Repeat dynamic determination of plasma NT-proBNP levels allows identification of patients at increased risk of poor outcomes for a more intensive observation and more aggressive pathogenetic therapy.

Aim: The aim of the study is to assess the efficiency of early invasive treatment versus conservative treatment for patients with non-ST acute coronary syndrome (ACS), and to study immediate results of percutaneous coronary intervention (PCI) in terms of the risk of adverse events., Material and Methods: The investigation includes 112 patients with non-ST ACS having risk of adverse outcome determined by the GRACE system. More than half of the patients (77/68.8%) underwent diagnostic coronary angiography within 72 hours of admission, and the decision was made on a subsequent treatment strategy (early invasive or conservative approach). In-hospital outcomes (cardiac deaths, nonfatal MI, reMI), cumulative frequency of these events have been studied according to the risk assessment scale GRACE and treatment strategy., Results: Low risk was determined in 33.9% of patients, intermediate--in 32.1%, and high--in 33.9%. On the whole, frequency of myocardial revascularization was assessed as 56.3%. Fifty-one (45.5%) patients received early invasive treatment, 12 (10.7%)--coronary artery bypass grafting (CABG). A conservative approach was used in 49 cases (43.8%). An early invasive treatment was given to 20 patients (52.6%) from each of the low- and high-risk groups, 11 (30.6%)--from the intermediate risk group. In-hospital cardiac deaths were observed only in the high-risk group, and this number was higher in case of conservative treatment versus early invasive treatment: 3 (30%) versus 1 (50%). Non-fatal MIs in the form of re(MI) were also diagnosed only in the high-risk group following conservative treatment: 2 (20.0%). Nevertheless, no reliable difference in the frequency of each complication was found (p = 0.095; p = 0.1). Significant differences in the high-risk group were proven while comparing the impact of early invasive and conservative approaches on the cumulative frequency of in-hospital death and (re)MI cases (50.0% versus 5.0%; p = 0.009). No benefits of an early invasive approach were identified for low-risk and intermediate risk groups., Conclusion: Early invasive approach compared with a conservative approach in high risk patients with non-ST acute coronary syndrome can improve clinical outcomes with a decrease in the total frequency of in-hospital death, reMI.

The review gives the results of large clinical studies of the prognostic value of hyperglycemia in patients with acute coronary syndrome and discusses the basic mechanisms determining the increased cardiovascular risk. The advantages of invasive treatment policy are also described in diabetic patients with an exacerbation of coronary heart disease.

We included 63 patients with chronic heart failure of ischemic origin (32 with left ventricular ejection fraction less than 40%) into prospective study with average duration of follow-up 27+/-10 months. Relative risk of lethal outcome was significantly increased in patients with initial endsystolic left ventricular dimension >6.0 m, enddiastolic left ventricular dimension >7.0 m, left atrial dimension >5.0 cm, left ventricular ejection fraction <35%, hemoglobin level <120 g/L, with disturbances of rhythm and conduction, and elevation of plasma levels of N-terminal pro-brain natriuretic peptide (NT-proBNP) >1000 mol/ml and interleukin-6 >20 g/ml. Relative risk of combined endpoint significantly increased at same values of echocardiographical parameters, plasma levels of NT-proBNP >500 mol/ml and interleukin-6 >10 g/ml.

Aim: To determine plasmic concentrations of NT-proBNP, TNFalpha and IL-6 in patients with coronary heart disease (CHD) complicated with chronic cardiac failure (CCF); to compare these parameters with hemodynamic and functional ones., Material and Methods: A total of 157 CHD patients (84.1% males, mean age 54.3 +/- 6.8 years) were divided into 3 groups matched by sex and age according to the presence of CCF and left ventricular (LV) or systolic dysfunction., Results: CCF patients with LV dysfunction or intact LV function had much higher plasmic concentrations of neurohumoral mediators than CHD patients without CCF. A plasmic NT-proBNP level over 1000 fmol/ml was associated with a 5.5-fold increase in the relative risk of LV diastolic dysfunction for CCF patients (rR 5.6; 95% CI 1.4-30.0; p = 0.0065) while an IL-6 level over 6.1 pg/ml was associated with a 9-fold increase in this risk (rR 8.9; 95% CI 2.3-35.4; p = 0.00001). Plasmic NT-proBNP and IL-6 levels went up in correlation with a CCF functional class. A plasmic level of TNFalpha correlated with anginal functional class., Conclusion: Changes in plasmic levels of the above neuromediators are associated with changes in some LV function and functional parameters of CCF patients.

Aim: To compare prognostic significance of troponin T (TnT) and MB creatine kinase (MB CK) elevations after percutaneous coronary interventions (PCI)., Material and Methods: Patients with ischemic heart disease (n=122) were followed for 9+/-3 months after PCI. Coronary angiography was repeated in 79% of cases. Composite criterion of prognostic significance comprised coronary death or nonfatal myocardial infarction., Results: Elevations of TnT , > or =0.03 ng/ml were noted in 55.5%, > or =0.1 ng/ml--in 21.9% of patients. Elevations of MB CK above upper limit of norm (ULN) were noted in 10.7% of patients. In 3 patients MB CK exceeded 3 ULN. Composite endpoint was registered in 53 patients (43.4%). There was no relation between any postprocedural elevation of MB CK and outcomes of follow-up. Levels of TnT between 0.03 and <0.1 hg/ml also were not related to prognosis. Post PCI TnT levels, > or =0.1 ng/ml were associated with significant worsening of prognosis during subsequent 6-12 months of follow-up.

Aim of the study was to assess significance of deviations of activated partial thromboplastin time (APTT) from optimal level (50-75 sec) after 48 hours of intravenous infusion of unfractionated heparin (UFH) in streptokinase treated patients with myocardial infarction (MI) for prognosis of nonfatal reinfarction and cumulative criterion comprising cardiac death, nonfatal MI and early postinfarction angina. Infusion of streptokinase (1,500,000 U in 30-60 min) was carried out after loading dose of aspirin (250 mg) and intravenous bolus (5,000 U) of UFH in 75 patients (age 34-76 years) admitted within 6 hours after onset of acute ST-elevation MI. UFH infusion was started prior to termination of administration of streptokinase and continued for 48 hours. During first 12 hours infusion rate was 1,000 or 800 U/hour in patients with body mass > or = 80 and < 80 kg, respectively. During initial 12 hours infusion rate was corrected if at 6 hours APTT was less than 40 or exceeded 150 sec. After 12 hours a nomogram was used for UFH dose adjustment according to APTT. Maximal number of optimal APTT values during UFH infusion just reached 50%. During first 12 hours prevailed values above 75 sec, after 24 and 36 hours -- values below 50 sec. Deviation of APTT from optimal level in 12 hours after onset of UFH infusion was the only independent predictor of nonfatal recurrent MI during following 30 days (relative risk [RR] 9.01, 95% confidence interval [CI]1.1 to 77.2; p=0.043). Independent predictors of cumulative criterion were level of risk of death according to TIMI scale (RR 1.47, 95% CI 1.-3 to 2.11; p=0.036) and deviation of APTT from optimal level in 12 hours after onset of UFH infusion (RR 3.24, 95%CI 1.05 to 10.5; p=0.046). It should be noted that rather than suboptimal excessive hypocoagulation by 12th hour of UFH infusion was associated with worse prognosis. APTT levels in 6, 24, and 36 hours of UFH infusion had no prognostic significance in relation to events assessed in the study.

Patients with left ventricular ejection fraction below 45% (mean 39+/-3.7%) were randomized either to captopril (n=33) or eprosartan after miocardial infarction (n=33) on days 3-7 of myocardial infarction. All patients were subjected to echocardiography and 40 to perfusion myocardial scintigraphy with (99m)TC-Technetril. Myocardial viability was defined as presence of perfusion reserve in dysfunctional segments during test with nitroglycerin. Dysfunctional myocardium was found to be viable in 62.5% of patients. Fifty six patients completed 3 months follow up and were restudied. By the time of the second study 28 patients continued captopril (37.5-150 mg, average dose 72+/-34.2 mg/day) and 28 - eprosartan (300-600 mg, average dose 471+/-151 mg/day). Captopril was stopped or its dose corrected in 28% of patients. In eprosartan group there were no side effects which required withdrawal of the drug. Similar increases of ejection fraction occurred on both groups (from 38+/-2.1 to 49+/-6.7%, p<0.001 and from 39+/-4 to 51+/-6.5%, p<0.001, in eprosartan and captopril groups, respectively). Magnitude of left ventricular ejection fraction change did not depend on the presence of viable myocardium. However in both treatment groups improvement of myocardial perfusion and decrease of left atrial dimensions were found only in patients with viable myocardium at initial study.

Aim: To examine efficacy of clopidogrel before thrombolytic therapy (TLT) in patients with acute myocardial infarction (AMI)., Material and Methods: A total of 72 patients (48 males and 24 females) admitted to hospital within 6 hours since the onset of acute myocardial infarction (AMI) were divided into three groups. Group 1 and 2 patients (n = 38 and 20, respectively) were given a prehospital stress dose of aspirin (250-500 mg), group 3 patients (n = 14) received this dose at admission. TLT with streptokinase or actilise (1,500,000 IU and 100 mg, respectively) was given to all the patients. Before TLT group 2 received a stress dose of clopidogrel (300 mg), after TLT--75 mg/day. 12-Lead ECG, CFK activity and troponine content examinations were made. The patients were observed for 30 days. The recovery of coronary circulation (CC) was evaluated by dynamics of a total lowering of the elevated ST segment., Results: CC completely recovered 60 min after TLT in 16, 10 and 7% patients of groups 1, 2 and 3, respectively. CC recovered partially in 24, 55 and 7% patients, respectively. In 90 min after TLT partial recovery of CC was observed in 21, 31 and 43%, respectively; in 180 min the effect was absent in 19, 15 and 38%, respectively. 30-Day lethality was 11.1% and was high in group 3. No lethal outcomes were seen in group 2., Conclusion: It is possible to achieve better myocardial reperfusion after TLT and improve 30-day outcomes in MI patients given combined antithrombocytic therapy.

Aim: To assess Efficacy of multifactorial preventive Interventions in achievement of target levels of low density lipoprotein cholesterol in survivors of myocardial infarction., Methods: Design of the study was open randomized comparative prospective. Two groups of patients with history of myocardial infarction were formed ("active intervention", n=88, "observation", n=48) and followed for 12 months. All interventions consisted in recommendatory and expository measures. Achievement of target low density lipoprotein cholesterol (LDLCH) levels, modifiable risk factors, blood lipids spectrum were assessed in 2-3, 5-6 and 12 months of observation., Results: Overall effect of undertaken multifactorial intervention on modifiable risk factors was positive. By the end of the period of observation number of risk factors per patient decreased from 3.8+/-0.99 to 2.8+/-1.29 (p<0.05). However target levels parameters in many cases were not reached. About half of patients could not decrease consumption of saturated fats and cholesterol, nearly 25% continued to smoke. More than 55% maintained excessive weight and 64% had abdominal obesity. Among patients of "observation" group only 5 (4.2%) began to take lipid lowering drugs. In active intervention group average LDLCH lowering was 23%, 38% of patients received lipid lowering drugs and 44% (of those who completed the study) achieved target LDLCH levels.

Infusion of esmolol (50-300 mcg/kg/min, mean 119-/+75.5 mcg/kg/min, average duration 3.2-/+1.22 h)) was carried out in 49 streptokinase treated patients within 6 hours of myocardial infarction. Infusion was associated with slowing of heart rate and lowering of mean dynamic systolic blood pressure (by 22%). No changes of stroke volume and index occurred. Complications requiring either cessation of infusion or decrease of its rate developed in 14.3% of patients (lowering of systolic blood pressure below 100 mm Hg in 5, complete atrio-ventricular block in 2) as a rule in the beginning of the infusion.

The influence of 4-month exercise training (ET) on the dynamics of lipids and lipoproteins of blood plasma regarding their initial level was studied in 64 postmyocardial infarction (PMI) patients. The initial 2 months bicycle exercise was performed in the moderate regimen (50-60% of individual ET), the next 2 months--in intensive regimen (70-90% of new threshold training). 46 control patients did no exercise. Two and four months of ET resulted in reduction of plasma cholesterol and its atherogenic fractions, an increase in high-density lipoprotein cholesterol level and exercise tolerance compared to the controls. Thus, ET in two-step regimen corrects lipid blood spectrum in PMI patients.

The study was undertaken to examine changes in ADP-induced aggregation of platelets, blood-circulating platelet aggregates, platelet phospholipids and cholesterol in patients with unstable angina depending on the therapy with disaggregatory agents. The patients from Group 1 (n = 23) received ticlopidine, 500 mg/day, in addition to antianginal therapy and heparin; those from Group 2 (n = 21) had aspirin, 320 mg/day, those from Group 3 (n = 36) took no disaggregahts. Ticlopidine was found to produce more marked effects on ADT-induced plasma platelet aggregation, in vivo reversible platelet aggregation, and reduced platelet levels of free cholesterol, as compared to aspirin.

Platelet functional parameters (platelet aggregation, blood circulating reversibly and irreversibly aggregated platelet complexes, thromboxane B2, 6-keto-PGF1 alpha) were examined in unstable angina treated with aspirin in a daily dose of 320 mg in relation to the outcome of the disease: Group 1, stabilization and Group 2, evolving myocardial infarction. Differences were found in the baseline platelet functional parameters between the groups. The findings suggest that platelet functional parameters show a varying response to aspirin depending on the outcome of the disease. Despite the effective inhibition of thromboxane A2 synthesis, aspirin was found to fail to prevent enhanced platelet aggregatory activity in case of myocardial infarction developed during the therapy.

The impact of a 4-week course of lovastatin (mevacor) therapy on platelet function was examined in 26 patients with coronary heart disease concurrent with hypercholesterolemia (the baseline plasma cholesterol level was 250 mg% or more). The agent was given in a daily dose of 20-40 mg. The agent in this dose was found to have no action on the thromboxane-prostacyclin balance in plasma, on the degree of ADP-induced aggregation and lipid peroxidation in platelets, phospholipid composition and levels of ester-bound cholesterol in platelet membranes. Free cholesterol tended to increase at the end of the 4th week of treatment. Despite the effective reduction of plasma levels of total and LDL cholesterols whose action on platelets is well known, there was no estimated decrease in the activity of platelets during lovastatin therapy.

The parameters of the structure and function of platelet membranes were examined in 30 patients with unstable vasospastic angina in relation to the outcome of the disease (myocardial infarction stabilization or development). The fractions of phospholipids (lysophosphatidylcholine, phosphatidylserine, sphingomyelin, phosphatidylcholine, phosphatidylethanolamine), the levels of platelet membranous free and esterified cholesterol, plasma malonic dealdehyde and thromboxane B2, the activity of platelet superoxide dismutase and catalase were determined. The exacerbation of vasospastic angina was found to appear as accumulation of cholesterol (mainly of its fraction), an increase in platelet membranous levels of phosphatidylcholine, phosphatidylethanolamine and sphingomyelin, accumulation of malonic dealdehyde. These changes were more profound in cases with subsequent myocardial infarctions. There were differences in the dynamics of the examined parameters in relation to the outcome of the disease.

The nature and frequency of cardiac arrhythmias were studied in 23 patients with coronary heart disease during anginal episodes accompanied by ECG ST-segment depression and elevation. All the ischemic episodes were divided into 2 periods: (1) that from the onset of ST-segment displacement to its maximum; (2) that from the first period to the return of ST segment to the baseline position. The predictive poor ventricular arrhythmias were more frequently recorded in the second period of ST-segment displacement. The occurrence of arrhythmias was demonstrated to be related to the degree of ST-segment elevation (depression) and the duration of the first period of ischemic episode in the second period of ST-segment displacement.

In patients with ischemic heart disease impairments in blood plasma lipid spectrum were more distinct in the chronic form of the disease. At the same time, the phospholipid composition was altered in thrombocytes as compared with that of persons free of ischemic heart disease and of stenosing coronary atherosclerosis.

Phosphocreatine (Neoton produced by "Schapparelli Farmaceutici") was infused intravenously to 27 patients with CHD at a dose of 2000 mg: 13 patients with unstable and 10 patients with stable angina pectoris. Phosphocreatine blocked ADP-induced platelet aggregation in these patients, but had no significant effect on the platelet aggregation induced by collagen, platelet activating factor or serotonin.

Reaction to graded bicycle exercise in patients with newly developed angina pectoris, patients with chronic IHD and subjects without IHD with normal coronary arteries was studied. Platelet activation by physical exercise was significantly more often (35.7%) in patients with newly developed angina pectoris than in patients with chronic IHD (12.8%) and patients without IHD (13%). It is shown that myocardial ischemia during physical exercise does not influence the frequency of the platelet activation signs determination. Development of platelet activation in physical exercise was promoted by minor disease duration, lower basic platelet functional activity and more evident increase in haematocrite in physical exercise.

Ca++ level in the platelets of patients with different forms of CHD (angina pectoris of new onset, including the spastic form, acute myocardial infarction) and of subjects without signs of CHD or coronary atherosclerosis was measured basally and after stimulation with ADP, platelet activation factor and serotonin. Simultaneously platelet aggregation induced by the same stimuli was studied. Basal platelet Ca++ did not differ significantly between the groups. Stimulation by ADP and serotonin increased Ca++ concentration, the change being greatest in patients with spastic angina pectoris. Augmentation of free platelet Ca++ in patients with acute myocardial infarction did not differ from that in subjects without CHD and coronary atherosclerosis, and in some cases it was even less pronounced. Free Ca++ level showed good correlation with platelet aggregation. It is suggested that the differences revealed are due to changes in the sensitivity of platelet receptors to the inductors used.

Platelet function (aggregation, circulating platelet aggregates, platelet factor 4, beta-thromboglobulin, thromboxane B2, 6-keto-PGF1 alpha, platelet count) was evaluated in patients with angina of new onset, as compared to individuals without coronary heart disease, and patients with angina of long standing (28 +/- 4.6 months). Some of the patients with angina of new onset were examined repeatedly 6 to 12 months after the onset of angina. Platelet activity was shown to be significantly higher in patients with stable angina of new onset, as compared to patients with lasting angina, where ADP and serotonin were used as inductors. Platelet aggregation, induced by platelet activation factor and collagen, was similar in all groups. Repeated investigation 6 to 12 months after the first anginal attacks demonstrated that most of platelet functional parameters declined or tended to decline.

Platelet function was studied in patients with diverse clinical patterns of unstable angina. In vasospastic angina, anginal attacks coincide with the highest increment in Ca2+ of platelets, and their high sensitivity to aggregation inductors, which declines as the condition stabilizes. Unstable angina without the vasospastic component is associated with reduced platelet sensitivity to aggregation inductors, particularly so in patients showing signs of intracoronary thrombosis. Spontaneous anginal attacks are accompanied with a rise of thromboxane B2 and a drop in the stable prostacyclin metabolite level.