This article presents the main results of large clinical studies that explored the efficacy and safety of antiplatelet agent, P2Y12 inhibitor, ticagrelor. The PLATO, ATLANTIC and PAGASUS-TIMI-54 studies' results formed the basis for inclusion of ticagrelor in the clinical recommendations for the management of acute coronary syndrome (ACS). These guidelines designate ticagrelor as the main drug that should be added to acetylsalicylic acid as a component of dual antiplatelet therapy (DAT) in patients with ACS. The new 2015 recommendations for the management of patients with non-ST elevation acute coronary syndrome not only give preference to tikagrelor over clopido-grel, but also make it possible for some patients with a high risk of coronary complications and low risk of bleeding to extend DAT for longer than 12 months. In addition, the article presents data on some ACS registers held in Russia to estimate the frequency of tikagrelor administration.

Despite the high level of cardiology development, cardiovascular diseases remain a major cause of death worldwide. The acute coronary syndrome both with and without ST elevation occupy an increasingly prominent place among them. Dysfunction of the arterialendothelium, chronic inflammation and damage of the atherosclerotic plaque cover, blood flow slowing, and formation of intravascular thrombus underlies various pathogenic forms of ACS. In this regard, the treatment and risk reduction of thrombotic complications of ACS is the main task of the physician in the management of this group of patients. The proposed article discusses optimizing antiplatelet therapy in patients with various ACS forms.

Despite the widespread introduction of primary percutaneous coronary interventions (PCI) and the use of new powerful antiplatelet drugs for the management of patients with acute coronary syndrome (ACS) at high risk, the relapse rate of coronary events associated with atherothrombosis remains sufficiently high. In the CURE [1] study the prevalence of myocardial infarction (MI), cere-brovascular accident (CVA) and cardiovascular death (CVD) among patients with ACS without ST elevation, who received aspirin and clopidogrel within 12 months, was 9.3%, and in the PLATO [2] study the frequency of above complications in a group of high-risk patients with ACS, who received a new P2Y12 inhibitor tikagrelor, amounted to 9.8%.

The review deals with the laboratory assessment of clopidogrel effect in patients with CHD. The article presents the results of major studies that have demonstrated the relationship between the residual platelet reactivity level and drug pharmacogenetics abnormalities causing coronary complications. It discusses proposals of the international expert organizations on the assessment of sensitivity to clopidogrel and possible modifications of antiplatelet treatment.

Despite the development of new oral anticoagulants, vitamin K antagonists (VKA) continue to be widely used for the treatment and prevention of throm-boembolic complications. On top of that, they have no alternative in patients with artificial heart valves. Receiving AVC results in the synthesis of modified factors of pro-thrombin-converting complex (prothrombin, factor X, IX and VII, as well as two components of the anticoagulant system — protein C and protein S) without capacity to bind with the phospholipid surface, which significantly reduces the likelihood of intravascular thrombosis, but the degree of anti-coagulation is individual and requires monitoring for each patient. Prothrombin test (PT test) is used to monitor the degree of anti-coagulation, which is based on determining the plasma clotting time in a patient after addition of thromboplastin and calcium chloride (prothrombin time). Tromboplastin is animal tissue extract containing tissue factor and phospholipids. In practice, the determination of the anti-coagulation degree by prothrombin time is no easy task. The fact of the matter is that various thromboplastin drugs have different sensitivity to the reduction of factors of prothrombin-converting complex; clotting time of normal and pathologic plasma depends on used thromboplastin and differs even for different series of thromboplastin supplied by the same manufacturer. In addition, prothrombin time depends on the method used (coagulometer). WHO had adopted a system of reporting the PT test results in the form of INR (International normalized ratio) specifically to measure the degree of anti-coagulation in patients who receive oral anticoagulant therapy.

The paper discusses the most common questions regarding the safety of therapy and patronage system in patients who receive warfarin in the question and answer form. Vitamin K antagonists now are the oral anticoagulants that are most commonly used in the actual clinical practice. Despite a large accumulated body of clinical experience, it is not always easy for a doctor to pick the individual dose of warfarin.

This study is aimed at exploring the use of thrombin generation assay (TGA) in platelet-poor plasma to assess the contribution of the protein C system to the hypercoagulation development in patients with coronary heart disease (CHD) after intracoronary stenting. The study material, the venous blood, was taken in 63 patients with CHD at the age of 53 to 77 before and on Day 1 after the planned percutaneous coronary intervention (PCI) who were treated with antiplatelet agents and antithrombotic agents in standard doses, and in 35 subjects of comparable age and sex without clinical manifestations of CHD who were not treated with these drugs for any other purpose. Laboratory examination included the standard coagulologic tests. To assess the effects of activated protein C system, the TGA in platelet poor plasma was modified by adding human recombinant trombomodulin (rh-TM) to the reaction mixture. The standard coagulologic tests revealed changes in hemostasis relevant to the pathogenesis of CHD and the effects of antithrombotic agents. The TGA results showed an increase in ETP and Peak Thrombin in patients with CHD after PCI with respect to the control and initial values which is evidence of the increased coagulation after the intervention. The test results also showed a reduction of TGA values per cent decline when adding TM. The ETR, Peak thrombin and ttPeak per cent decline was the most significant under the influence of TM which was evidence of the contribution of protein C activity reduction to the development of hypercoagulation after PCI. The modified TGA in platelet-poor plasma used in this study can be applied in clinical practice for estimating the plasma-coagulation hemostasis status and reduction in sensitivity to TM, which characterizes the protein C system activity by degree of decrease in results of the test that was performed in plasma without and with the addition of rh-TM.

The term "Venous Thrombosis" (in English literature "Venous Thromboembolism") represents two diseases which are closely related to each other in terms of triggering events and clinical manifestations: lower extremity deep vein thrombosis (DVT) and pulmonary embolism (PE). It is known that PAT (symptomatic or asymptomatic) is discovered in most patients with DVT, and the clinical picture of PAT in most cases reveal (symptomatic or asymptomatic) DVT. Among cardiovascular diseases, venous thrombosis (VT) is ranked 3rd most common in the world with an annual incidence of 100-200 cases per 100,000 population, while fatal PE results in an annual rate of 60 deaths per 100,000 population [1]. It should be borne in mind that these figures are clearly underestimated, given the difficulties of diagnostics and the high incidence of asymptomatic or oligosymptomatic flow of DVT and PE. In addition, the fatal outcome is often the first and only manifestation of PE, and PE firmly holds third place among causes of sudden death [2]. The risk of PE markedly increases with age starting at 40 years old, and this risk double during each subsequent decade of life, and the number of patients with DVT and PE and, probably, deaths from these causes is expected to grow in the future [3].

This article discusses the significant features and use of new oral anticoagulant dabigatran etexilate for the treatment of venous thromboembolic complications (VTC). The article presents the results of 4 randomized clinical studies: RE-COVER, RE-COVER II, RE-MEDY and RESONATE. The RE-COVER and RE-COVER (II) studies compared the effectiveness and safety of dabigatran and warfarin in patients with acute episode of VTC, and RE-MEDY and RESONATE studies assessed the prolongation of dabigatran therapy in patients with VTC, who completed the main 3-6-month course of anticoagulant therapy. In addition, REMEDY study estimated efficacy of dabigatran compared with warfarin, and RE-SONATE study estimated one compared with placebo. RE-COVER, RE-COVER II and RE-MEDY showed that the efficacy of dabigatran (150 mg 2 times a day) for the prevention of recurrent and fatal episodes of VTС was not less than that of warfarin; on top of that, dabigatran was more efficient in reducing the risk of hemorrhag-ic complications. In RE-SONATE study, dabigatran showed a 92% reduction in risk of the VTC relapse compared to placebo, but a 2.9-fold increase in risk of large or small clinically significant bleeding.

The article presents the review of clinical studies that determined the role of apixaban in the early treatment and long-term secondary prophylaxis of deep vein thrombosis and lower limbs and and/or pulmonary arteries embolism. It also defines a patient population for whom apixaban administration is justified on the basis of pilot studies and the clinical data accumulated to date at various clinics.

The article presents the results of its own study of the effect of long-term (not less than 30 days) enoxa-parin therapy (1 mg/kg administered subcutaneously every 12h) on the risk of recurrent venous thromboembolic complications (VTC) and recanalization of thrombosed deep veins. The enoxaparin therapy was compared with a standard approach to treatment (unfractionated heparin for not less than 5 days followed by the administration of warfarin). The extended enoxaparin therapy was significantly more effective than standard treatment due to its impact on the risk of recurrent deep vein thrombosis (DVT) and recanalization of thrombosed deep veins. On top of that, the effect of enoxaparin in the first month of treatment of VTC episodes last for the next 11 months. As a result, the extension of enoxaparin therapy was associated with an 88% reduction in the risk of DVT recurrence during 12 months of anticoagulant therapy and a 2.5-fold increase in the probability of recanalization of venous occlusions by the end of the first year of treatment compared with the standard therapy with unfractionated heparin and warfarin.

About 10% of the adult population is diagnosed with chronic kidney disease (CKD), and its presence is associated with a high risk of developing cardiovascular diseases including ventricular fibrillation (VF). The long-term monitoring of patients has found a clear association between the degree of renal failure and risk of VF development. ARIC (1) study showed that a relative risk of VF development in patients with glomerular filtration rate (GFR) 15-29 ml/min was 3.2 (95% CI 2.0-5.0), and in patients with normal GFR 1.3 (95% CI 1.1-1.6), p < 0.0001. GFR reduction is an independent predictor of VF development. The mechanism underlying the link between renal failure and risk of VF development is not fully clear.