TGF-ß Isoforms and GDF-15 in the Development and Progression of Atherosclerosis.

The effect of oxidised lipoproteins on the endothelium, monocytes, platelets, and macrophages is a key factor in the initiation and development of atherosclerosis. Antioxidant action, lipoprotein metabolism, and chronic inflammation are the fields of research interest for better understanding the development of the disease. All the fields are related to inflammation and hence to the secretion of cytokines, which are being investigated as potential diagnostic markers for the onset of atherosclerosis. Pathways of vascular damage are crucial for the development of new laboratory readouts. The very early detection of endothelial cell damage associated with the onset of atherosclerosis, allowing the initiation of therapy, remains a major research goal. This article summarises the latest results on the relationship of tumour growth factor beta (TGF-ß) isoforms and growth differentiation factor 15 (GDF-15) to the pathogenesis of atherosclerosis: which cells involved in atherosclerosis produce them, which effectors stimulate their synthesis and secretion, how they influence atherosclerosis development, and the relationship between the levels of TGF-ß and GDF-15 in the blood and the development and extent of atherosclerosis.

Anti-Cancer Properties of Resveratrol: A Focus on Its Impact on Mitochondrial Functions.

Cancer is one of the most serious public health issues worldwide, demanding ongoing efforts to find novel therapeutic agents and approaches. Amid growing interest in the oncological applications of phytochemicals, particularly polyphenols, resveratrol-a naturally occurring polyphenolic stilbene derivative-has emerged as a candidate of interest. This review analyzes the pleiotropic anti-cancer effects of resveratrol, including its modulation of apoptotic pathways, cell cycle regulation, inflammation, angiogenesis, and metastasis, its interaction with cancer stem cells and the tumor microenvironment. The effects of resveratrol on mitochondrial functions, which are crucial to cancer development, are also discussed. Future research directions are identified, including the elucidation of specific molecular targets, to facilitate the clinical translation of resveratrol in cancer prevention and therapy.

Novel Knowledge about Molecular Mechanisms of Heparin-Induced Thrombocytopenia Type II and Treatment Targets.

Heparin-induced thrombocytopenia type II (HIT II), as stated in the literature, occurs in about 3% of all patients and in 0.1-5% of surgical patients. Thrombosis develops in 20-64% of patients with HIT. The mortality rate in HIT II has not decreased using non-heparin treatment with anticoagulants such as argatroban and lepirudin. An improved understanding of the pathophysiology of HIT may help identify targeted therapies to prevent thrombosis without subjecting patients to the risk of intense anticoagulation. The review will summarize the current knowledge about the pathogenesis of HIT II, potential new therapeutic targets related to it, and new treatments being developed. HIT II pathogenesis involves multi-step immune-mediated pathways dependent on the ratio of PF4/heparin and platelet, monocyte, neutrophil, and endothelium activation. For years, only platelets were known to take part in HIT II development. A few years ago, specific receptors and signal-induced pathways in monocytes, neutrophils and endothelium were revealed. It had been shown that the cells that had become active realised different newly formed compounds (platelet-released TF, TNFα, NAP2, CXCL-7, ENA-78, platelet-derived microparticles; monocytes-TF-MPs; neutrophils-NETs), leading to additional cell activation and consequently thrombin generation, resulting in thrombosis. Knowledge about FcγIIa receptors on platelets, monocytes, neutrophils and FcγIIIa on endothelium, chemokine (CXCR-2), and PSGL-1 receptors on neutrophils could allow for the development of a new non-anticoagulant treatment for HIT II. IgG degradation, Syk kinase and NETosis inhibition are in the field of developing new treatment possibilities too. Accordingly, IdeS and DNases-related pathways should be investigated for better understanding of HIT pathogenesis and the possibilities of being the HIT II treatment targets.

Relationship between Oxidative Stress and Left Ventricle Markers in Patients with Chronic Heart Failure.

Oxidative stress is proposed in the literature as an important player in the development of CHF and correlates with left ventricle (LV) dysfunction and hypertrophy in the failing heart. In this study, we aimed to verify if the serum oxidative stress markers differ in chronic heart failure (CHF) patients' groups depending on the LV geometry and function. Patients were stratified into two groups according to left ventricular ejection fraction (LVEF) values: HFrEF (<40% (n = 27)) and HFpEF (≥40% (n = 33)). Additionally, patients were stratified into four groups according to LV geometry: NG-normal left ventricle geometry (n = 7), CR-concentric remodeling (n = 14), cLVH-concentric LV hypertrophy (n = 16), and eLVF-eccentric LV hypertrophy (n = 23). We measured protein (protein carbonyl (PC), nitrotyrosine (NT-Tyr), dityrosine), lipid (malondialdehyde (MDA), oxidizes (HDL) oxidation and antioxidant (catalase activity, total plasma antioxidant capacity (TAC) markers in serum. Transthoracic echocardiogram analysis and lipidogram were also performed. We found that oxidative (NT-Tyr, dityrosine, PC, MDA, oxHDL) and antioxidative (TAC, catalase) stress marker levels did not differ between the groups according to LVEF or LV geometry. NT-Tyr correlated with PC (rs = 0.482, p = 0.000098), and oxHDL (rs = 0.278, p = 0.0314). MDA correlated with total (rs = 0.337, p = 0.008), LDL (rs = 0.295, p = 0.022) and non-HDL (rs = 0.301, p = 0.019) cholesterol. NT-Tyr negatively correlated with HDL cholesterol (rs = -0.285, p = 0.027). LV parameters did not correlate with oxidative/antioxidative stress markers. Significant negative correlations were found between the end-diastolic volume of the LV and the end-systolic volume of the LV and HDL-cholesterol (rs = -0.935, p < 0.0001; rs = -0.906, p < 0.0001, respectively). Significant positive correlations between both the thickness of the interventricular septum and the thickness of the LV wall and the levels of triacylglycerol in serum (rs = 0.346, p = 0.007; rs = 0.329, p = 0.010, respectively) were found. In conclusions, we did not find a difference in serum concentrations of both oxidant (NT-Tyr, PC, MDA) and antioxidant (TAC and catalase) concentrations in CHF patients' groups according to LV function and geometry was found. The geometry of the LV could be related to lipid metabolism in CHF patients, and no correlation between oxidative/antioxidant and LV markers in CHF patients was found.

Reactive Oxygen Species Induced Pathways in Heart Failure Pathogenesis and Potential Therapeutic Strategies.

With respect to structural and functional cardiac disorders, heart failure (HF) is divided into HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). Oxidative stress contributes to the development of both HFrEF and HFpEF. Identification of a broad spectrum of reactive oxygen species (ROS)-induced pathways in preclinical models has provided new insights about the importance of ROS in HFrEF and HFpEF development. While current treatment strategies mostly concern neuroendocrine inhibition, recent data on ROS-induced metabolic pathways in cardiomyocytes may offer additional treatment strategies and targets for both of the HF forms. The purpose of this article is to summarize the results achieved in the fields of: (1) ROS importance in HFrEF and HFpEF pathophysiology, and (2) treatments for inhibiting ROS-induced pathways in HFrEF and HFpEF patients. ROS-producing pathways in cardiomyocytes, ROS-activated pathways in different HF forms, and treatment options to inhibit their action are also discussed.

Phenotypic and Functional Heterogeneity of Monocyte Subsets in Chronic Heart Failure Patients.

Chronic heart failure (CHF) results when the heart cannot consistently supply the body's tissues with oxygen and required nutrients. CHF can be categorized as heart failure (HF) with preserved ejection fraction (HFpEF) or HF with reduced ejection fraction (HFrEF). There are different causes and mechanisms underlying HF pathogenesis; however, inflammation can be regarded as one of the factors that promotes both HFrEF and HFpEF. Monocytes, a subgroup of leukocytes, are known to be cellular mediators in response to cardiovascular injury and are closely related to inflammatory reactions. These cells are a vital component of the immune system and are the source of macrophages, which participate in cardiac tissue repair after injury. However, these monocytes are not as homogenous as thought and can present different functions under different cardiovascular disease conditions. In addition, there is still an open question regarding whether the functions of monocytes and macrophages should be regarded as causes or consequences in CHF development. Therefore, the aim of this work was to summarize current studies on the functions of various monocyte subsets in CHF with a focus on the role of a certain monocyte subset in HFpEF and HFrEF patients, as well as the subsets' relationship to inflammatory markers.

The Difference of Cholesterol, Platelet and Cortisol Levels in Patients Diagnosed with Chronic Heart Failure with Reduced Ejection Fraction Groups According to Neutrophil Count.

Background and Objectives: It is known that neutrophils are involved in the pro-inflammatory processes and thus, can have a great impact on the pathophysiology of heart failure (HF). Moreover, hypercholesterolemia heightens neutrophil production, thereby accelerating cardiovascular inflammation. However, there is a lack of information about the relation of low inflammation to the state of stress, hypercholesterolemia, and pro-thrombotic statement in patients with chronic HF. Therefore, we aimed to determine whether platelet, cholesterol and cortisol levels differ in a different inflammatory condition groups according to the neutrophil count in patients diagnosed with CHF with reduced ejection fraction (CHFrEF), and whether there is a correlation between those readings. Materials and Methods: The average of neutrophil count was 4.37 × 109 L; therefore, 180 patients were separated into two groups: one with relatively a higher inflammatory environment (neutrophil count ≥ 4.37 × 109 L (n = 97)) and one with a relatively lower inflammatory environment (neutrophil count < 4.38 × 109 L (n = 83)). We also determined the levels of lymphocytes, monocytes, platelet count (PLT), mean platelet volume (MPV), platelet aggregation, the levels of cortisol and cholesterol and the concentrations of C reactive protein (CRP) and fibrinogen. Results: We found that CRP, fibrinogen and cortisol concentrations were statistically significantly higher in the group with higher neutrophil counts. However, there were no differences among cholesterol concentration and other markers of platelet function between the groups. We also showed that PLT, leukocyte and monocyte counts were higher in the group with a higher neutrophil count, and the PLT correlated with other cell type count and CRP. In addition, the neutrophil count correlated with concentrations of fibrinogen, evening cortisol and CRP. Conclusions: Cortisol, fibrinogen and CRP levels, PLT and monocyte counts were higher in the CHFrEF patient group with higher neutrophil counts. The cholesterol levels and platelet function readings did not differ between the groups. The neutrophil count correlated with evening cortisol concentration.

Platelet Activity and Its Correlation with Inflammation and Cell Count Readings in Chronic Heart Failure Patients with Reduced Ejection Fraction.

Background and objectives: There has been an increasing interest in the role of inflammation in thrombosis complications in chronic heart failure (HF) patients. The incidence of thrombosis in HF has been shown to be the highest in patients classified as NYHA IV (New York Heart association). It is stated that inflammation is regulated by platelet-induced activation of blood leukocytes. We aimed to compare the platelet and cell count readings in chronic HF with reduced ejection fraction (HFrEF) patients according to NYHA functional class and to evaluate the correlation between those readings. Materials and methods: A total of 185 patients were examined. The results of heart echoscopy (TEE) testing; fibrinogen, N-terminal pro b-type natriuretic peptide (NT-proBNP), C reactive protein (CRP), and cortisol concentrations; complete blood counts; and a 6 min walking test were assessed and platelet aggregation was determined. Results: Mean platelet volume (MPV) increased with deterioration of a patient's state (p < 0.005). Lymphocyte count and percentage were the lowest in the NYHA IV group (p < 0.005). Neutrophil and monocyte percentage and count were the highest (p < 0.045) in the NYHA IV group. Adenosine diphosphate (ADP)- and ADR-induced platelet aggregation was higher in the NYHA III group compared to NYHA II and I groups (p < 0.023). NYHA functional class correlated with mean platelet volume (MPV) (r = 0.311, p = 0.0001), lymphocyte count (r = -0.186, p = 0.026), monocyte count (p = 0.172, p = 0.041), and percentage (r = 0.212, p = 0.011). CRP concentration correlated with NT-proBNP (r = 0.203, p = 0.005). MPV correlated with fibrinogen concentration (r = 0.244, p = 0.004). Conclusions: (1) MPV could be considered as an additional reading reflecting a patient's condition, however the use of MPV to identify patients at risk of hypercoagulable state should be evaluated in more extensive studies; (2) increased neutrophil and monocyte counts could indicate a higher inflammatory state in chronic HFrEF.

Selenium Anticancer Properties and Impact on Cellular Redox Status.

(1) Background: In this review, we provide information published in recent years on the chemical forms, main biological functions and especially on antioxidant and prooxidant activities of selenium. The main focus is put on the impact of selenoproteins on maintaining cellular redox balance and anticancerogenic function. Moreover, we summarize data on chemotherapeutic application of redox active selenium compounds. (2) Methods: In the first section, main aspects of metabolism and redox activity of selenium compounds is reviewed. The second outlines multiple biological functions, asserted when selenium is incorporated into the structure of selenoproteins. The final section focuses on anticancer activity of selenium and chemotherapeutic application of redox active selenium compounds as well. (3) Results: optimal dietary level of selenium ensures its proper antioxidant and anticancer activity. We pay special attention to antioxidant activities of selenium compounds, especially selenoproteins, and their importance in antioxidant defence. It is worth noting, that data on selenium anticancer properties is still contraversive. Moreover, selenium compounds as chemotherapeutic agents usually are used at supranutritional doses. (4) Conclusions: Selenium play a vital role for many organism systems due to its incorporation into selenoproteins structure. Selenium possesses antioxidant activity at optimal doses, while at supranutritional doses, it displays prooxidant activity. Redox active selenium compounds can be used for cancer treatment; recently special attention is put to selenium containing nanoparticles.

The Effect of Oxidant Hypochlorous Acid on Platelet Aggregation and Dityrosine Concentration in Chronic Heart Failure Patients and Healthy Controls.

Background and objective: One of the reasons for thrombosis in chronic heart failure (CHF) might be reactive forms of oxygen activating platelets. The aim of this study was to evaluate the effect of oxidant hypochlorous acid (HOCl) on platelet aggregation and dityrosine concentration in CHF patients and healthy controls. Materials and Methods: CHF patients (n 67) and healthy (n 31) were investigated. Heart echoscopy, 6-min walking test, complete blood count, platelet aggregation, and dityrosine concentration were performed. Platelet aggregation and dityrosine concentration were measured in plasma samples after incubation with different HOCl concentrations (0.15, 0.0778, and 0.0389 mmol/L). Results: Platelet aggregation without oxidant was lower (p = 0.049) in CHF patients than in controls. The spontaneous platelet aggregation with oxidant added was higher in CHF patients (p = 0.004). Dityrosine concentration was also higher (p = 0.032) in CHF patients. Platelet aggregation was the highest in samples with the highest oxidant concentration in both healthy controls (p = 0.0006) and in CHF patients (p = 0.036). Platelet aggregation was higher in NYHA III group in comparison to NYHA II group (p = 0.0014). Concentration of dityrosine was significantly higher in CHF samples (p = 0.032). The highest concentration of dityrosine was obtained in NYHA IV group samples (p 0.05). Intensity of platelet aggregation, analyzed with ADP, was correlated with LV EF (r 0.42, p = 0.007). Dityrosine concentration was correlated with NYHA functional class (r 0.27, p 0.05). Conclusions: The increase in platelet aggregation in CHF and healthy controls shows the oxidant effect on platelets. The increase in dityrosine concentration in higher NYHA functional classes shows a higher oxidative stress in patients with worse condition.

Multiplicity of effects and health benefits of resveratrol.

Resveratrol is mainly found in grapes and red wine, also in some plants and fruits, such as peanuts, cranberries, pistachios, blueberries and bilberries. Moreover, nowadays this compound is available as purified preparation and dietary supplement. Resveratrol provides a wide range of benefits, including cardiovascular protective, antiplatelet, antioxidant, anti-inflammatory, blood glucose-lowering and anticancer activities, hence it exhibits a complex mode of action. During the recent years, these properties have been widely studied in animal and human models, both in vitro and in vivo. This paper is intended to present information published during the recent years on the biological activities and multiple effects of resveratrol.

Effect of physical training on indices of platelet aggregation and fibrinogen concentration in patients with chronic heart failure.

OBJECTIVE: The aim of this study was to determine the effect of long-term physical load on the changes in the fibrinogen concentration and platelet aggregation. MATERIAL AND METHODS: Platelet aggregation was investigated in 144 patients while fibrinogen concentration in 138 patients with CHF. The patients were divided into the groups of the trained patients and the controls and were investigated as follows: on admission to the hospital (stage 1); after treatment in the hospital (stage 2); after 3 months (stage 3); after 6 months (stage 4); and after 1 year (stage 5). The indices were investigated before and after physical load. RESULTS: It was determined that fibrinogen concentration significantly increased after physical load in all the treatment stages in both groups of the patients (P=0.045). In the course of the treatment, fibrinogen concentration gradually decreased in the group of the trained patients (P=0.02). Platelet aggregation investigated with ADP significantly increased after physical load in all the stages in both groups of the patients and decreased during the different investigation stages in the groups of the untrained (P=0.02) and trained patients. Platelet aggregation investigated with ADR consistently decreased before physical load during the different investigation stages in the groups of the trained (difference is not significant) and untrained patients (P=0.02). CONCLUSIONS: Physical training reduces fibrinogen concentration in patients with CHF. It remains unclear whether physical training can have an effect on the decrease in platelet aggregation in patients who have long-term physical training applied.

The effect of Polyscias filicifolia bailey biomass tincture on the protein synthesis process in the heterogeneous system from the isolated pig heart.

BACKGROUND AND OBJECTIVE: An insufficient supply of oxygen to the heart influences the process of protein synthesis. The aim of this study was to determine the effect of the Polyscias filicifolia Bailey biomass tincture on the protein synthesis process in a heterogeneous translation system from the isolated pig heart. MATERIALS AND METHODS: The effect of anoxia was evaluated after 20- and 90-minute anoxia. With the aim to determine the effect of Polyscias, the pig hearts were perfused with a buffer containing the Polyscias filicifolia Bailey biomass tincture. To determine the rate and the level of translation, the incorporation of [(14)C]-leucine into translational products in a cell-free system was measured. RESULTS: The protein synthesis level decreased by 23%-42% when the translation system containing cytosol from the anoxic heart was used. When the translation system containing a ribosomal fraction after 20-minutes anoxia was used, the protein synthesis level was the same as in the control. In the case of 90-minute anoxia, it decreased by 16%. The protein synthesis rate and the level in the translation system containing cytosol from the heart after 20-minute anoxic perfusion with the buffer containing Polyscias was the same as in the control. CONCLUSIONS: A decrease in the protein synthesis rate and the level after 20-minute anoxia was determined by changes in cytosol. On the other hand, 90-minute anoxia caused changes in cytosol and the ribosomal fraction. The Polyscias filicifolia Bailey biomass tincture restored the protein synthesis process acting on the components of the translation system in cytosol and the ribosomal fraction.

[Changes in parameters of coagulation system after treatment of chronic heart failure with ß-adrenoblockers, angiotensin-converting enzyme inhibitors, calcium antagonists, diuretics, anticoagulants, antiagregants, cardiac glycosides, and physical exercise]. / ß-adrenoblokatoriu, AKF slopikliu, kalcio antagonistu, diuretiku, antikoaguliantu, antiagregantu, sirdi veikianciu glikozidu ir fizinio kruvio poveikis kresejimo sistemos rodmenims sergant letiniu sirdies nepakankamumu.

Scientific research has proved that coagulation system is more active in patients with chronic heart failure than in healthy people. Therefore, the aim of this article was to review the data in literature about changes in coagulation system after treatment of chronic heart failure with ß-adrenoblockers, angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, cardiac glycosides, diuretics, anticoagulants, and antiagregants. It is known that ß-adrenoblockers used separately decrease platelet aggregation and angiotensin-converting enzyme inhibitors reduce P-selectin expression as well. Low-molecular-weight heparin decreases the concentrations of prothrombin fragments, D-dimers; orally administered anticoagulants reduce the concentrations of interleukin 6, von Willebrand factor, intercellular adhesion molecules, fibrinogen 1+2 and increases the concentration of plasminogen activator inhibitor-1. Both anticoagulants reduce the levels of VII:C factors and thrombin-antithrombin III complex. The use of aspirin together with clopidogrel reduces the concentration of intercellular adhesion and platelet-endothelial cell adhesion molecules and expression of P-selectins; however, these concentrations do not vary while using aspirin alone. The treatment with ACE inhibitors together with calcium antagonists and ß-adrenoblockers decreases activated partial thromboplastin time, concentrations of D-dimers, plasminogen activator inhibitor-1, vascular cell adhesion molecules, CD63 and expression of L- and P-selectins. While analyzing the effect of abovementioned agents, it is necessary to mention that data reported by different authors are not consistent. Therefore, the effect of particular drugs on the particular parameters of coagulation system has not been completely elucidated.

The coagulation system changes in patients with chronic heart failure.

Though heart failure can mainly be caused by systolic or diastolic dysfunction, the impairments of the neurohormonal, immune, and hemostatic systems are observed too. Therefore, it is not easy to determine etiology of the syndrome. Parameters that can be helpful to predict chronic heart failure, to evaluate its course and the risk of complications are still being searched. The aim of this article is to review the recent studies in order to find the links between the coagulation system and the development of chronic heart failure. Stress is a key factor for the development of most diseases including chronic heart failure too. Signals of emotional and physical stress via particular structures trigger an increase in concentrations of the following hormones: noradrenaline, renin, angiotensin II, aldosterone, vasopressin. It is proved that it causes the disorders of the coagulation system: an increase in the following factors of plasma coagulation (fibrinogen, VII, VIII, fibrinopeptide A, thrombin-antithrombin complex), fibrinolysis (D-dimer), endothelium (interleukin 1, endothelin 1, vascular cell adhesion molecules, endothelial growth factor), platelet activity (von Willebrand factor, intercellular adhesion molecules, platelet factor 4, P-selectin, thromboxane A(2), thromboglobulin, CD63P) and cytokines (tumor necrosis factor, interleukin 6) and decrease in E-selectin. The role of particular coagulation factors for the development of chronic heart failure has not been understood yet. Thus, it is necessary to carry out further studies.

Coagulation alterations in treating arrhythmias with radiofrequency ablation.

OBJECTIVE: To determine an influence of radiofrequency ablation on changes in coagulation system. MATERIAL AND METHODS: We investigated 30 patients with cardiac arrhythmias. Platelet aggregation, fibrinogen and D-dimer level were analyzed before, right after, 24 and 72 h after radiofrequency ablation. Platelet aggregation was explored in whole blood and platelet-rich plasma using adenosine diphosphate (ADP), epinephrine, and collagen for induction. RESULTS: Platelet aggregation induced by ADP and collagen in whole blood plasma increased significantly (P<0.01) (by 45% and 43%, respectively) in 24 h after radiofrequency ablation and remained increased in 72 h after radiofrequency ablation (by 11% and 35%, respectively) (P<0.01) as compared with baseline results. Spontaneous aggregation of platelet-rich plasma as well as ADP- and collagen-induced platelet aggregation tended to decrease right after radiofrequency ablation. Epinephrine-induced platelet aggregation significantly decreased by 17.5% after radiofrequency ablation (P<0.01) and started to increase in 24 h after radiofrequency ablation. In 72 h after radiofrequency ablation, platelet aggregation induced by different agonists increased by 7-45% significantly (P<0.05), and values were higher than baseline ones. Fibrinogen level after radiofrequency ablation did not differ from that of the baseline (3.08+/-0.7 g/L), but D-dimer level increased significantly (from 0.39+/-0.3 to 1.29+/-2.4 mg/L, P<0.01). In 24 h after radiofrequency ablation, an increase in fibrinogen level and a decrease in D-dimer level were found. Fibrinogen level increased to 3.32+/-0.6 g/L significantly in 72 h after radiofrequency ablation (P<0.05). Meanwhile, D-dimer concentration decreased to 0.78+/-0.8 mg/L, but it was still significantly higher (P<0.05) than the baseline value. CONCLUSION: Despite diminished platelet aggregation and increased D-dimer level right after radiofrequency ablation, a risk of thrombosis increased in the next few days after radiofrequency ablation.

[Possibilities of platelet function assays]. / Trombocitu funkcijos tyrimo galimybes.

The aim of this article is to review various methods used and started to introduce into practice for determining platelet function, their possibilities, advantages, and disadvantages. Nowadays, in platelet function investigations, devices and their systems with unequal possibilities, operating in different principles, are used. However, because of a wide variety of platelets defects, none of them gives the accuracy of 100%. In order to avoid mistakes, several assays are used. Analysis of platelets function testing is represented in two ways: according to its investigation object and investigation methods and according to the most frequently used platelet function assays. The most important criteria are presented in two different tables.

Influence of radiofrequency catheter ablation on platelet aggregation.

The objective of this article was to find out how radiofrequency catheter ablation (RFA) influences platelet aggregation (PA), and the dependence on the total energy (TE) of RFA used and the cause of arrhythmia. We investigated 97 patients. PA was analyzed before, after, and in 24 hours after RFA. ADP- and epinephrine-induced PA significantly decreased after RFA by 5% and 8.9% (P < .001), respectively, and increased in 24 hours close to baseline. PA induced by ADP and collagen did not radically depend on the TE. Epinephrine-induced PA decreased after RFA by 0%, 8% (P < .05), and 16.9% (P < .01) in groups of patients where the TEs used were <4000 J, 4000 to 15,000 J, and >15,000 J, respectively. There were no significant differences in PA between groups based on the cause of arrhythmia. ADP- and epinephrine-induced PA significantly decreased after RFA and returned close to baseline in 24 hours. Epinephrine-induced PA was inversely associated with the TE used for RFA.

Influence of aspirin or heparin on platelet function and postoperative blood loss after coronary artery bypass surgery.

The aim of the study was to assess the effect of aspirin or heparin pretreatment on platelet function and bleeding in the early postoperative period after coronary artery bypass grafting (CABG) surgery. Seventy-five male patients with coronary artery disease who underwent CABG with cardiopulmonary bypass (CPB) were studied. The patients were divided into three groups: Group 1 (n=25) included patients receiving aspirin pretreatment, Group 2 (n=22) received heparin pretreatment, and Group 3 (n=28) included patients who received no antiplatelet or anticoagulant pretreatment. Twenty-four hours after surgery, all patients were administered aspirin therapy that was continued throughout their hospitalization period. We assessed the following preoperative blood coagulation indices: activated partial thromboplastin time (aPTT), international normalized ratio (INR), and fibrinogen. We compared platelet count and platelet aggregation induced by adenosinediphosphate (ADP) before surgery, 1 h after surgery, 20 h after surgery and on the seventh postoperative day. We assessed drained blood loss within 20 postoperative hours. Preoperative blood coagulation indices did not differ among the groups. Platelet count was also similar. One hour after surgery, platelet count significantly decreased in all groups (p<0.001), after 20 postoperative hours it did not undergo any marked changes, and on the seventh postoperative day, it significantly increased in all groups (p<0.001). Before surgery, the lowest index of ADP-induced platelet aggregation was found in Group 1 (p<0.05). One hour after surgery, platelet aggregation significantly decreased in all groups, most markedly in Group 3 (p<0.001), yet after 20 h, its restitution tendency and a significant increase in all groups was noted. On the seventh day, a further increase in the statistical mean platelet aggregation value was noted in Groups 2 and 3. Comparison of platelet aggregation after 20 postoperative hours and on the seventh day after surgery revealed a significantly higher than 10% increase of the index in 32% of patients in Group 1 (p<0.05), 27.3% of patients in Group 2 (p<0.05) and in 35.7% of patients in Group 3 (p<0.001). The lowest statistically significant value of postoperative blood loss was noted in Group 2 (p<0.01). Our study has shown that aspirin or heparin pretreatment had no impact on the dynamics of platelet function in the early postoperative period after CABG. The lowest postoperative blood loss was noted in patients pretreated with heparin.

[Influence of preoperative treatment with aspirin or heparin on platelet function and intensity of postoperative bleeding in early period after coronary artery bypass surgery]. / Aspirino ar heparino, vartojamo iki operacijos, itaka trombocitu funkcijai bei kraujavimo intensyvumui po aortos vainikiniu jungciu operaciju.

OBJECTIVE: The aim of the study was to evaluate influence of preoperative treatment with aspirin or heparin on platelet function and intensity of postoperative blood loss in early period after coronary artery bypass grafting (CABG). MATERIAL AND METHODS: Study involved 75 patients (men) with ischemic heart disease, who underwent CABG. Patients were divided into three groups: aspirin pretreated (I group, n=25), heparin pretreated (II group, n=22) and III group (n=28) had no antiplatelet or anticoagulant pretreatment. At 24 h after surgery all patients started treatment with aspirin (ASS 100, Bayer), which lasted all hospitalization period. We have evaluated preoperative coagulation parameters: activated partial thromboplastin time, international normalized ratio, and fibrinogen level. Also we have compared platelet count, platelet aggregation induced by adenosine diphosphate during preoperative period, at 1 h, 20 h and at 7 day after surgery. RESULTS: Preoperative coagulation parameters were comparable in all groups. Platelet count was also similar. One hour after surgery platelet count remarkably decreased in all groups (p<0.001); at 20 hours after surgery changes remained the same and at 7 day a significant increase was observed in all groups (p<0.001). The lowest rate of preoperative platelet aggregation was found in I group (p<0.05). At 1 hour after surgery platelet aggregation decreased significantly in all groups, particularly in III group (p<0.001). At 20 hours after surgery platelet aggregation had a tendency to reach previous level and increased substantially in all groups. We have found more than 10% increase in platelet aggregation at 7 day compared to 20 hours postoperatively. These changes were observed in 32% (p<0.05), 27.3% (p<0.05) and 35.7% (p<0.001) of patients in the group I, II and III, respectively. Postoperative blood loss was significantly lowest in II group (p<0.01). CONCLUSIONS: Our investigation shows that preoperative treatment with aspirin or heparin had no remarkable influence on dynamics of platelet function in early period after CABG. The least blood loss was observed in patients with heparin pretreatment.