THE INFLUENCE OF ANXIETY AND DEPRESSIVE CONDITIONS ON AFTERINFARCTION REMODELING IN PATIENTS WITH STEMI

Depression after AMI increases the frequency of re-hospitalization because of acute coronary syndrome, heart failure, MI, and is a risk factor for cardiac arrest and death. The objective of the study was to define the influence of anxiety-depressive disorders (ADD) on afterinfarction remodeling and the participation of sST2 fibrosis factor in this process. 100 STEMI patients were enrolled to the study, 81 (81 %) male and 29 (29 %) female, of average age of 58,94 ± 10,16 years. Examinations were performed twice: during 1–3 days after PCI with infarct-related artery stenting and included clinical-anamnesis data, blood analyses. The sST2 level was defined by immune-fermentative method with usage of «Presage ST2 Assay», Critical Diagnostics, USA. For ADD objectivization, HADS (Heart Anxiety and Depression Scale) and Teylor questionary were used. In 6 month 6-minute walk test and the volume fraction of interstitial collagen (VFIC) were done. Conclusion: ADD in patients with STEMI aggravates the course of postinfarction period and entails the progression of fibrotic-hypertrophic processes and corresponding remodeling of myocardium, decrease of physical tolerance

Experience of the application of pedagogical control as a way of diagnosing the effectiveness of students 'academic activity at the department of medical and bioorganic chemistry at KHNMU

У статті на основі аналізу літературних джерел вказується на значення правильної організації і управління навчально-пізнавальною діяльністю студентів- медиків та роль у цьому процесі одної з важливих складових - педагогічного контролю. Автори діляться досвідом застосування педагогічного контролю при вивченні хімічних дисциплін на своїй кафедрі: наголошують на значенні контролюючих заходів різних форм як засобу діагностування стану навчальної роботи для студентів і для викладачів.Based on the analysis of literary sources, the article indicates the importance of the proper organization and management of educational and cognitive activities of medical students and the role in this process of one of the important components - pedagogical control. The authors share their experiences with use of pedagogical control in the study of chemical disciplines at their department: they emphasize the importance of monitoring activities of various forms as a way of diagnosing the state of academic work for students and teachers

THE ROLE OF A NEW BIOMARKER GROWTH DIFFERENTIATION FACTOR 15 IN PROGNOSIS OF PATIENTS WITH ACUTE CORONARY SYNDROME AND TYPE 2 DIABETES MELLITUS

Numerous studies confirm worse results in diabetic patients with acute coronary syndrome (ACS) compared with non-diabetic patients. Different mechanisms underlie the adverse outcomes of ACS and diabetes mellitus. In this connection, a special place is occupied by the study of new biomarkers that reflect the complex pathogenic processes in these patients. Purpose: to investigate the role of the biomarker GDF 15 in prognosis of adverse outcomes in type 2 diabetes mellitus (DM2T) patients with ACS. Materials and methods: 73 patients with different forms of ACS were screened. Levels of biomarkers: GDF 15, N-terminal pro brain natriuretic peptide (NT-pro BNP) and C-reactive protein (C-RP) were determined. The follow up period was 1 year. Endpoint was defined as lethal outcome. Results: significant differences in GDF 15 level has been found, prognostic value of GDF 15 was estimated in patients with DM2T, using a ROC-analysis. Threshold level of GDF 15 has been determined as 3894 pg/ml, with sensitivity of 64 % and specificity of 75 %. Conclusion: Patients with ACS and DM2T more often had a history of different cardiovascular diseases and risk factors compared to patients without diabetes. GDF 15 level was significantly higher in patients with ACS who had history of DM2T

Мозковий нейротрофічний фактор та його поліморфізм Val66Met (rs6265). Значення для серцево-судинної системи

Brain derived neurotrophic factor (BDNF) is a neurotrophin that determines proliferation and survival of the cholinergic, serotoninergic and dopaminergic neurons. Deficit of BDNF results in the decrease of neuron plasticity and impaired cognitive function. In large amount, BDNF is detected in hippocampus, cerebral cortex, basal forebrain, fibroblasts, astrocytes, different types of neurons, Schwann cells, smooth muscle cells. It has been shown that BDNF and its receptors also expressed in un-neuronal tissues and different types of cells (in heart, atherosclerotic vessels, macrophages, lymphocytes, thrombocytes, endothelial cells, smooth vessel cells), which all together defines the role of neurotrophin in cardiovascular system. In embryonic period, the BDNF insufficiency worsens intramyocardial vessels development. Through BDNF, the blood flow regulation of revascularization in ischemic tissue increases and left ventricular function after event improves. The level of ВDNF in the blood reflects its concentration in the brain. The low protein level was independent predictor of 4-year coronary death and all-case mortality. The high serum BDNF levels associated with the decrease of cardiovascular risk. It has been shown that at the most СNS diseases such as Alzheimer’s, Parkinson’s, Huntington’s diseases, the pathological process develops due to the low level of BDNF in the brain, accompanied by the impaired function of vessel. Both cardiovascular diseases and depression-anxiety disorders are complex violations caused by the genetic and environment factors. In this context single nuclear polymorphism Val66Met of BDNF gene is possible candidate associated with psychopathology and combines this condition with cardiovascular events: substitution of valine by methionine in codone 66 (Val66Met) of proBDNF molecule affects the intracellular processing and BDNF secretion.Brain derived neurotrophic factor (BDNF) — нейротрофин, который обусловливает пролиферацию и выживание холинергических, серотонинергических и дофаминергических нейронов. Его дефицит снижает пластичность нейронов и нарушает когнитивные функции. В большом количестве BDNF определяется в гиппокампе, церебральной коре, базальных отделах переднего мозга, а также на фибробластах, астроцитах, нейронах разных типов и локализации, шванновских и гладкомышечных клетках. Показано, что BDNF и его рецепторы также экспрессируются в ненейрональных тканях и разных типах клеток (в сердце, атеросклеротических сосудах, макрофагах, лимфоцитах, тромбоцитах, эндотелиальных клетках, гладкомышечных клетках сосудов), что определяет роль нейротрофина в сердечно-сосудистой системе. Дефицит BDNF в эмбриональный период ухудшает развитие внутримиокардиальных сосудов. Благодаря BDNF происходит усиление кровотока и регуляция реваскуляризации в ишемизированной ткани, улучшение функции левого желудочка после ишемического события. Уровень ВDNF в крови отображает его концентрацию в головном мозге. Низкий уровень протеина был независимым предиктором 4-летней коронарной смертности и смертности от всех причин. Высокая концентрация BDNF в сыворотке ассоциировалась со снижением риска сердечно-сосудистых событий. Показано, что при большинстве заболеваний центральной нервной системы, в частности болезни Альцгеймера, Паркинсона и Хантингтона, к развитию патологического процесса приводит снижение концентрации BDNF в головном мозге, что сопровождается нарушением функции сосудов. Как сердечно-сосудистые заболевания, так и тревожно-депрессивные состояния, являются комплексными нарушениями, обусловленными генетическими факторами и факторами окружающей среды. В этом контексте однонуклеотидный полиморфизм Val66Met гена BDNF является возможным кандидатом, который ассоциируется с развитием психопатологии и объединяет это состояние с сердечно-сосудистыми событиями: замена валина на метионин в кодоне 66 (Val66Met) молекулы проBDNF влияет на внутриклеточный процессинг и секрецию BDNF.Brain derived neurotrophic factor (BDNF) — нейротрофін, який зумовлює проліферацію і виживаність холінергічних, серотонінергічних та дофамінергічних нейронів. Його дефіцит знижує пластичність нейронів і порушує когнітивні функції. У великій кількісті BDNF визначається у гіпокампі, церебральній корі, базальних відділах переднього мозку, а також на фібробластах, астроцитах, нейронах різного типу і локалізації, шванівських клітинах і клітинах гладеньких м’язів. Показано, що BDNF та його рецептори також експресуються в ненейрональних тканинах і різних типах клітин (у серці, атеросклеротичних судинах, макрофагах, лімфоцитах, тромбоцитах, ендотеліальних клітинах, гладеньких м’язах судин), що визначає роль BDNF у серцево-судинній системі. Дефіцит BDNF в ембріональний період погіршує розвиток внутрішньоміокардіальних судин. Завдяки BDNF відбувається посилення кровотоку та регуляція реваскуляризації в ішемізованій тканині, поліпшення функції лівого шлуночка після ішемічної події. Рівень ВDNF у крові відображує його вміст у мозку. Низький рівень BDNF був незалежним предиктором 4-річної коронарної смертності та смертності від усіх причин. Висока концентрація BDNF у сироватці асоціювалася зі зниженням ризику кардіоваскулярних подій. Показано, що при багатьох захворюваннях центральної нервової системи, зокрема хворобах Альцгеймера, Паркінсона і Хантингтона, до розвитку патологічного процесу призводить зниження концентрації BDNF у мозку, що супроводжується порушенням функції судин. Як серцево-судинні захворювання, так і тривожно-депресивні стани, є комплексними порушеннями, спричиненими генетичними чинниками та чинниками довкілля. У цьому контексті однонуклеотидний поліморфізм Val66Met гена BDNF є можливим кандидатом, який асоціюється з розвитком психопатології та поєднує цей стан із серцево-судинними подіями: заміна валіну на метіонін у кодоні 66 (Val66Met) молекули проBDNF впливає на внутрішньоклітинний процесинг та секрецію BDNF

ALLELE STATUS OF ALDOSTERONE SYNTHASE (CYP11B2) GENE POLYMORPHISM AND CARDIAC REMODELING AFTER ST SEGMENT ELEVATION MYOCARDIAL INFARCTION

Aldosterone plays an important role in the development of reparative and reactive fibrosis and cardiac remodeling (CR) after myocardial infarction. The objective of the study is to investigate the structural and functional parameters of the myocardium, heart rate variability (HRV), exercise intolerance, levels of sST2 in association with polymorphism of CYP11B2 gene of aldosterone-synthase in ST-myocardial infarction (STEMI) patients during a 6-months follow-up period. 85 STEMI patients were enrolled: 68 (80 %) male and 17 (20 %) female, mean age was 58,94 ± 10,16 years. Examinations were performed twice: during 1–3 days after PCI with infarct-related artery stenting and included clinical assessment, ultrasound diagnostic, immunofermentative blood analyses (sST2), polymerase chain reaction in real time (polymorphism –T344C of the CYP11B2 gene). After 6-months of observation, 57 patients were reexamined – clinical assessment, ultrasound diagnostic, HRV were performed. CYP11B2 TT-genotype in 6 months after STEMI is associated with a maladaptive character of after infarction remodeling

Edoxaban versus warfarin in patients with atrial fibrillation

Contains fulltext : 125374.pdf (publisher's version ) (Open Access)BACKGROUND: Edoxaban is a direct oral factor Xa inhibitor with proven antithrombotic effects. The long-term efficacy and safety of edoxaban as compared with warfarin in patients with atrial fibrillation is not known. METHODS: We conducted a randomized, double-blind, double-dummy trial comparing two once-daily regimens of edoxaban with warfarin in 21,105 patients with moderate-to-high-risk atrial fibrillation (median follow-up, 2.8 years). The primary efficacy end point was stroke or systemic embolism. Each edoxaban regimen was tested for noninferiority to warfarin during the treatment period. The principal safety end point was major bleeding. RESULTS: The annualized rate of the primary end point during treatment was 1.50% with warfarin (median time in the therapeutic range, 68.4%), as compared with 1.18% with high-dose edoxaban (hazard ratio, 0.79; 97.5% confidence interval [CI], 0.63 to 0.99; P<0.001 for noninferiority) and 1.61% with low-dose edoxaban (hazard ratio, 1.07; 97.5% CI, 0.87 to 1.31; P=0.005 for noninferiority). In the intention-to-treat analysis, there was a trend favoring high-dose edoxaban versus warfarin (hazard ratio, 0.87; 97.5% CI, 0.73 to 1.04; P=0.08) and an unfavorable trend with low-dose edoxaban versus warfarin (hazard ratio, 1.13; 97.5% CI, 0.96 to 1.34; P=0.10). The annualized rate of major bleeding was 3.43% with warfarin versus 2.75% with high-dose edoxaban (hazard ratio, 0.80; 95% CI, 0.71 to 0.91; P<0.001) and 1.61% with low-dose edoxaban (hazard ratio, 0.47; 95% CI, 0.41 to 0.55; P<0.001). The corresponding annualized rates of death from cardiovascular causes were 3.17% versus 2.74% (hazard ratio, 0.86; 95% CI, 0.77 to 0.97; P=0.01), and 2.71% (hazard ratio, 0.85; 95% CI, 0.76 to 0.96; P=0.008), and the corresponding rates of the key secondary end point (a composite of stroke, systemic embolism, or death from cardiovascular causes) were 4.43% versus 3.85% (hazard ratio, 0.87; 95% CI, 0.78 to 0.96; P=0.005), and 4.23% (hazard ratio, 0.95; 95% CI, 0.86 to 1.05; P=0.32). CONCLUSIONS: Both once-daily regimens of edoxaban were noninferior to warfarin with respect to the prevention of stroke or systemic embolism and were associated with significantly lower rates of bleeding and death from cardiovascular causes. (Funded by Daiichi Sankyo Pharma Development; ENGAGE AF-TIMI 48 ClinicalTrials.gov number, NCT00781391.)

Ezetimibe added to statin therapy after acute coronary syndromes

BACKGROUND: Statin therapy reduces low-density lipoprotein (LDL) cholesterol levels and the risk of cardiovascular events, but whether the addition of ezetimibe, a nonstatin drug that reduces intestinal cholesterol absorption, can reduce the rate of cardiovascular events further is not known. METHODS: We conducted a double-blind, randomized trial involving 18,144 patients who had been hospitalized for an acute coronary syndrome within the preceding 10 days and had LDL cholesterol levels of 50 to 100 mg per deciliter (1.3 to 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.3 to 3.2 mmol per liter) if they were not receiving lipid-lowering therapy. The combination of simvastatin (40 mg) and ezetimibe (10 mg) (simvastatin-ezetimibe) was compared with simvastatin (40 mg) and placebo (simvastatin monotherapy). The primary end point was a composite of cardiovascular death, nonfatal myocardial infarction, unstable angina requiring rehospitalization, coronary revascularization ( 6530 days after randomization), or nonfatal stroke. The median follow-up was 6 years. RESULTS: The median time-weighted average LDL cholesterol level during the study was 53.7 mg per deciliter (1.4 mmol per liter) in the simvastatin-ezetimibe group, as compared with 69.5 mg per deciliter (1.8 mmol per liter) in the simvastatin-monotherapy group (P<0.001). The Kaplan-Meier event rate for the primary end point at 7 years was 32.7% in the simvastatin-ezetimibe group, as compared with 34.7% in the simvastatin-monotherapy group (absolute risk difference, 2.0 percentage points; hazard ratio, 0.936; 95% confidence interval, 0.89 to 0.99; P = 0.016). Rates of pre-specified muscle, gallbladder, and hepatic adverse effects and cancer were similar in the two groups. CONCLUSIONS: When added to statin therapy, ezetimibe resulted in incremental lowering of LDL cholesterol levels and improved cardiovascular outcomes. Moreover, lowering LDL cholesterol to levels below previous targets provided additional benefit