[THE BIOMARKERS OF MYOCARDIAL DAMAGE AND THEIR ROLE IN THE PROGRESSION OF HEART FAILURE (REVIEW)].

Despite the success achieved in the study and treatment of chronic heart failure, this syndrome still remains one of the most difficult and predictable unreliable pathologies. Moreover, in recent years there has been a tendency of growth of such patients. Based on the above, the attention of scientists focuses on new concepts that involve the study of new biomarkers of cardiac damage and the definition of their role in the progression of heart failure. Based on studies conducted by numerous authors, the paper analyzes the importance of new biomarkers of myocardial damage in the development of heart failure. The manuscript describes biomarkers of damage (troponin T, galectin 3, lipocalin, Cystatin C): nature: the causes and mechanisms of their growth, increase and activity. Biomarkers of myocardial damage are shown to have diagnostic and high predicted values. Their temporary definition provides additional information for stratifying the risks of possible complications. It also gives us the opportunity to allocate patients with high risks in a timely manner and eliminate possible adverse complications.

[Metabolic issues of ischemia induced myocardial dysfunction].

Myocardial ischemia represents most common cause of necrosis of cardiomyocytes, cardio sclerosis and heart failure. Main clinical manifestation of myocardial ischemia is systolic and/or diastolic dysfunction. It has been shown, that local disturbance of myocardial contractility is not always determined by cell necrosis and cardio sclerosis, as improvement of coronary perfusion may lead to restoration of contractile function of myocardium. Present review outlines aspects of phenomenon of ischemic preconditioning, hibernation and myocardial stunning (so called new ischemic syndromes) that are suggested to be determinants of ischemia induced myocardial dysfunction. No-reflow (Less known type of myocardial stunning) is considered also. However, further studies of molecular mechanisms of ischemic syndromes are necessary for development of new methods of protection of myocardium against ischemic or reperfusion injury.

[Ventricular arrhythmias and sudden cardiac death].

Sudden cardiac death (SCD) - this natural death caused by cardiac reasons and which is characterized by sudden loss of consciousness within first hour after revealing of sharp clinical symptoms. A primary factor of SCD is not traumatic. It occurs suddenly and unexpectedly. The high risk of development of sudden cardiac death is basically associated with ventricular arrhythmias. Electrophysiological anomalies in cells lead to development of ventricular ectopic activity or ventricular tachycardia which comes to the end with fibrillation. The ultimate goal of antiarrhythmic drug therapy is to restore normal rhythm and conduction Treatment of ventricular arrhythmia provides application of antiarrhythmic medicines, beta-adrenoblokators, amiodarone, lidocaine, sotalole, implantation cardioverters - defibrillators (ID), catheter ablation, surgical manipulations. ID therapy is recommended for primary prevention developments SCD in patients with ventricular fibrillation against a background of the acute miocardial infarction.

[Prevention of thrombolitic compications with atrial fibrillation].

This study presents the modern principles of prevention and treatment of thrombolitic complications in patients with atrial fibrillation. The adequate tactics and algorithm of antithrombotic therapy in the case of variety versions of this disease is considered in this study. It described the efficiency and safety of oral anticoagulants (antagonist Vit K) varfarin with the purpose to inform the practical doctors with principals of prevention and treatment of hemorrhagic complications. This publication appears as a fragment from the series of atrial fibrillation management and destinated for physicians and cardiologist.

[Role of immune inflammatory activity in chronic heart failure progress].

Significant role of immune inflammatory reactions along with activation of the RAAS (rennin-angiotensin-aldosterone system) and the sympatho-adrenal system in CHF (chronic heart failure) pathogenesis is considered in the present survey article. Together with haemodynamic disorders activation of inflammatory reactions, which involve anti-inflammatory cytokines, is shown to be one of the main factors affecting CHF course and prognosis. Alteration of cytokine level is associated with injury level, gravity of the disease course and its clinical outcome. Prognostic value of determination of inflammation mediators as predictors of cardiovascular diseases and clinical outcomes is evaluated. Urgency of search for new medication in addition to "traditional preparations" used for the treatment of CHF is shown.

The relationship between endothelial dysfunction and 24-hour blood pressure rhythm in patients with arterial hypertension.

The purpose of the study was an investigation of relationships between duration of arterial hypertension (AH), 24-hour blood pressure (BP) rhythm and endothelial function. 18 (mean age 50+/-8.7; 8%-male, 10%-female) outpatients with AH were included in the study. All subjects underwent off-therapy 24-hour ambulatory BP monitoring and vascular Doppler echography of the brachial artery. Hypercholesterolemic subjects, diabetics, smokers and patients with Raynaud's phenomenon were excluded from the study. Compared with dipper women, non-dipper women showed statistically significant lowering of FMD (11.8+/-4.2% vs. 3.4+/-3.85%, p<0.005). The same fact was observed in men (16.5+/-3.45% dipper vs. 4.0+/-1.08% non-dipper, p<0.05). Association of the duration of arterial hypertension with FMD was significant (7.9+/-4% (<10 y) vs. 2.0+/-3% (>10 y); p= 0.017). Compared with dipper patients, non-dipper subjects showed an impaired endothelial function (11.4+/-2% vs. 3.5+/-2.6%; p=0.0006). The present data confirm the presence of disturbed endothelium-dependent vasodilatation in arterial hypertension. The study showed significant relation between duration of arterial hypertension and FMD. Furthermore, these results demonstrate that the main factor, which leads to endothelial dysfunction, is the shortage in the lowering BP during the night.