[Fat cardiomyopathy in patients with severe degree of obesity. Case report].

Currently, the world is constantly increasing the number of people with obesity. As was shown by the Framingham study, obesity is a risk factor for many cardiovascular diseases. The effect of obesity on the structure and function of the heart is manifested in the form of cardiac remodeling, the effect on energy metabolism in the heart and infiltration of both myocardium with lipids, and an increase in the accumulation of adipose tissue in the pericardium, imbalance of adipokines and activation of inflammatory markers. Cardiac remodeling occurs primarily due to thickening of the left ventricle (LV) walls and an increase in the LV myocardium mass. Systolic dysfunction of the heart is less common in obese individuals compared with diastolic dysfunction. However, more modern methods (tissue Doppler, visualization of the deformation of the chambers of the heart strain imaging) reveal a subclinical decrease in systolic function in people with obesity. It is not fully known whether obesity is associated with systolic dysfunction, regardless of other risk factors. In any case, it has been proven that heart failure in people with obesity can develop independently of other risk factors. As an illustration, we give an example when the presence of obesity and concomitant pathology (arterial hypertension, diabetes) led to the development of systolic dysfunction with a decrease in the LV ejection fraction to 35% (fat cardiopathy), which show the potential for the influence of both obesity itself and in combination with concomitant diseases to lead to severe systolic heart failure.

[The «obesity paradox¼ and its degree of proof].

The article gives a critical assessment of the so-called obesity paradox. Methodological errors that occur in the organization of studies that studied the obesity paradox and the formation of comparison groups are highlighted. There are also examples of the disappearance of the obesity paradox when taking into account additional risk factors. The organization of prospective studies or more careful consideration of all currently known risk factors for cardiovascular diseases (CVD) will significantly improve the results of the study of the effect of overweight and obesity on mortality in patients with CVD. Thus, despite the biological possibility of the existence of a positive effect of adipose tissue in CVD, the presence of a large number of errors identified in the analysis of the work of researchers obesity paradox require to reconsider the existence of this phenomenon, it should be taken into account the possibility that the obesity paradox may be a consequence of improper design studies to investigate this phenomenon.

[Desaggregant Therapy of Patients With Ischemic Heart Disease: Unsolved Problems].

At present, choice of antiplatelet therapy in ischemic heart disease (IHD) patients depends on the IHD form, accepted treatment guidelines, contraindications, and cost of drugs. Usually, there is no regular control of the action of antiplatelet drugs. However, in many patients such therapy does not improve the long-term outcome. Increasing dosage of antiaggregants has no positive effect on prognosis. Presently attempts have been made to improve survival by introduction of double or triple drug combinations. Furthermore, although long-term treatment with combination of aspirin and clopidogrel, or both drugs plus one of the new oral anticoagulants (thrombin or a factor inhibitors) has no significant positive effect on total mortality, such therapy significantly increases risk of massive internal and particularly intracranial bleeding. In view of small decreasing effect of such therapy on the rate of reinfarction and stroke, one should search for new approaches. One of such approaches is selection of an antiplatelet drug taking into consideration its effect on the aggregative reactivity of platelets. There are considerable data proving that high residual platelet reactivity (RPR) during antiplatelet therapy is associated with elevated risk of diseases caused by arterial thrombosis. Our research demonstrates that one can overcome high RPR by substituting clopidogrel for aspirin and vice versa or by using combination of these drugs. Indeed, in patients with high RPR during aspirin or clopidogrel monotherapy this combination is associated only with slight increase of number of patients with target level of platelet reactivity. It can be supposed that in this group of patients one of oral anticoagulants (e.g. rivaroxaban) should be used in combination with clopidogrel.

[Control of myocardial ischemia in patients with effort angina and polyvascular atherosclerotic involvement].

In patients with ischemic heart disease with various degree of severity of atherosclerotic involvement of peripheral arteries maintenance of target levels of arterial pressure and heart rate with the help of therapy which includes cardioselective -adrenoblocker as a preparation of choice with addition if necessary of a calcium antagonist and angiotensin converting enzyme inhibitor allows to successfully control myocardial ischemia and heart rate under conditions of everyday life.

[N-terminal pro-brain natriuretic peptide and cardiac involvement in patients with hypertensive disease].

The purpose of this study was to define a correlation between N-terminal proBNP level and extent of cardiac abnormalities. A total of 40 patients with hypertension were included in the study (60.5+/-7.6 years of age; 18 men, 22 women). It was found that patients with hypertension had increased plasma N-terminal proBNP level, that it increased with age and tended to be higher in patients with concentric hypertrophy compared with those with normal geometry and eccentric hypertrophy; however, the differences were not significant. N-terminal proBNP concentration depended on ventricular septal thickness and left ventricular wall thickness. Analysis of association between N-proBNP level and parameters of myocardial diastolic function showed that increased plasma peptide levels correlated with degree of diastolic dysfunction in patients with altered left ventricular relaxation.

[Effect of hypotensive therapy on metalloproteinase activity of the blood in patients with arterial hypertension].

Aim of the study--investigation of dynamics of levels of serum markers of myocardial fibrosis matrix metalloproteinase-1 (MMP-1), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1)--at the background of 3 months hypotensive therapy in 39 patients with arterial hypertension and paroxysmal form of atrial fibrillation. Twenty patients received sotalol, 19--retard form of verapamil. After 3 months of hypotensive therapy in all patients and separately in groups of patients receiving sotalol and verapamil no significant changes of MMP-1 and TIMP-1 occurred. However in patients with most pronounced hypotensive effect according to 24-hour blood pressure monitoring significant elevation of MMP-1 and lowering of TIMP-1 levels took place. This was associated with improvement of ventricular diastolic function. In most patients longer period of therapy (more than 3 months) is required for achievement of regression of damage to the heart.

[Effect of hypotensive drugs on painless ischemia of the myocardium and diastolic function of the left ventricle].

UNLABELLED: Aim of the study was comparative assessment of hypotensive, antiischemic efficacy and effect on left ventricular (LV) diastolic function of calcium antagonists, angiotensin converting enzyme inhibitor and blockers of beta-adrenoreceptors. RESULTS: The data obtained evidence that at monotherapy most pronounced lowering of arterial pressure is observed during use of verapamil CR or amlodipine. Therapy with all studied drugs led to significant decrease of number of episodes of ST-segment depressions, their duration and amplitude during 24 hours. Greatest decrease of frequency of episodes of ST-segment depression was observed during therapy with heart rate reducing calcium antagonists. Disturbed LV diastolic function improved under action of calcium antagonists and beta-adrenoblockers did not change during therapy with angiotensin converting enzyme inhibitor. Diminishment of severity of disturbance of diastolic function under influence of pulse slowing calcium antagonists was associated in the first place with augmentation of LV filling in the first phase of diastole, but during therapy with amlodipine and beta-adrenoblockers - with decrease of contribution of systole of the left atrium. beta-adrenoblockers and diltiazem improved LV diastolic function in patients with episodes of painless myocardial ischemia. CONCLUSION: Comparative assessment of hypotensive action of preparations from three groups revealed that greatest lowering of arterial pressure occurred during monotherapy with verapamil SR and amlodipine. The stadied drugs differently affected damage of a target organ - the heart - in patients with AH.

[Therapy of patients with chronic coronary artery disease and the actual state of the problem in practical public health].

This review presents the analysis of the results of large controlled studies of the efficiency of lipid-lowering agents, disaggregants, and anti-ischemic drugs for treatment of coronary artery disease (stenocardia). It has been shown that not all preparations in one group are equally efficient. The review also adduces comparative data on the use of the listed groups of pharmaceuticals in different European countries and Russian Federation.

[Metalloproteinase activity of the blood in patients with arterial hypertension with paroxysmal form of atrial fibrillation].

Aim of the study was to investigate interrelationship between serum markers of myocardial fibrosis: matrix metalloproteinase -1 (MMP-1), tissue inhibitor of metalloproteinase-1 (TIMP-1) and parameters of echocardiography in patients with arterial hypertension (AH) and paroxysmal form of atrial fibrillation (n=39). We revealed positive correlation of levels of TIMP-1 with thickness of interventricular septum in diastole (r=0,47, p=0,02), peak velocity of late filling of the right ventricle (r=0,46, p=0,01), and negative relation between MMP-1 levels and degree of mitral and tricuspid regurgitation (r=0,43, p=0,005 and r=0,38, p=0,04, respectively). In the group of patients with increased left ventricular myocardial mass index (LVMMI) TIMP-1 level was significantly higher than in patients with normal LVMMI (p < 0,05). In the group combining patients with concentric and eccentric LV hypertrophy TIMP-1 level was significantly higher than in the group combining patients with LV concentric remodeling and normal geometry (p < 0,05). No correlations were revealed between MMP-1 and TIMP-1 levels and parameters of diastolic dysfunction. In patients with AH increase of serum concentrations of TIMP-1 was associated with increased thickness of interventricular septum, increase of LVMMI, and with prognostically unfavorable types of LV remodeling.

[Effect of cordaron on systolic and diastolic functions of the left ventricle in patients with a mixed form of chronic low cardiac output and cardiac arrhythmias]. / Vliianie kordarona na sistolicheskuiu i diastolicheskuiu funktsii levogo zheludochka u bol'nykh so smeshannoi formoi khronicheskoi serdechnoi nedostatochnosti i narusheniiami ritma serdtsa.

AIM: To study effects of cordaron on central hemodynamics reflecting systolic and diastolic functions of the left ventricle (LV) in patients with a mixed form of chronic cardiac failure--a systolic dysfunction and LV diastolic dysfunction type I. MATERIAL AND METHODS: 14 patients with a mixed form of chronic heart failure (CHF) and cardiac arrhythmia were followed up for 6 months. All the patients received ACE inhibitors, diuretics, nitrates and, additionally, cordaron in a supporting dose 200-300 mg/day. Control of central hemodynamics was made with echocardiography before, 1, 3 and 6 months of therapy. RESULTS: For 6 months of therapy LV ejection fraction increased by 16%. LV diastolic function improved, primarily, due to a rise of the E max (by 52% for 6 months of therapy). This reflected early diastolic filling of the LV. Improvement of LV diastolic function was associated with heart rate decrease. CONCLUSION: Cordaron used in addition to ACE inhibitors, diuretics, nitrates improves both systolic and diastolic LV function in patients with a mixed form of CHF.

[Assessment of efficacy of treatment of patients with chronic ischemic heart disease]. / Otsenka éffektivnosti lecheniia bol'nykh khronicheskoi ishemicheskoi bolezn'iu serdtsa.

The lecture summarizes data on approaches to organization of studies in which evidence based data on efficacy and safety of therapy of patients with ischemic heart disease can be obtained. Some novel approaches to improvement of quality of assessment of benefits of treatment are suggested. It is stressed that results of studies of a drug can not be transferred to another one even belonging to the same group. Indications to various methods of estimation of antiischemic action of drugs and their limitations are also described.

[Postinfarction remodeling of the left atrium and left ventricle: effects of long-term treatment with beta adrenergic blockers and angiotensin converting enzyme inhibitors]. / Postinfarktnoe remodelirovanie levogo predserdiia i levogo zheludochka serdtsa: vliianie dlitel'nogo lecheniia beta-adrenoblokatorami i ingibitorami angiotenzinprevrashchaiushchego fermenta.

AIM: To study changes in left atrial volume, geometry and function in myocardial infarction (MI) patients treated with beta-adrenoblocker and ACE inhibitor. MATERIAL AND METHODS: 65 patients with Q-wave myocardial infarction (MI) were followed up for 6 months. Regular check-ups included clinical examination, ECG, echo-CG, dopplercardiography. RESULTS: In MI patients left ventricular remodeling is associated with left atrial remodeling. The greatest inhibition of remodeling in patients with symptoms of cardiac failure was reached with captopril therapy. Atenolol in this respect is less effective. If cardiac failure in MI patients is absent, atenolol impact on the remodeling is stronger than that of captopril. CONCLUSION: In postmyocardial infarction patients remodeling occurs in both heart chambers. The presence of cardiac failure affects remodeling inhibition rate, especially under treatment with beta-adrenoblocker.