Aim. To assess the prevalence and clinical value of various types of left ventricular (LV) myocardial dyssynchrony in patients with systolic chronic heart failure (CHF).

Material and methods. In total, 71 patients with Functional Class (FC) II–IV CHF (LV ejection fraction (EF) <35%). The main CHF causes were coronary heart disease, CHD (65%) and non-coronary myocardial pathology (NCMP) which resulted in cardiac dilatation (35%). In 50% of the patients, QRS complex duration was

Aim. To assess the severity and potential mechanisms of left ventricular (LV) myocardial remodelling and diastolic dysfunction in symptom-free young patients with mitral valve prolapse (MVP), but no arterial hypertension or significant mitral regurgitation.

Material and methods. The study included 78 patients with MVP (mean age 19,7±1,6 years; 72% males). The control group, comparable by age and sex distribution, included 80 healthy people. Longitudinal diastolic strain rate (SRe) was assessed using the speckle tracking method (Vivid 7 Dim, EchoPAC’06, GE). Serum levels of transforming growth factors (TGF)

Aim. To identify whether mitral regurgitation (MR) is associated with coronary stenosis localisation in women with coronary heart disease (CHD) and postinfarction cardiosclerosis.

Material and methods. Among 15283 patients included in the “Coronary Angiography Register” © from 1991 to 2012, the women with CHD and postinfarction cardiosclerosis (age 31–72 years) were selected: 94 without MR and 53 with moderate or severe MR.

Results. Patients with MR were significantly older (mean age 57,6±8,5 vs. 52,2±8,5 years; p=0,001), had higher NYHA classes (III–IV) of chronic heart failure, CHF (46,2 vs. 18,5%; p=0,001), and a higher prevalence of repeat myocardial infarction (22,6 vs. 7,1%; p=0,010) than the patients without MR. According to echocardiography data, MR patients demonstrated higher values of left ventricular (LV) asynergy (28,7±14,7 vs. 22,4±12,2%; p=0,016) and linear cardiac dimension indices, including LV indices (30,7±3,0 vs. 27,2±2,7 mm/m 2; p<0,001). This clinical group also shown a reduction inLVcontractility (54,7 vs. 17,9%; p<0,001). MR patients were also characterised by multiple localisation of post-infarction cardiosclerosis (33,3 vs. 17,4%; p=0,035). According to coronary angiography data, stenosis of left coronary artery trunk was observed only in women with MR (9,4 vs. 0%; p=0,008). Multivariate analyses demonstrated an independent association between MR, higher NYHA classes, and increasedLVdimension indices.

Conclusion. In women with CHD and post-infarction cardiosclerosis, moderate and severe chronic MR was associated with higher NYHA classes of CHF and increasedLV dimension indices.

Recently, researchers have been increasingly interested in the association between the incidence of cardiovascular events (such as myocardial infarction, MI) and leptin – an adipocyte-produced hormone, which normally is involved in the body mass regulation.

Aim. To assess the role of leptin in the clinical course of acute myocardial infarction with ST segment elevation (STEMI) on ECG.

Material and methods. The study included 89 men aged 23–77 years. All patients underwent coronary angiography (CAG) in the first 12 hours of STEMI. Based on the CAG findings, 80 patients underwent percutaneous coronary interventions (PCI). All participants were divided into two groups, based on the plasma levels of leptin.

Group 1 (n=42) had elevated leptin levels (>5,63 ng/ml), while Group 2 (n=47) had normal leptin levels (<5,63 ng/ml).

Results. In MI patients, leptin concentration was a predictor of the in-hospital diagnosis of Type 2 diabetes mellitus (DM-2). The plasma leptin concentration in the first 24 hours of MI was associated with the levels of interleukin-1-beta, potassium, creatinine, triglycerides, haemoglobin, body mass index, and left ventricular enddiastolic dimension.

Conclusion. Leptin levels in the acute phase of STEMI could be used for the prediction of MI complications and DM-2.

Aim. To assess 30-day and long-term outcomes of various revascularisation strategies in patients with myocardial infarction and ST segment elevation (STEMI) and multi-vessel coronary pathology (MVCP), in regard to the severity of coronary stenosis, as assessed by the SYNTAX scale.

Material and methods. The 30-day and long-term outcomes of various strategies of primary percutaneous coronary intervention (PCI) were assessed in 227 STEMI patients, in regard to the severity of their coronary stenosis (as assessed by the SYNTAX scale). Group 1 included 40 patients who underwent multi-vessel stenting (MVS) as a part of their primary PCI, while Group 2 included 187 patients with indications for staged revascularisation (SR).

Results. At baseline, the MVS and SR subgroups with severe coronary stenosis (SYNTAX score

Aim. To study the prevalence of coronary atherosclerosis in patients referred to planned non-cardiac interventions of intermediate and high risk.

Material and methods. This retrospective analysis included 397 medical histories of patients who underwent planned interventions on aorta, carotid arteries, and peripheral arteries, PA (341 men and 56 women; mean age 60,0±13,0 years). Carotid endarterectomy (CEA) was performed in 161 patients (40,6%); PA intervention in 160 (40,3%); and abdominal aortic reconstruction in 76 (19,1%). Comparisons were performed by coronary angiography (CAG) results and immediate intervention results.

Results. According to the CAG data, coronary artery (CA) stenosis

Aim. To investigate the association between plasma levels of galectin-3 and parameters of endogenous inflammation and nitrosylation oxidative stress (NOS) in patients with decompensated chronic heart failure (CHF).

Material and methods. In total, 197 CHF patients with myocardial infarction in medical history were divided into 3 groups: Group 1 (n=56) with Functional Class (FC) II CHF IIA; Group 2 (n=72) with FC III CHF IIA; and Group 3 (n=69) with FC IV CHF IIB. The control group (CG) included 39 healthy individuals. Plasma levels of galectin-3, 3-nitrotyrosine, low-density lipoprotein (LDL) oxidation, EC-SOD activity, interleukin-6, and high-sensitivity C-reactive protein (hsCRP) were measured.

Results. In Groups 1, 2, and 3, plasma levels of galectin-3 were significantly higher than in CG: by 39% (p<0,05), 164% (p<0,001), and 428% (p<0,001), respectively.

The activity of NOS increased in parallel with CHF FC: by 24% (p<0,05) in Group 1, by 81% (p<0,01) in Group 2, and by 152% (p<0,001) in Group 3. There was a strong positive correlation between galectin-3 and 3-nitrotyrosin and between galectin-3 and LDL oxidation across all three groups. The activity of endogenous inflammation also increased in parallel with CHF FC. A strong positive correlation between galectin-3 and hsCRP, as well as between galectin-3 and interleukin-6, was also observed.

Conclusion. Galectin-3 levels correlate with CHF severity and are associated with the key parameters of NOS and endogenous inflammationn. Therefore, galectin-3 could be regarded as a marker and mediator of these pathological processes.

The assessment of the current disease severity in patients with the syndrome of acute decompensation of chronic heart failure (acute decompensated heart failure, ADHF) and the prediction of the risk of adverse events or in-hospital death remains one of the most important problems of current clinical practice. The need to consider the current disease severity while selecting the therapeutic strategy justifies the search for the most convenient and user-friendly risk scales. 

Aim. To identify the optimal risk scale for the use in patients with ADHF syndrome. The paper focusses on the key risk scales which assess the severity, prognosis, and death risk in this clinical group. The emphasis is on the instruments which can be easily used in the routine clinical practice and which do not require additional examination. 

Material and methods. The data on ADHF patients came from the City Clinical Hospital No. 4 Register. This epidemiological study included both retrospective analysis of the patients hospitalised earlier and the analysis of the data from currently hospitalised ADHF patients. Over 12 months, 1034 patients were included in the study: 662 retrospective cases and 372 currently hospitalised patients (54% women and 46% men; age 58–80 years). 

The following risk scales were used: Russian “Shocks”,USclassification (“warm and dry”), Killip and Kimball (1967), Forrester and Stevenson (1977), Seattle HF Model, and EFFECT. 

Results. Among the analysed risk scales, the most accurate prognosis was observed for the EFFECT scale, particularly for the estimation of the 30 and 360-day risk of death. The predicted 30-day number of deaths was 153, compared to the observed number of 148 (p=0,01). For the 360-day risk, the respective numbers were 352 and 337 (p=0,01). 

Conclusion. Based on the results obtained, all examined scales can be classified into two types: Type I – for the assessment of the current disease severity (with the “warm and dry” classification as the most informative and use-friendly scale); and Type II – for the prediction of life expectancy and death risk at Day 30 and Day 360 (with EFFECT scale as the best-performing instrument).

The paper presents the data on effectiveness and safety of long-term dabigatran
use for the prevention of thromboembolic complications in patients with atrial
fibrillation (AF). The criteria for selecting an optimal dose of dabigatran are
discussed. The authors summarise the results of the current international and
Russian clinical guidelines on dabigatran use in AF patients.

The paper is focussed on the role of increased sympathetic activation in the pathogenesis of arterial hypertension (AH), its exacerbations (hypertensive crises), and complications. One of the effective methods of interrupting pathogenetic “vicious circles” in AH is the blockage of peripheral alpha-adrenoreceptors. One of the medications of choice for urgent treatment of hypertensive crises, as well as for long-term ambulatory treatment, is urapidil – a peripheral sympatholytic with characteristics of a central serotonin receptor agonist.

The paper addresses the role of calcium channel blockers (CCB) in the treatment of patients with arterial hypertension and concomitant pathology. The authors present the findings of the recent studies on CCB effects on renal function, bronchial function, and systemic inflammation. This additional information on comorbidities is essential for the doctors’ choice of optimal individualised therapy.

Aim. To study coagulation and vascular-platelet haemostasis in patients with rheumatoid arthritis (RA) and coronary heart disease (CHD), who receive various non-steroidal anti-inflammatory drugs (NSAID) in combination with low doses of aspirin. 

Material and methods. The study included 79 patients (59 women and 20 men; mean age 61,0 years; mean disease duration 8,5 years) with confirmed RA diagnosis. All participants received disease-modifying anti-inflammatory therapy and NSAID, as well as standard pharmacological CHD therapy. The parameters of coagulation and vascular-platelet haemostasis were compared by the type of administered NSAID (diclofenac, tenoxicam, nimesulide, or meloxicam). In total, 40 patients with increased platelet aggregation but no previous antiaggregant therapy were administered aspirin (100 mg/day). Platelet aggregation was reassessed at Day 7–8 of aspirin therapy. The control group included 25 untreated healthy men (mean age 55 years). 

Results. Activated coagulation haemostasis was observed in 58,2% of patients with RA and CHD, as manifested in increased levels of fibrinogen, soluble fibrin monomer complexes (SFMC), factor XII-dependent fibrinolysis, and von Willebrand factor, compared to controls. The therapy with most NSAID was linked to similar changes in coagulation haemostasis. The patients receiving diclofenac, nimesulide, and meloxicam demonstrated an activation of vascular-platelet haemostasis, as manifested in a significant increase of spontaneous platelet aggregation and ADPinduced platelet aggregation, compared to controls. Among patients receiving tenoxicam, there was a tendency towards a reduction in ADP-induced platelet aggregation (aspirin-like effect). Among patients already receiving diclofenac, nimesulide, or meloxicam, aspirin administration typically resulted in reduced platelet aggregation. In total, 42,4% of the patients did not respond to aspirin therapy. 

Conclusion. Patients with RA and CHD who receive NSAID are also in need of antiaggregant therapy. The latter should be administered under control of vascularplatelet haemostasis, as in a substantial proportion of these patients (42,4%), aspirin effectiveness is not adequate.

Diagnostic criteria are presented for the syndromes related to mutations of fibrillin gene type 1 (such as Marfan syndrome, ectopia lentis, MASS phenotype, mitral valve prolapse syndrome, stiff skin syndrome, Shprintzen-Goldberg syndrome) and for the acromelic group of dysplasias (such as geleophysic dysplasia, Weill-Marchesani syndrome, and acromicria).

The paper is focussed on the therapeutic choice of angiotensin receptor antagonists (ARA). The author presents the data on the comparison between different sartans and their benefits which are not explained by the blood pressure reduction. The findings from large multi-centre studies (EUTOPIA, DOHSAM, and OLIVUS-Ex) are also discussed. The evidence presented justifies specific ARA choices, despite the fact that at a first glance, this medication class appears homogeneous.

The paper focusses on the problem of impaired bone metabolism in patients with chronic heart failure. The authors discuss the importance of this problem, prevalence of osteoporosis, pathophysiological mechanisms of bone metabolism impairment, and common risk factors of heart failure and osteoporosis. The therapeutic strategy in patients with heart failure and osteoporosis is described.

Practitioners are often faced with a combination of coronary heart disease (CHD), chronic heart failure (CHF), and anaemic syndrome. These patients are typically characterised by a worse prognosis of acute and chronic CHD, as well as by a rapid progression of CHF and chronic renal failure (CKF).

This review is focussed on the epidemiology of anaemia in CHD and CHF patients; the aetiology and pathogenesis of anaemia in CHD and CHF; and the changes of cardiovascular parameters in patients with anaemic syndrome. Despite the abundance of studies on CHD and CHF clinical course and prognosis in anaemic syndrome, very little is known about the effects of anaemia treatment on the clinical course and prognosis of CHD. The review presents the external evidence and original results on the prognosis of acute and chronic CHD in anaemic patients. A modern view on anaemia treatment in various CHD forms is also presented.