This document is an updated and extended version of the clinical guidelines by the Expert Committee of the Society of Cardiology of the Russian Federation, the Schmidt-Kudryashov All-Russian Association of Thrombosis, Haemorrhage, and Vascular Pathology, and the Russian Flebologists’ Association. The previous version was approved in 2006, at the joint meeting of the Schmidt-Kudryashov All-Russian Association of Thrombosis, Haemorrhage, and Vascular Pathology, and the Russian Flebologists’ Association.

To assess the effects of electro-mechanical heart remodelling on atrial fibrillation development, 190 patients with coronary heart disease (CHD), arterial hypertension (AH), and recurrent atrial fibrillation (AF) were examined (the main group). The comparison group included 181 patients with CHD and AH, but no AF. The patients underwent standard clinical examination, standard 12-lead electrocardiography with the assessment of time and dispersion indices of atrioventricular conductivity, echocardiography, and Doppler echocardiography with heart remodelling type analysis. The findings were analysed by AF presence and paroxysm frequency. The main group demonstrated an increase in end-diastolic volumes of left atrium and ventricle, as well as in dispersion indices of atrial and atrioventricular conductivity. The prevalence of concentric hypertrophy, left ventricular dilatation, and left ventricular diastolic dysfunction in men and women from the main group was higher than in their peers from the comparison group. The results obtained could be used for differential treatment and prevention of cardiovascular events in patients with CHD, AH, and recurrent AF.

The features of endothelial function and metabolic factors, such as insulin resistance and dyslipidaemia, were studied in 67 patients with arterial hypertension (AH) and obesity. It has been shown previously that in AH patients with metabolic disturbances, decreased endothelium-dependent vasodilatation, increased microalbuminuria, and elevated von Willebrand factor levels could facilitate the development and progression of endothelial dysfunction. Metabolic factors, such as insulin resistance and high blood pressure, become the markers of endothelial dysfunction in AH patients.

The parameters of carbohydrate, protein, lipid metabolism and haemostasis were analysed in patients with Type 1 and 2 diabetes mellitus (DM-1, DM-2), who demonstrated the progression of micro- and macroangiopathy over the five-year follow-up period. Micro- and macroangiopathy progression was associated with haemostatic and metabolic disturbances, and also had some DM type-specific features. The disturbances of protein metabolism and haemostasis were as important as carbohydrate and lipid metabolism disturbances in predicting angiopathy progression.

The associations between adiponectin levels and atherosclerotic remodelling of carotid arteries were investigated in 50 patients with coronary heart disease. Among patients with increased adiponectin levels, carotid atherosclerosis was less severe (significantly lower mean values of total plaque volume), while arterial wall elasticity was higher (lower mean values of arterial stiffness, Icompl), compared to individuals with lower adiponectin concentrations.

To assess the link between angina pectoris and traditional or rheumatoid arthritis-associated risk factors, 64 female patients were examined. Angina syndrome was diagnosed in 53%, being linked to such factors as age, menopause, obesity, dyslipidaemia, arterial hypertension, animal fat consumption, as well as to rheumatoid arthritis duration, the number of involved joints, severity of joint dysfunction, and steroid and methotrexate therapy.

Atypical clinical course of myocardial infarction (MI) is used as an example, in order to demonstrate the benefits of systematic diagnostic approach in the acute MI phase. A new cardiac diagnostic complex, using the modern information technologies, allows automatic calculation of vector electrocardiogram (VECG) loop parameters, as well as detailed analysis of specific VECG parts magnified 3000 times. VECG method, as an addition to standard ECG, demonstrated myocardial damage in the reciprocal zone, disturbed conductivity and repolarisation, and cardiac overload, which gave an opportunity to specify the degree and the spread of pathological changes in the myocardium.

Clinical effectiveness, safety, and the impact on left ventricular (LV) systolic and diastolic function were assessed for Propanorm® and Cordarone® in patients with atrial fibrillation (AF), arterial hypertension (AH), coronary heart disease (CHD), and chronic heart failure (CHF) with preserved ejection fraction (EF). In total, 218 patients were randomised, and 189 were included in the study (132 in the Propanorm® group, and 57 in the Cordarone® group). The follow-up period lasted for 12 months. Primary end-points included all-cause mortality, cardiovascular mortality, fatal and non-fatal myocardial infarction or stroke, and hospitalisation due to decompensated CHF or recurrent AF. Secondary end-points included AF episode frequency, their duration, ventricular rate (VR) during AF paroxysms, blood pressure levels, dynamics of CHD and CHF functional class (FC), LV systolic and diastolic function, treatment safety and adverse effects in patients with CHF and preserved LV EF. At 12 months, Propanorm® effectiveness, in terms of AF paroxysm prevention, reached 61,4% and was similar to that for Cordarone®. In 31,8% of the patients from the Propanorm® group, the number of tachyarrhythmia episodes decreased by 82,4%, the total paroxysm duration was reduced by 86,6%, and VR during the paroxysm decreased by 16,1%. Improved LV diastolic filling resulted in the increased proportion of FC I CHF patients (by 50%), and reduced hospitalisation rates (by 72,9%) among the patients from the Propanorm® group. In patients with AH, CHD, and CHF with preserved LV EF, Propanorm® demonstrated a better safety profile, compared to Cordarone, since the respective adverse effect incidence was 1,5% vs. 45,6%.

Metabolic syndrome (MS) is an important problem of the modern medicine, due to its substantial impact on cardiovascular risk. Visceral fat tissue is an endocrine organ, producing a wide spectrum of biologically active substances – adipokines, which influence atherosclerosis progression, thrombosis, insulin resistance, and other processes. The aim of this study was to assess the activity of adipokines, endothelial dysfunction markers, and systemic inflammation, in patients with arterial hypertension (AH) and MS, who received an ACE inhibitor zofenopril. This open study of pleiotropic and antihypertensive effects of zofenopril included 32 patients with Stage I-II AH and MS (18 men, 14 women; mean age 54 years (from 48 to 60,5 years)). Zofenopril demonstrated not only a good antihypertensive effect, but also a significant (p=0,001) decrease in leptin levels, from 18,7 ng/ml (12,8;34,0) to 17,5 ng/ml (12,5;30,6); some increase (p=0,12) in adiponectin levels, from 10,4 mkg/ml (7,5;14,1) to 13,6 mkg/ml (6,5;17,7); a significant (p=0,001) reduction in endothelin-1 activity, from 0,38 fmol/l (0,25;1,03) to 0,34 fmol/l (0,14;0,88); and a slight decrease (p=0,03) in intercellular adhesion molecule (ICAM) levels, from 323,9 ng/ml (242,25;512,31) to 315,47 ng/ml (187,31;424,38).

This study was aimed at the assessment of antiarrhythmic (AA) effectiveness of myocardial revascularisation (MR), as well as the evaluation of the Mexicor (M) role in the complex management of coronary heart disease (CHD) patients with high-grade ischemic ventricular arrhythmia (VA). In total, 34 patients underwent MR, based on the clinical, instrumental, and angiographic indications. Another 20 patients, who refused MR, or did not have clinical and angiographic indications for it, received conservative treatment, with an addition of M (300 mg/d). AA effectiveness of MR and M was assessed during Holter ECG monitoring, stress tests, and radionuclide examination. MR effectiveness, regardless of the intervention type, was maximal in the early post-surgery period (79,4%) and decreased later, reaching 55,8% after 12 months. In patients who did not undergo MR, M therapy demonstrated good AA effectiveness (75-100%). Therefore, the restoration of coronary circulation and myocardial metabolism agrees with the principles of complex etiopathogenetic treatment of ischemic VA.

Administration of L-carnitine in patients with anterior acute myocardial infarction (AMI) prevents left ventricular remodelling. Current study was aimed to assess the effect of L-carnitine administration on mortality and heart failure in patients with anterior AMI. CEDIM 2 trial was a randomized, double-blind, multicentre, placebo-controlled trial planned to enrol 4,000 patients with acute anterior AMI. The trial was interrupted after the enrolment of 2,330 patients because of the lower than expected enrolment rate. The primary end point was a composite of death and heart failure at 6 months; 5-day mortality was the secondary end point. During the 6-month follow-up, the primary endpoint was not significantly different between the L-carnitine and placebo group (9,2 vs. 10,5%, p=0,27). A reduction in mortality was seen in the L-carnitine arm on day 5 (secondary end-point) from randomization (HR=0,61, 95% CI 0,37–0,98, p=0,041). In CEDIM 2 trial L-carnitine therapy led to a reduction in early mortality (secondary end-point) without affecting the risk of death and heart failure at 6 months in patients with anterior AMI, leading to a non-significant finding with respect to the primary end-point.

In total, 316 patients with Q wave myocardial infarction (MI) were randomised into three groups. For six months after hospital discharge, 103 patients from the control group received standard therapy (aspirin, enalapril, metoprolol, and simvastatin). Group 1 (n=103) also received trimetazidine, and Group 2 (n=206) was administered ramipril, carvedilol, and trimetazidine. The end-point incidence was assessed during the two-year follow-up period (repeat MI, unstable angina, death, and the combination of these end-points). The Group 2 therapy (ramipril, carvedilol, and trimetazidine) was the most effective in terms of the end-point incidence reduction. The effectiveness of the Group 1 treatment (enalapril, metoprolol, and trimetazidine) was slightly lower, while the control group therapy (standard treatment, plus enalapril and metoprolol) was the least effective.

The study aimed to assess the effects of long-term and course mildronate therapy (500 mg/d) on cognitive function in elderly patients with arterial hypertension (AH) and cognitive dysfunction. This open, randomised, controlled comparative study in parallel groups (long-term therapy for 52 weeks, or two three-month courses over a year vs. standard therapy for 52 weeks) included 180 elderly patients with AH and cognitive dysfunction. Neuro-psychological examination included MMSE test, Reitan test, Wechsler test, test for speech activity, memory (10 words), and serial count, kinetic test, and MFI-20 test for asthenia assessment. Depression and anxiety symptoms were assessed with Beck and Tailor scales, respectively. Long-term mildronate therapy was the only treatment regimen improving all cognitive function parameters, compared to baseline and the control group. In the course mildronate therapy group, some cognitive function parameters did not change significantly, compared to baseline; however, the final values were not significantly different from those in the long-term mildronate therapy group. Course therapy was more effective than standard treatment in terms of improving the asthenia and anxiety scale parameters.

Aim. To analyse how effectively the three main risk factors – arterial hypertension (AH), hypercholesterolemia, and Type 2 diabetes mellitus (DM-2) are controlled among male and female patients with coronary heart disease (CHD), who are residents of the Ingush Republic. Material and methods. The study included 300 men and 230 women (mean age 54±0,4 and 55,7±0,5 years, respectively) – residents of the three Ingush Republic regions. The standard questionnaire included items on sociodemographic parameters, behavioural risk factors, and pharmaceutical therapy. Blood pressure (BP) was measured in a sitting position, with a 5-minute interval between two measurements. In all patients, blood levels of total cholesterol (TCH, mmol/l)) and glucose (mmol/l) were measured. Adequate control of AH, hypercholesterolemia, and DM-2 was defined as the achievement of target levels of BP, TCH, and fasting glucose during the treatment. Results. Among CHD patients, hypercholesterolemia was the most prevalent risk factor in both men (95%) and women (81%). Only 11,3% of men and 21% of women received lipid-lowering therapy (typically, statins). Target TCH levels were achieved in 1% and 2%, respectively. AH was registered in 77,3% and 65% of male and female CHD patients, respectively. In men with CHD and AH, 93% received antihypertensive therapy (18%, 49%, and 26% received one, two, or three medications, respectively). Target BP levels were observed in 43% of the treated men. In women with CHD and AH, 28%, 60%, and 7% received one, two, or three antihypertensive medications, respectively; target BP levels were achieved in 49%. DM-2 prevalence reached 17% in men and 13% in women. Among patients with CHD and DM-2, target fasting glucose levels were registered in 41% of men and 21% of women. Conclusion. Among CHD patients, target BP levels were achieved in every second participant, while target glucose levels were observed in 30%, and target TCH concentrations were registered in less than 2%.

We investigated whether prevention of cardiac and vascular remodelling associated with inhibition of angiotensin II is independent of the blood pressure (BP) lowering action of angiotensin II type 1 (AT1) receptor blockade. Spontaneously hypertensive rats, 8 weeks old, were treated with olmesartan, atenolol, or vehicle in their drinking water for 56 days. At the end of each treatment, arterial pressure and heart rate were measured, the ratio of heart weight to body weight was calculated, collagen deposition in the heart was determined histochemically using picrosirius red staining, and wall-to-lumen ratio in isolated mesenteric arteries was measured by a video graphic approach. At 3 weeks after the initiation of treatment, rats medicated with olmesartan showed lower values of systolic BP compared with rats given atenolol or vehicle, whereas no difference in directly measured BP were observed at the end of study in anesthetized rats given olmesartan or atenolol. Rats given atenolol showed sustained bradycardia, whereas cardiac hypertrophy and collagen deposition was prevented only in spontaneously hypertensive rats given olmesartan. Olmesartan or atenolol reduced arteriolar wall-to-lumen ratio (olmesartan: 11,5±0,4%; atenolol: 13,3±0,6%; vehicle: 18,4%±1,1); however, this effect was greatest in rats medicated with the angiotensin II type 1 antagonist. Although control of BP is a factor in the prevention of cardiac and vascular hypertrophy, our studies suggest that blockade of angiotensin II receptors may attenuate the structural changes in the heart and blood vessels of hypertensive animals independent of a reduction in BP.

In the United States, a vast segment of the adult population is classified as having the cardiometabolic syndrome, and currently there are epidemic rates of both type 2 diabetes mellitus and obesity. Hypertension is closely linked with these metabolic disorders and is a strong independent predictor of incident type 2 diabetes. In addition, hypertension is an important contributor to increasing cardiovascular disease risk in patients with the cardiometabolic syndrome. Lowering elevated blood pressure in patients with the cardiometabolic syndrome or diabetes is a critical component of reducing global cardiovascular risk. However, aggressive management of hypertension in these patients is often challenging, and the presence of these conditions is associated with poor blood pressure control. The utility of β-blockers in patients with these conditions continues to be a subject of intense debate, given the adverse metabolic effects associated with conventional β-blockers. Data on vasodilating β-blockers, however, suggest that these agents have favourable or neutral metabolic effects and generally more favourable effects when compared with non-vasodilating members of this class. These agents may expand the utility of β-blockers to patient populations traditionally considered not to be optimal candidates for β-blocker therapy – a fact which has important clinical implications, because more antihypertensive agents are needed to diversify the therapeutic options available for clinicians treating hypertension in patients with the cardiometabolic syndrome or type 2 diabetes.