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High prevalence of atrial fibrillation (AF) and low effectiveness of antiarrhythmic therapy are the reasons for searching a new therapeutic strategy focused on this arrhythmia. Recent studies have demonstrated the link between anatomical atrial structure changes and pro-inflammatory cytokine levels, that led to a new direction in AF pathogenesis investigation. Whether AF paroxysm is primary, or on the contrary, inflammation provokes AF, is still unknown. Inflammation might be not the only cause of atrial arrhythmogenicity but it plays an important role in myocardial predisposition for AF paroxysm. Results of multi-center studies have shown that early administration of ACE inhibitors, angiotensin receptor antagonists, and statins in cardiac patients significantly reduces AF risk, and could be a promising therapeutic strategy.

Aim. To study the real-world pharmaceutical reduction of high cardiovascular disease (CVD) risk in patients with Type 2 diabetes mellitus (DM-2).Material and methods. In total, 200 DM-2 patients agreed to participate in the study, including survey, anthropometry, and laboratory tests.Results. In two-thirds of the patients, carbohydrate metabolism was decompensated due to inadequate disease awareness, inadequate or absent glycemia self-control, and rare prescription of combined therapy. The main reasons for not achieving target blood pressure (BP) levels included high rates of monotherapy, low doses of antihypertensive drugs, inadequate treatment compliance, and low rates of BP self-control. Statins were taken by 23% of the patients, and aspirin medications – by 16%.Conclusion. In real-world clinical settings, a substantial proportion of DM-2 patients require intensified treatment, in accordance with the concept of multi-factorial risk reduction.

Vascular wall infiltration with lipoproteins, in particular with low-density lipoprotein (LDL) cholesterol (LDLCH), plays an important role in atherosclerosis pathogenesis. Elevated LDL-CH levels are associated with increased risk of coronary heart disease (CHD). Based on the evidence from experimental and clinical studies, there is a direct link between LDL-CH reduction and decreased incidence of cardiovascular events. Statins are medications of choice for LDL-CH reduction; however, statin monotherapy does not always result in target LDLCH level achievement, due to pharmaco-genetic factors and adverse effects of the therapeutically effective statin doses. In these clinical situations, a combination of low-dose statins with other lipid-lowering agents is effective. Recently, high effectiveness of statin combination with ezetimibe (inhibitor of intestine CH absorption) has been demonstrated. It is explained by targeting both mechanisms which determine blood CH levels (intestine absorption and hepatic synthesis), with a substantial reduction in LDL-CH levels as a result.

Various clinical forms and complications of atherosclerosis remain the leading causes of morbidity and mortality in both developed and developing countries. HMG-CoA reductase inhibitors (statins) are the key components of pharmaceutical treatment in patients with dyslipidemia (DLP) and atherosclerosis. Statins have been thoroughly studied not only in randomised clinical trials with “hard” end-points, but also in the so called regression studies. The latter tested the hypothesis of qualitative and quantitative changes in coronary arteries (CA) due to aggressive reduction (-40-50% from baseline) of low-density lipoprotein (LDL) cholesterol levels. The results of the first regression studies justified the increase of statin doses in clinical practice, as well as led to large randomised clinical trials of statin therapy. In current regression studies, vascular atherosclerosis is monitored using such methods as intima-media thickness assessment, magnetic resonance imaging, and intravascular ultrasound. Reduced progression of carotid atherosclerosis (METEOR Study, rosuvastatin 40 mg/d; ENHANCE Study, ezetimibe 10 mg/d plus simvastatin 20 mg/d) and CA atherosclerosis (REVERSAL Study, atorvastatin 80 mg/d), as well as atherosclerosis regression (ASTEROID Study, rosuvastatin 40 mg/d), was demonstrated. Aggressive lipid-lowering effect (-40-50%), observed for high statin doses in modern regression clinical trials, was well-tolerated, with no severe adverse events. The results and principles of regression studies could be widely used in clinical practice, to optimise the treatment of severe DLP and atherosclerosis.

Such periinterventional complications of percutaneous coronary intervention (PCI) as myocardial infarction (MI), “no-reflow/slow-flow” phenomenon, and stroke, affect long-term survival. Therefore, their risk should be effectively stratified and reduced. The existing approaches for predicting the risk of periinterventional complications are typically focussed on assessing the fatal outcome probability and do not consider modifiable risk factors, which restricts their use to evaluation of PCI benefits and risk only. Periinterventional statin therapy reduces the risk of periinterventional MI both in patients with stable angina and individuals with acute coronary syndrome. This beneficial action could be related to anti-inflammatory, antioxidant, antithrombotic, NO- and immunomodulating effects of statins. The evidence on cardioprotective effects of periinterventional beta-blocker therapy is contradictory for PCI patients. Existing data on the link between beta-blocker treatment and increased risk of “slow flow” phenomenon, coronary artery spasm, heart failure, and arterial hypotension point to the need for optimisation of the pulse-reducing component of pharmaceutical PCI support. One of the promising methods for solving this problem could be administration of ivabradine – a medication with confirmed anti-ischemic and antianginal action, but no effects on myocardial contractility or blood pressure level.

Clinical trials of modern antiarrhythmics often demonstrate their ineffectiveness in life-threatening ventricular arrhythmias and sudden cardiac death (SCD), as well as inadequate pharmacological control in atrial fibrillation (AF). Together with cholesterol-lowering effect, statins demonstrate various pleiotropic effects (anti-inflammatory, anti-proliferative, endothelial function improvement, etc.). Statins can reduce the risk of life-threatening arrhythmias and SCD in patients with acute myocardial infarction, after coronary revascularization and implantation of cardioverter-defibrillator. Statin therapy may decrease recurrent AF risk.

Based on СОURAGE study results (Clinical Outcomes Utilizing Percutaneous Coronary Revascularization and Aggressive Guideline-Driven Drug Evaluation), modern tactics for management of patients with coronary heart disease (CHD) and stable angina are discussed (percutaneous coronary intervention, PCI, or aggressive drug therapy with statins, aspirin, ACE inhibitors etc.). The role of secondary drug prevention, according to modern guidelines, is highly appraised. The emphasis is put on the leading role of lipid-lowering therapy with statins and ezetimibe. No significant difference was observed for complication rates in PCI group (n=1149) and optimal drug therapy (n=1138). Cumulative incidence of primary events during 4,6 years of follow-up was 19,0% and 18,5% in PCI and drug therapy groups, respectively (р=0,62). Therefore, in patients with stable CHD, PCI as a first-line strategy does not reduce the risk of death, myocardial infarction, or cardiovascular events, if combined with drug treatment.

Aim. To analyse cardiovascular risk levels in patients with arterial hypertension (AH); to assess atorvastatin effectiveness in AH patients without cardiovascular events (CVE).Material and methods. In total, 612 CVE-free patients with AH were examined. The participants with SCORE risk level of 5-9% received atorvastatin (10 mg/d) and standard antihypertensive therapy. The authors examined the effects of atorvastatin on blood pressure levels, lipid profile, endothelium-dependent vasodilatation (EDVD) in the brachial artery reactive hyperemia test, intima-media thickness (IMT) of common carotid arteries, C-reactive protein (CRP) concentration, and heart rate variability (HRV).Results. At the end of the study, the atorvastatin group demonstrated a significant decrease in mean levels of total cholesterol (CH), low-density lipoprotein CH and CRP was observed, as well as an increase in EDVD. In addition, in the atorvastatin group, the reduction of sympathetic component of low-frequency and especially very low-frequency HRV was more manifested than in the standard therapy group. In CVE-free patients with AH, atorvastatin therapy (10 mg/d) effectively normalised lipid profile, neuro-humoral and sympatho-adrenal activity parameters, and also demonstrated anti-inflammatory effect.Conclusion. The majority of AH patients have high and very high risk levels and, therefore, require a complex approach towards cardiovascular risk factor modification.

Aim. То assess clinical effectiveness of simvastatin in coronary heart disease (CHD) patients with paroxysmal atrial fibrillation (AF). Material and metliods. Thirty-two CHD patients (mean age 53+2,7 years) with paroxysmal AF and cardioversion-restored sinus rhythm were randomized into two groups. Group I (n=12) included patients receiving standard antiarrhythmic therapy and simvastatin. Group II - only standard therapy. Examination methods included: physical examination; standard 12-lead ECG with QT interval, QT dispersion (QTd), corrected QT (QTc), and QTc dispersion measurement; ECG-monitoring with assessment of heart rate (HR), incidence and features of extrasys toles, and number of ischemic ST depression episodes. laboratory tests included lipid profile and hepatic transaminase levels assessment. Results. During the follow-up period, recurrent AF incidence was significantly lower (p