After 3 years since the release of the first consensus on the management of patients with hyperuricemia and high cardiovascular risk. During this time, new data appeared that confirm the importance of uric acid control as a risk factor for cardiovascular complications and allow optimizing the algorithm for managing such patients. Studies since the first consensus emerged have identified new hyperuricemia thresholds for cardiovascular risk. The present consensus regulates the prescription of urate-lowering therapy depending on the severity of the detected hyperuricemia. However, although a large body of data demonstrates a positive effect of urate-lowering therapy on the cardiovascular prognosis, there is a need for additional evidence to support the treatment of asymptomatic hyperuricemia.

Aim: evaluate the frequency of prescription and long-term efficacy of different types of specific therapy in patients with pulmonary arterial hypertension (PAH) associated with congenital heart defects (CHD).

Materials and methods. The retrospective part of the study included patients first admitted to the National Medical Research Center of Cardiology in the period 2015-2017 — 30 patients with Eisenmenger syndrome, 25 with left-to-right shunt, 26 with residual PAH. 58 patients were followed up 12 and 24 months after the first hospitalization.

Results. The most commonly prescribed drugs for PAH-CHD pts were sildenafil and bosentan as monotherapy and in combination. By the 24th month of followup there was a twofold increase of patients with combined specific therapy in all groups, the largest increase in patients with residual PAH. After 24 months, all modes of therapy showed positive dynamics with an increase in distance in the 6-minute walk testing, functional class improvement, a decrease in the mean pulmonary artery pressure, a decrease in the size of the right ventricle, and normalization of the left heart. The survival rate of patients with Eisenmenger syndrome was 80,5%, PAH-CHD with bidirectional shunt — 93,5%, residual PAH — 47,9%, idiopathic pulmonary hypertension — 48%.

Conclusion. Patients with Eisenmenger syndrome receive specific monotherapy for a long time, while maintaining low/intermediate risk, are characterized by the best survival. Patients with residual PAH have the most severe hemodynamic impairment, rapid progression of the disease, despite the ongoing combination specific therapy, and low survival.

Background. Treatment of patients with arterial hypertension (AH) associated with type 2 diabetes mellitus (DM2) and non-alcoholic fatty liver disease (NAFLD) is a complex clinical challenge. The complementary and aggravating effect of these comorbidities often prevents the realization of the antihypertensive potential of the drugs used and their combinations, and therefore it is necessary to search for additional ways to intensify therapy.

Aim. To assess the efficiency of combined pharmacotherapy in patients with AH associated with DM2 and NAFLD, depending on the CYP2C9 gene polymorphism.

Materials and methods. The study included 68 patients with uncontrolled AH associated with DM2 and NAFLD (Fatty Liver Index (FLI) > 60) who received prior antihypertensive therapy. All subjects were prescribed a combination of azilsartan medoxomil with amlodipine at doses of 40/5 mg/day. The duration of therapy was 24 weeks. Those included in the study underwent control of office blood pressure (BP) at the initial visit, after 4, 8 and 24 weeks of treatment; 24-hour BP monitoring (ABPM) — initially and after 24 weeks. Venous blood samples were taken from patients, followed by DNA isolation from leukocytes by phenol-chloroform extraction. Determination of polymorphic variants of the CYP2C9 gene was carried out on an amplifier Rotor Gene — Q. The TaqMan method (allele discrimination) and a set of primers and probes were used.

Results. As a result of genetic testing, the following distribution of polymorphic variants of the CYP2C9 gene was revealed: *1/*1 was found in 73,5% of patients, *1/*2 in 14,7%, *1/*3 in 11,8%. It was shown that after 4 weeks of therapy with a polymorphic variant of the *1/*1 CYP2C9 gene, the achievement of the target level (TL) of BP was registered in 62% of patients, with polymorphisms *1/*2 and *1/*3 — in 30% and 25%. After increasing the dose of azilsartan medoxomil and amlodipine to 80/10 mg/day, respectively, and 8 weeks from the start of treatment in the *1/*1 group, the number of BP targets achieved increased to 88%, in the *1/*2 groups and *1/*3 — up to 60% and 62,5%. Antihypertensive therapy was intensified with prolonged release indapamide at a dose of 1,5 mg/day, and according to the results of 24 weeks of therapy, patients with a polymorphic variant of the CYP2C9 *1/*1 gene achieved the TLBP in 96% of cases, with *1/*2 and *1/*3 — In 90% and 87,5%, respectively. At the same time, in patients with polymorphism of the CYP2C9 gene *1/*1, *1/*2 and *1/*3, positive dynamics of all ABPM parameters was revealed. However, in the *1/*1 variant, more pronounced positive changes were observed in the systolic BP time index during the day and the diastolic BP time index during the day, and the diastolic BP time index at night.

Conclusions. As a result of a 24-week study, the majority of patients who had the polymorphic variant *1/*1 of the CYP2C9 gene showed a more pronounced efficacy of the studied combination of drugs. Patients with *1/*2 and *1/*3 polymorphisms often required triple therapy to achieve TLBP. At the same time, further studies are needed to study the dependence of the antihypertensive effects of drugs on polymorphisms of the corresponding genes, which may help identify groups of patients who need more intensive antihypertensive therapy already at the start of treatment.

The aim of this study is conducting a comparative analysis of the effect of 24 weeks of therapy of glucagon-like peptide-1 receptor agonists (aGLP-1) semaglutide and a sodium-glucose co-transporter 2 inhibitors (SGLT2) empaglifosin on the left heart chambers and the severity of epicardial adipose tissue (EAT) in patient with arterial hypertension (АН), obesity and diabetes mellitus (DM).

Materials and methods: 91 patients (40.7% women and 59.3% men) aged 44-65 years with type 2 DM (glycated hemoglobin level over 6.5%) and obesity (WC over 80 cm in women and over 94 cm in men) were successively included in the study. All patients received standard antihypertensive and hypolipidemic therapy, in addition, all patients were on metformin monotherapy at a dose of 1000-2000 mg/day (during the follow-up, the therapy did not change). Anthropometric measurements, echocardiography were carried out to evaluate the structural and functional parameters of LV using transmitral and tissue Doppler and determine the thickness of EAT. After a preliminary examination, all patients were randomized on two groups: the 1st group was prescribed semaglutide therapy with an initial dose of 0.25 mg and gradual titration every 4 weeks to 1.0 mg, the 2nd group was prescribed empagliflozin at a dose of 10 or 25 mg. After 24 weeks, all patients were re-examined.

Results: semaglutide and empagliflozin improved a structural and functional condition of the left heart chambers — LV mass, LV mass index (LVMI), the LA index volume, practically all of indicators of the LV diastolic function (E/A ratio, LV-filling pressure, Еmlat , Emsept velosity) in patients with AH, obesity and DM 2 types. In addition, in the semaglutide group, a pronounced decrease in the EAT thickness with 0.76 cm [0.56; 0.8] to 0.71 cm [0.5; 0.74] (p < 0.001), which was not observed in the empagliflozin group. Apparently, semaglutide and empagliflozin positive effect on the left heart chambers achieved by the different mechanisms. In the 1st group by means of decrease LVMI and EAT thickness, in the 2nd group through reduction heart preload and LV-filling pressure according improve LV relaxation.

Conclusion: the new sugar-lowering agents should be prescribed to patients with type 2 DM and CVD or a high risk of CVD development taking into account their impact on the cardiovascular prognosis, and in some cases considering the need for a combination of these drugs.

Renovascular hypertension (RH) is one of the most common secondary forms of arterial hypertension, in most cases caused by atherosclerotic renal artery stenosis (ARAS). The development of a course of hypertension resistant to antihypertensive therapy with an unfavorable prognosis of deterioration of kidney function and cardiovascular complications is characteristic. The review discusses the pathophysiological mechanisms of RH development in ARAS, draws attention to the important role of the renin-angiotensin system (RAS) activation, which determines the nature of the course of the disease, the high frequency of target organ damage. Modern approaches to the drug treatment of this form of hypertension, the validity and benefits of the use of drugs that block the effects of RAS in patients with RH of atherosclerotic genesis, constituting a category of high risk of cardiovascular complications, are The issues of the effectiveness of the use of these drugs in order to reduce the risk of cardiovascular complications and improve the long-term prognosis of the course of this form of hypertension are discussed.