Large artery damage is a major contributory factor to cardiovascular morbidity and mortality of patients with hypertension. As shown ASCOT and other study, beta-blockers appear to be less effective than other drugs in improving outcome in hypertensive patients, and a potential explanation may be that beta-blockers are less effective in reducing arterial stiffness. However, the aim of this study was to prove otherwise while assessing the direct effect of cardioselective beta-adrenoblocker betaxolol (Lokren) on arterial distensibility in patients with mild, moderate and severe hypertension. 50 hypertensive patients (mean age 54.7±14.3 years, 28 male, 32 female) received betaxolol in individual titrated doses 10–40 mg (mean dose 14.7±6.8mg) daily for 3 months. The examination comprised routine tests, ECG, blood glucose, total cholesterol, triglycerides. The assessment of arterial stiffness was done by way of measuring brachial-ankle pulse wave velocity (baPWV). Systemic arterial compliance was estimated through brachial Augmentation Index (AIb), Endothelial function was calculated based on flow-mediated dilatation (FMD) parameters. The treatment produced a significant reduction in systolic (–27.2 mmHg) and diastolic BP (–12.3 mmHg). No fluctuation of AIbwas monitored which should be attributed to the pulse decrease from 74.3 to 60.6 beats/min (p < 0.001). Significant decrease of baPWV (by 8.1

Subclinical hypothyroidism is associated with an increased risk of coronary heart disease, myocardial infarction, chronic heart failure and mortality. However experts still debate appropriateness of levothyroxin replacement therapy of subclinical hypothyroidism with thyrotropin - TSH (concentrations below 10 mIU/L). A controversy also exists on the value of upper TSH reference level in blood serum.

Aim. To study effect of concomitant type 2 diabetes mellitus on the number of circulating progenitor cells (CPC) in patients with coronary heart disease (CHD) and postinfarction heart failure (ischemic cardiomyopathy).Methods. The number of CPC (CD34+ cells) was determined by flow cytophotometry in 47 patients with CHD including 14 with CHD + DM2; 12 patients without CHD and DM2 made up the control grouP. Enzyme-linked immunosorbent assay was used to measure N-terminal precursor of brain natriuretic peptide (NT-proBNP), immunoreactive insulin (IRI) and C-peptide levels.Results. The number of CPC in patients with ischemic cardiomyopathy without DM2 was 33.4% greater than in controls. In patients with cardiomyopathy and DM2 the number of CPC depended on the quality of diabetes compensation. It was lowest in case of decompensated DM2 (HbA(1c) = 9.5 +/- 1.8%). In patients with compensated/subcompensated DM2 (HbA(1c) = 6.8 +/- 0.3%) it was significantly higher than in controls and patients with ischemic cardiomyopathy without DM2 (mean 46.5 (p=0.006) and 40.0% (p=0.02) respectively).Conclusion. The number of CPC in peripheral blood of patients with ischemic cardiomyopathy and DM2 correlated with the level of DM compensation. It was lowest in patients with decompensated DM2 and exceeded the normal number in patients with CHD without DM2. The number of CPC inversely correlated with blood glucose level. Positive correlation of CPC number with IRI and C-peptide levels was documented in control subjects and patients with CHD without DM2.

Aim. To compare the effects of ACE inhibitors zofenopril and perindopril on endothelial function and oxidative stress (OS) in patients with stable CHD and AH. Material and methods. In total, 40 patients with stable CHD (Functional Class II-III effort angina) and Stage 1-2 AH received zofenopril (7,5-30 mg/d; mean dose 18,6±8,8 mg/d; n=17) or perindopril (2-8 mg/d; mean dose 4,1±2,1 mg/d; n=23) for 12 weeks. At baseline and in the end of the study, all patients underwent reactive hyperemia test (RHT), to assess flow-dependent vasodilatation of brachial artery, and the measurement of OS parameters (malone dialdehyde, MDA, in low-density lipoproteins, MDALDL) and antioxidant parameters (superoxide dismutase (SOD) and glutathione peroxidase (GPO) activity in erythrocytes). Results. In both groups, a similar reduction in systolic and diastolic blood pressure levels was observed. In the zofenopril group, a significant elevation in brachial artery diameter increase during RHT, a significant increase in GPO activity, and some reduction in MDALDL levels were observed, which points to antioxidant system (AOS) activation and OS reduction. No similar changes of these parameters were observed in the perindopril group. Conclusion. In patients with stable CHD and AH, zofenopril, but not perindopril, reduced OS severity and increased AOS system activity, which was associated with improved endothelial-dependent vasodilatation.

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Randomized trial ESCAPE adressed the lipid-lowering efficacy, safety and tolerability and vascular effects of simvastatin (ZOCOR®, MSD) 20 and 80 mg/day in the long-term treatment of 50 patients with coronary heart disease and familial hypercholesterolaemia (FH). The study lasted for 76 weeks and demonstrated a reduction in low-density lipoprotein cholesterol (LDL-c) level by 32,7 % in patients treated with simvastatin 20 mg/day, and by 44,5 % in patients treated with simvastatin 80 mg/day (p < 0,001 for both groups). Long-term treatment with simvastatin 20 and 80 mg/day was well tolerated, there were no clinical significant adverse effects observed.

In a framework of multicenter study ATLANTIKA in a group of patients we carried out noninvasive ultrasound test of endothelium dependent vasodilatation (EDVD) of brachial artery before and at the background of therapy with atorvastatin. Aim of the study was to assess and compare effects of incremental (10-80 mg/day) and stable (10 mg/day) doses of atorvastatin on functional state of endothelium. The group of observation comprised 148 patients A 86 men, 62 women aged 59.5 (55;66) years, who were included into ATLANTIKA study and randomized to 3 groups: group A - active therapy with stable dose of atorvastatin (10 mg/day) (n=52), active therapy with titration of atorvastatin dose from 10 to 80 mg/day (n=50), group C - common therapy which could include lipid lowering drugs (n=46). At baseline there were no statistically significant differences between groups in main demographical, laboratory and instrumental parameters. Median EDVD was 5.4 (3.5; 8.0), 5.1 (3.9; 7.6) and 5.6 (3.2; 8.1)% in groups A, B, and C, respectively. After 12 and 24 weeks of observation statistically significant increases of brachial artery EDVD occurred only in group B (by 27.2 and 31.9%, respectively). There was no statistically significant positive dynamics of EDVD in groups A and C. Results of the presented work show that for achievement of statistically significant positive vascular effect it is necessary to titrate dose of atorvastatin until target level of low density lipoprotein cholesterol (< 2.5 mmol/l) is achieved. Vascular effect of therapy with atorvastatin in a fixed dose 10 mg/day is inferior to that of aggressive therapy, however it is substantially superior to common treatment.

Aim. To study atorvastatin (10 and 20 mg/d) effects on lipid, C-reactive protein, and fibrinogen levels, vascular wall structure and function in patients with coronary heart disease (CHD) and primary hyperlipidemia (PHL). Material and methods. In total, 50 CHD and PHL patients were randomized into two stable-dose atorvastatin groups (10 or 20 mg/d) for 24 weeks. Atorvastatin effects on lipid levels, endothelial function, vascular wall distensibility and stiffness, as well as treatment tolerability, were examined. Results. Twenty-four-week atorvastatin therapy (10 or 20 mg/d) reduced low-density lipoprotein cholesterol (LDL-CH) level by 34,9% and 43,9%, respectively (p<0,001). At baseline, vascular wall functional parameters did not differ significantly, reaching 7,2% and 6,4% for endothelium-dependent vasodilatation (EDVD), 21,3 and 18,7 10-3/kPa for vascular wall distensibility (DC) of common carotid artery (CCA); 8,0 and 9,1 Units for vascular wall stiffness (beta-index), respectively. Three-month therapy was associated with significant increase in EDVD – by 40,2% in 10 mg/d group, and by 51,3% in 20 mg/d group. After 24 weeks of the treatment, CCA distensibility increased by 45,3% (p<0,01) and 43,6% (p<0,01) in 10 and 20 mg/d groups, respectively. Vascular wall stiffness decreased by 23,4% (p=0,008) and 25,7% (p=0,002), respectively. There was no significant association between LDL-CH decrease and EDVD, distensibility or stiffness dynamics. During 24-week follow-up, 2 adverse events (4%), linked to atorvastatin therapy, were registered. Conclusion. In CHD and PHL patients, atorvastatin (10-20 mg/d) increased EDVD by 40-51%, CCA distensibility by 43-45%, reduced vascular wall stiffness by 23-26%, and was well tolerated.

Aim. To elucidate effect of two doses of atorvastatin (10 and 20 mg/day) on endothelial function, distensibility and stiffness of vascular wall. Material and methods. Patients (n=50) with documented ischemic heart disease and hyperlipidemia were randomized to 10 or 20 mg/day of atorvastatin (Atoris, KRKA). Endothelial function and common carotid artery wall distensibility and stiffness were assessed at baseline and after 12 and 24 weeks of treatment. Results. Administration of both 10 and 20 mg/day doses of atorvastatin for 6 weeks was associated with significant lowering of total cholesterol (CH), triglycerides (TG) and low density lipoprotein (LDL) CH (24.5, 18.4, 34.9% and 29.1, 28.2, 40.9%, respectively). After 24 weeks LDL CH lowering from baseline reached 34.9 and 43.9% (p < 0.001) and that of TG - 22 and 15%, in 10 and 20 mg/day groups, respectively. There were no significant differences between 10 and 20 mg/day groups in baseline values of endothelium dependent vasodilation (EDV), carotid artery distensibility and stiffness (7.28 and 6.64%, 21.60 and 20.15, 8.04 and 9.19U, in 10 and 20 mg/day groups, respectively). After 3 months of treatment there occurred significant 38.4% (10 mg/day) and 45.4% (20 mg/day) increases of EDV. Significant 27.6% (10 mg/day) and 28.8% (20 mg/day) enhancement of vascular distensibility was noted after 24 weeks. Vascular wall stiffness decreased 33.4% (P=0.008) and 31.3% (p=0.002) in 10 and 20 mg/day groups, respectively.

Thirty patients with grades 1-3 arterial hypertension were examine to evaluate in patients with arterial hypertension the effectiveness and safety of treatment in patients with angiotensin-converting enzyme (ACE) inhibitor enalapril and the thiazide-type diuretic chlortalidone and to study the impact of this therapy on the great arteries. This combined therapy could reduce systolic blood pressure (BP) from 166,9 ± 22,8 to 135,7 ± 14,1 mm Hg, diastolic BP from 101,8 ± 22,8 to 135,7 ± 14,1 mm Hg (p