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Nedogoda et al. Vessel Plus 2018;2:37  I  http://dx.doi.org/10.20517/2574-1209.2018.36                                                Page 3 of 9

               Patients with at least one of the following criteria could not be involved in the study: increased sensitivity
               to angiotensin-converting enzyme inhibitors (ACEI), angiotensin receptor blockers (ARBs), calcium
               antagonists (CAs) and hydrochlorothiazide; instable angina, recent myocardial infarction less than 1-month-
               old, cardiogenic shock, clinically significant aortic stenosis; decompensated heart failure; severe AH (BP
               above 170/100 mmHg) that requires a 3-component combination AHT, severe comorbidities; alcohol abuse,
               pronounced impairments of the kidney function (level of creatinine in the blood 2 times higher than the
               upper normal limit), liver function (activity of alanine and aspartate aminotransferases in the blood 2 times
               higher than the upper normal limit); malignant neoplasms; pregnancy or lactation; inability to understand
               the essence of the programme and give informed consent to participate therein.


               The study involved 60 patients (26 men and 34 women, mean age 55.2 ± 6.5 years and body mass index
                            2
               28.8 ± 4.6 kg/m ).
               The study included 4 patients visits to the physician: V1 - entry visit, V2, V3, V4 - follow-up visits 4, 12 and
               24 weeks after the entry visit. At the first visit, the previous AHT was discontinued and the fixed-dose
               combination of lisinopril 10 mg + amlodipine 5 mg + rosuvastatin 10 mg was prescribed to every patient.
               In the course of the study, the physician had the opportunity to intensify the lipid-lowering therapy by
               prescribing the fixed-dose combination of lisinopril 10 mg + amlodipine 5 mg + rosuvastatin 20 mg in
               cases when the target low-density lipoproteins (LDL) of ≤ 2.5 mmol/L was not reached for the high-risk
               patientsafter 4 weeks of therapy (at Visit 2).


               Initially and after the course therapy, all the patients underwent 24 h BP monitoring, examination of the
               vessel wall elasticity, echocardiography and laboratory testing.


               The 24 h BP monitoring was performed using the Spacelabs 90207 device (USA). During the daytime hours
               (from 7 to 23 o’clock), measurements were made every 15 min, during the night (from 23 to 7 o’clock) - every
               30 min. A special cuff was used to measure the BP in the patients with excessive body weight.

               The PWV, AI and central aortic pressure were determined using the SphygmoCor device [23,24] .

               In 2010, a group of Spanish researchers published modified SCORE scales for the calculation of vascular
                                                                               [25]
               age for European countries with high and low cardiovascular disease levels . The method of vascular age
               calculation from these scales involves calculating the absolute cardiovascular risk (ACVR) from the standard
               SCORE scales and then comparing the percentage of ACVR with the age of the vessels from the modified
               SCORE scale. To perform these calculations, the following data are required: patient’s gender, passport age,
               smoking status, levels of systolic BP and total cholesterol (TC).

               Serum adipocytokines were determined by enzyme immunoassay using Mediagnost kits, leptin high
               sensitive (0.05-5 ng/mL) and BCM diagnostics adiponectin. Blood was drawn into a plastic test tube
               without a stabilizer. After centrifugation at 1000 RPM for 10 min, 1 mL of serum was collected. Before the
               determination of leptin and adiponectin levels, the samples were stored at -20 °C.

               The insulin resistance was estimated by the homeostasis model assessment (HOMA) index. The study was
               conducted strictly on an empty stomach, after an 8-12 h period of night fasting. Plasma glucose and plasma
               insulin were studied. The glucose level was determined by the hexokinase method (La Roche reagents, La
               Roche automatic analyzer). Plasma insulin was determined by enzyme immunoassay [Insulin ELISA (Mercodia
               AB, Sweden)]. The homeostasis model assessment of insulin resistance (HOMA-IR) index was calculated using
               the following formula: HOMA-IR = fasting glucose (mmol/L) × fasting insulin (μIU/mL)/22.5.
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