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Biomedical subjects

A V Susekov

Publications and source records attributed to A V Susekov.

At least 19 recordsLinked to original sources
PubMed2006

[Randomized FARVATER Study. Part 1. Effect of 10 and 20 mg/day atorvastatin on levels of lipids, C-reactive protein, and fibrinogen in patients with ischemic heart disease and hyperlipidemia].

Main aim of the clinical study FARVATER was comparison of effects of 10 and 20 mg/day of atorvastatin on levels of lipids, high-sensitivity C-reactive protein (CRP), fibrinogen (F), and structural-functional state of vascular wall in patients with documented and primary hyperlipidemia (HLP). Fifty patients (mean age 60.8 years) with documented ischemic heart disease and HLP were randomized to continuous administration of 10 and 20 mg/day atorvastatin for 24 weeks. Initial levels of total cholesterol (TC), triglycerides (TG), low density lipoprotein cholesterol (LDLCH), high density lipoprotein cholesterol (HDL CH), CRP and F were 6.22, 1.86, 4.15, 1.24 mmol/l, 1.46 and 2.93 g/l, respectively. After 6 weeks lowering of TCH, TG and LDLCH was significant both in 10 (24.5, 18.4, and 34.9%, respectively) and 20 mg (29.1, 28.2, and 40.9%, respectively) groups. After 24 weeks TG levels decreased by 22 and 15% in 10 and 20 mg subgroups, respectively. Changes of HDLCH (+11 and +12% in patients treated with 10 and 20 mg, respectively) were not significant. There were no significant changes of CRP and F levels. Seven side effects (4%) were registered during 24 weeks; 2 were related to study drug (allergy and symptomless elevation of creatine kinase).

Adult↗
PubMed2003

[Atorvastatin in the treatment of patients with hereditary hypercholesterolemia].

Efficacy and tolerability of atorvastatin (20 mg/day) were assessed in a 3 month study on 19 patients (5 men, 14 women, mean age 52.3 years) with familial hypercholesterolemia. Average baseline levels of total cholesterol (CH) and low density lipoprotein (LDL) CH were 10.7 and 8.6 mmol/l, respectively. By the end of 3 months levels of CH, LDL CH, triglycerides and atherogeneity index decreased by 32, 41, 16 and 45%, respectively. This was accompanied by 21% increase of high density lipoprotein CH level. There were no cases of AST or ALT activity elevation above 3 upper limits of normal values. However 1 patient had asymptomatic elevation of ALT activity up to 53 U/l which did not cause interruption of therapy. Creatine kinase remained normal throughout the study period. Three patients (16%) stopped taking atorvastatin because of side effects. Thus in patients with familial hypercholesterolemia the dose of atorvastatin 20 mg/day was sufficiently well tolerated and provided effective control of lipid levels.

Adult↗
PubMed2002

[Simvastatin (40 mg/day) in patients with hereditary hypercholesterolemia: effect on high density lipoprotein cholesterol].

AIM: To study effect of simvastatin of the level of high density lipoprotein (HDL) cholesterol (CH). MATERIAL AND METHODS: Simvastatin (40 mg/day) was given for 3 months to 15 patients (3 men, 12 women, mean age 56-/+10.3 years) with hereditary type II hypercholesterolemia after washout from lipid lowering therapy. Initial level of HDL CH was below and above 1.0 mmol/l in 7 and 8 patients, respectively. Blood lipids, activity of liver enzymes and creatine kinase were determined after 1 and 3 months of therapy with simvastatin. Safety and tolerability of simvastatin were also studied. RESULTS: Simvastatin was well tolerated. In 1 patient the drug was stopped because of pain in the liver and nausea. In patients with initially low HDL CH levels of total and low density lipoprotein (LDL) CH significantly decreased by 29.6 and 36.8%, respectively, after 3 months, while level of HDL CH increased by 20% after 1 month of therapy. In patients with initially normal HDL CH levels of total and LDL CH significantly decreased by 31.1 and 32.6%, respectively, while those of triglycerides and HDL CH did not change. CONCLUSION: In patients with hereditary hypercholesterolemia 40 mg/day of simvastatin besides pronounced lowering of LDL CH level caused significant increase of HDL CH (up to 20% in 1 month) in patients with initially low level of this parameter.

Anticholesteremic Agents↗
PubMed2002

[Effect of atorvastatin on endothelial function in patients with familial hypercholesterolemia].

AIM: To study the influence of treatment with HMG-CoA reductase inhibitor atorvastatin on endothelial function in patients with familial hypercholesterolemia type IIa. MATERIALS AND METHODS: Sixteen patients (5m/11w, 51-/+3 years) with familial hypercholesterolemia were studied before and after 3 months of therapy with atorvastatin 20 mg/day. EDRF release test (D.Celermajer, 1992) was used to assess flow-mediated endothelium-dependent vasodilatation (FMD) of the brachial artery in response to reactive hyperemia. Plasma nitrite/nitrate (NOx) levels were measured as an indirect index of nitric oxide (NO) production in vivo using HPLC. RESULTS: Atorvastatin treatment resulted in a 32% reduction in total serum cholesterol (CH), 41% reduction in low density lipoprotein (LDL) CH, 16% reduction in triglycerides and a 21% increase in high density lipoprotein CH. Flow mediated dilatation (FMD) was impaired at baseline (5.8-/+0.9%) and significantly improved up to 9.5-/+0.9% after 3 month atorvastatin therapy (p<0.002). Change in FMD inversely correlated with baseline FMD (r = -0.58, p<0.05). There was no significant correlation between FMD and neither total serum CH nor LDL CH levels at baseline. During atorvastatin therapy significant reduction of plasma NOx levels occurred from 53.4-/+5.1 mcmol/l at baseline (range 42.6-86.2 mcmol/l) to 35.5-/+5.1 mcmol/l (18.4-46.0 mcmol/l) after treatment (p<0.02, n=7). CONCLUSION: In patients with familial hypercholesterolemia atorvastatin produced beneficial effect on endothelial function (increase in flow-mediated dilatation, decrease in NOx).

Adult↗
PubMed2002

[Simvastatin in management of patients with primary hypercholesterolemia: tolerability and efficacy of daily doses 10-80 mg].

AIM: To analyze retrospectively data on lipid lowering efficacy, tolerability and safety of different doses of simvastatin in patients with primary hyperlipidemia. MATERIAL AND METHODS: Thirty five patients (mean age 54.9-/+8.5 years, 15 men, 20 women) received simvastatin for 3-6 months in doses 10 (n=12), 20 (n=8), 40 (n=10) and 80 (n=5) mg/day. Average lowering of low density lipoprotein cholesterol was 28.9, 37.6, 39.7, and 46.2% on doses 10, 20, 40 and 80 mg/day, respectively. Elevation of activity of transaminases (AST and ALT) above 3 upper limits of normal (ULN) accompanied by right upper quadrant pain occurred in 1 patient and the drug (10 mg/day) was stopped. Symptomless elevation of AST and ALT activities above 2 ULN was registered in 2 other patients receiving 10 and 20 mg/day. The dose of 80 mg/day was well tolerated - none of 5 patients had symptoms of myopathy or elevated creatinekinase activity.

Anticholesteremic Agents↗
PubMed1998

[Variability of the hypolipidemic action of simvastatin and fluvastatin in patients with primary hyperlipoproteinemia].

AIM: To reveal the metabolic parameters of lipoproteins (L), which determine the benefits of hypolipidemic effects of simvastatin (S) and fluvastatin (F); to trace changes in the activity of lecithin-cholesterol acyltransferase (LCA) and cholesterol (C) ester transfer (CET) from high density lipoproteins to very low density lipoproteins (VLDL) and low density lipoproteins (LDL) and the levels of apoE in the blood and in some L classes during therapy with the above drugs. MATERIALS AND METHODS: Thirty six patients took S, 10 mg/day, and 25 received F, 20 mg/day, for 3 months. The levels of lipids were measured by enzyme assays, apoprotein (apo) was determined by immunoturbidimetry and immunodiffusion. RESULTS: The hypocholesterolemic and hypotriglyceridemic effect of S (19.6 and 25.5, respectively) and F (19.0 and 30.5%) were similar. With S, the reduction in the blood levels of C and LDL C positively correlated with the baseline apoE levels. With F, it did with C and LDL C before treatment. Lower blood apoE was found with S and F and lower HDL apoE/(VLDL + LDL) ratio was detected only with F. F treatment significantly lowered the activity of CET and LCA; before and after S treatment, they did not differ significantly. CONCLUSION: Analyzing the relationship between the benefits of the hypolipidemic effect and the baseline parameters of L metabolism indicates that the changes in serum C, LDL C and HDL C are due to the composition of HDL particles and the distribution of apoE among different L classes in the patient to a greater degree.

Adult↗
PubMed1998

[Lipanor treatment of atherogenic hyperlipoproteinemia].

AIM: The study of the hypolipidemic efficiency, safety and tolerance of ciprofibrate (lipanor) in therapy of atherogenic hyperlipoproteinemia. MATERIALS AND METHODS: The trial included 14 hypertensive postmenopausal females, 14 patients with diabetes mellitus type II, 14 males with coronary heart disease and primary hyperlipoproteinemia (total cholesterol > 6.5 mmol/l, triglycerides < 4.5 mmol/l under low-cholesterol diet). Lipanor was given for 12 weeks in a daily single dose 100 mg in the morning. Lipids and other biochemical indices were measured in a fasting state after 1 and 3 months of lipanor treatment. RESULTS: After 1 month of lipanor treatment there was a 22-30%, 24-49% decrease in the level of low-density lipoprotein cholesterol, triglycerides, respectively. High-density lipoprotein cholesterol increased by 16%. The hypolipidemic effect of lipanor persisted for 3 months during which triglycerides continued to fall (up to 38.5%). Lipanor was well tolerated, only one patient with diabetes mellitus had hyperactivity of creatine phosphokinase manifesting with clinical symptoms (the drug was discontinued). 3 patients developed mild side effects. Alkaline phosphatase activity inhibited in all the groups by 25-41%. CONCLUSION: Lipanor is a highly effective, safe hypolipidemic drug with good tolerance. It can be recommended for correction of atherogenic hyperlipoproteinemia in patients at high risk of atherosclerosis progression.

Cholesterol↗
PubMed1993

[The choice of the optimal regimen for apheresis of the low-density lipoproteins in patients with familial hypercholesterolemia by using mathematical modelling].

The study was undertaken to enhance the effectiveness of a low-density lipoprotein apheresis procedure by using the mathematical approach to choosing an individual sorption regimen for each patient when the cholesterol concentration given by a physician was achieved in the shortest time. The experimental estimation of time course of changes in plasma cholesterol levels at the column inlet and outlet during low-density lipoprotein apheresis allowed the optimal parameters of the procedure to be calculated. The adequacy of the proposed methods to the real data was examined by the paired t-test (p < 0.0001). The optimal regimen was chosen for 5 patients with familial hypercholesterolemia. It is shown that the optimization of the regime will reduce the time of the procedure to 47 min, by removing the same amount of a substance.

Adolescent↗
PubMed1992

[Use of immunosorption for selective decrease of lipoprotein (A) levels in patients with coronary atherosclerosis].

Lipoprotein (a) [L(a)] is an atherogenic lipoprotein, its human plasma concentration correlates with the occurrence of coronary heart disease. The procedure for selectively removing L(a) with an anti-L(a) immunosorbent was performed to treat 3 patients who had high L(a), normal total cholesterol and other lipoprotein levels. All the patients had coronary stenosis as documented by angiography. After L(a)-apheresis, the level of L(a) decreased by 72%, while that of other plasma components, including low density lipoproteins virtually unchanged. Thus, the procedure of L(a)-apheresis is an effective and safe method for lowering human blood L(a) concentrations. In addition, this in vivo model allows information on L(a) metabolism to be obtained.

Adult↗