Репозиторий Университета

© 2018, Silicea-Poligraf. All rights reserved. Aim. Assessment of prognostic significance of endothelial dysfunction markers: stable metabolites of nitric oxide (NOx), von Willebrand factor (vWF), endothelin-1 (E1), homocysteine and tissue plasminogen activator (tPA) in essential hypertension (EAH) patients not taking antihypertension therapy systematically. Material and methods. Totally, 12 EAH patients investigated (45 males, 79 females) (mean age 51,4±6,5 y.o., mean duration of AH 7,9±7,3 y.). Concentration of NOx in plasma was measured by spectrophotometry, and of vWF, homocysteine, E1 and tPA — by immune enzyme assay. Results. By the increase of SCORE risk level, there was significant increase of concentrations of NOx, E1, homocysteine and vWF in EAH patients (p<0,05), there were no changes in tPA levels (p>0,05). In 8 (8±1,1) years after baseline assessment, 115 patients were assessed second time. Of those 13 (11,3%) had cardiovascular events (CVE) and 5 (4,3%) died. By single factorial regression, the rate of CVE in EAH patients relate to homocystein level (р=0,01), NOx (р=0,001) and vWF (р=0,001). By multifactorial analysis, prognostic statistical significance is found for NOx (relative risk (RR) =3,8, р=0,006) and vWF (RR =3,5, р=0,005). In ROC-analysis there were found threshold levels of NOx (>46,6 mcM/L, AUC =0,863) and vWF (>1,68 mg/dL, AUC =0,738), the increase of which is followed by CVE development risk for the levels of NOx >46,6 mcM/L 3,8 times (sensitivity 81,9% and specificity 65,8%), vWF >1,68 mg/dL — 3,5 times (sensitivity 74,3% and specificity 62,7%). Combination of the parameters point on the risk increase up to 6,5 times (р=0,00007). Conclusion. NOx with the threshold of >46,6 mcM/L (RR =3,8) and vWF >1,68 mg/dL (RR =3,5) do show independent prognostic value for 5-year CVE risk assessment in EAH patients that can be applied as an additional method for risk stratification to estimate a group for more aggressive therapy and CVE prevention.

© 2018 Vserossiiskoe Obshchestvo Kardiologov. All rights reserved. Aim. Assessment of the markers levels of endothelial dysfunction (ED): stable metabolites of nitric oxide (NOx), endothelin-1 (E1), homocysteine (HC), von Willebrand factor (vWF) and tissue plasminogen activator (tPA) in blood plasma of smoker and nonsmoker patients with arterial hypertension (AH) of low and moderate risk, not taking antihypertension therapy regularly. Material and methods. Totally, 124 AH patients included, 45 males and 79 females, mean age 51,4±6,5 y. O., mean AH duration 7,9±7,3 y. Controls included 35 healthy volunteers (20 males, 15 females). Concentration of NOx in plasma was measured with spectrophotometry, and of vWF, HC, E1 and tPA-with immune enzyme assay. Results. To evaluate the relation of smoking and ED markers levels, AH patients and controls were selected to subgroups according to smoking status: smoker (35,5%) and non-smoker (64,5%) AH patients; smoker (38%) and non-smoker (62%) controls. In smoker AH patients comparing to non-smoking there were significantly higher concentrations of NOx-48,2±18,8 mcM/L and 40,3±21,2 mcM/L, respectively (p<0,05), E1-1,2±0,16 and 0,6±0,2 fM/L, resp. (p<0,05), HC-25,7±6,04 and 16,2±6,5 mcM/L, resp. (p<0,05), vWF-1,39±0,7 and 1,1±0,6 mg/dL, resp (p<0,05) and tPA-13,05±6,2 and 8,5±6,2 mcM/L, resp. (p<0,05). There was correlation in the AH group, of NOx concentration and smoking (r=0,46, p<0,05), and tobacco smoking duration (r=0,83, p<0,05). Also, there were positive correlations of HC and smoking (r=0,4, p<0,05). In control group smokers had higher HC-20,7±5,3 and 17,2±4,7 mcM/L, resp. (p<0,05), vWF-1,3±0,8 and 0,8±0,6 mg/dL, resp. (p<0,05) and tPA-11,1±6,5 and 6,6±5,2 mcM/L, resp. (p<0,05). There were no significant changes in NOx and E1. Conclusion. In smokers of both AH and control groups the levels of HC, vWF and tPA were significantly higher in comparison with nonsmokers. In smoker AH patients the mean concentrations of NOx and E1 are higher than in non-smoker patients. Levels of ED are related with not only the fact of smoking itself (p<0,05), but smoking duration (p<0,05).

© Russian Association of Endocrinologists, 2018. BACKGROUND. Intensive glycaemic control in patients with type 1 diabetes may lead to hypoglycaemia and thus increase the risk of cardiovascular and cerebrovascular events. Platelet activation and/or decreased activity of physiological anticoagulants during hypoglycaemia may play a role in the development of cardiovascular or cerebrovascular complications. AIMS. To investigate induced platelet activity, the activity of physiological anticoagulants, and the von Wil-lebrand factor in patients with type 1 diabetes with the hyperinsulinaemic-hypoglycaemic clamp. MATERIALS AND METHODS. We examined 11 patients with type 1 diabetes without macro- and micro-vascular complications (6 males, 5 females, mean age 23.7 ± 5.6 years, A1C 9.7 ± 2.3%). Induced platelet aggregation, physiological anticoagulants (Protein S, Protein C, AT III) and the von Willebrand factor were studied at hyperglycaemic, euglycaemic, and hypoglycaemic stages during use of a hyperinsulinaemic (1 mU/kg/min) hypoglycaemic clamp. RESULTS. Platelet aggregation to all agonists increased significantly during the hypoglycaemic stage, compared with the euglycaemic or hyperglycaemic stages. There was no difference in platelet aggregation between the euglycaemic and hyperglycaemic stages. Platelet aggregation to all agonists increased during the hypoglycaemic stage compared with the hyperglycaemic period: thrombin-23.9%, ADP-30.6%, arachidonic acid-30.9%, collagen-69.4% and ristocetin-70.8%. During hypoglycaemia aggregation to ADP, arachidonic acid and collagen remained within normal limits (upper quartile); aggregation to thrombin was significantly above normal limits and aggregation to ristocetin remained significantly below lower limits. Protein S activity was significantly increased during hypoglycaemia compared with euglycaemia (p = 0.046) and hyperglycaemia (p = 0.046). Antithrombin-III activity decreased significantly at the euglycaemic and hypoglycaemic stages, compared with the hyperglycaemic period, but still remained significantly elevated above the upper threshold. Protein C and vWf activity did not change significantly. CONCLUSIONS. In patients with type 1 diabetes platelet aggregation and protein S activity increases significantly at the hypoglycaemic stage of the hyperinsulinaemic-hypoglycaemic clamp. Platelet activation is directly caused by hypoglycaemia and not by decreasing glucose levels. Increased protein S activity is a compensatory response to platelet activation.