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Review [Platelet activation and hypercholesterolemia in the pathogenesis of deep vein thrombosis] 2006
Martínez M, Labiós M, Gabriel F. · Departamento de Biopatología Clínica, Hospital Universitario La Fe, Valencia, España. · Med Clin (Barc). · Pubmed #17169286 No free full text.
Abstract: Currently it is accepted that deep vein thrombosis is a multifactorial event in which the presence of activated platelets and also plasmatic lipids seems to play a pivotal role that it is not well established in the scientific bibliography. Due to the non consensus state about these topics between the different groups working in these aspects, the topic involving deep vein thrombosis-platelets-lipids, and also their interactions, still is an interesting area of investigation, in which it is necessary to carry out studies with the aim of establishing risk factors, initial diagnostic methods and clinical assays to probe the efficacy of new therapies.
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Clinical Conference Effect of a modified fibrate (Biniwas Retard) on hemorheological alterations in hyperlipemic patients. 1999
Labios M, Martínez M, Vayá A, Gabriel F, Guiral V, Aznar J. · Hypertension Unit, Hospital Clínico Universitario, Valencia, Spain. · Clin Hemorheol Microcirc. · Pubmed #10599590 No free full text.
Abstract: The effect of a binifibrate (Biniwas Retard, Wasserman) on the plasma lipids and hemorheological profile of 30 primary hyperlipemic patients was studied. Our results indicate that the patients under study had evident rheological alterations as well as the expected lipid alterations. Treatment with Biniwas (2 x 550 mg/day) for six months not only substantially improved the alterations in the lipid balance but also tended to normalize the patients' hemorheological alterations, and there was a statistically significant correlation between the two effects. Apart from the decrease in plasma viscosity (1.20 +/- 0.05 vs 1.29 +/- 0.07 mPa.s, p < 0.001), the most noteworthy effects of Biniwas treatment were the decrease in red blood cell aggregability (8.7 +/- 1.2 vs 9.3 +/- 1.1, p < 0.05) and increased deformability (55 +/- 3 vs 47 +/- 5%, p < 0.001). Both changes may be due to modifications in the lipid composition of the erythrocyte membrane due to cell-plasma lipid exchange.
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Article Effect of atorvastatin upon platelet activation in hypercholesterolemia, evaluated by flow cytometry. 2005
Labiós M, Martínez M, Gabriel F, Guiral V, Martínez E, Aznar J. · Department of Internal Medicine, Clinic University Hospital, Valencia, Spain. · Thromb Res. · Pubmed #15668185 No free full text.
Abstract: Hyperlipidemia is a well established risk factor for cardiovascular disease and atherothrombotic events, in which platelet activation also plays a significant role. However, very few studies have addressed platelet activation in hypercholesterolemia, the potential effect of lipid lowering drugs upon platelet hyperfunction, and the question of whether changes in the latter are correlated to normalization of plasma lipids. This study used whole blood flow cytometry to assess in vivo and in vitro platelet activation in a group of 33 patients with hypercholesterolemia, and also the ex vivo effect of atorvastatin (20 mg/day) upon such activation. A control group of 40 normolipidemic volunteers matched in terms of age, sex and added risk factors to the patient group was used. The results showed that hypercholesterolemic patients had in vivo a significantly greater percentage of GPIIb/IIIa- and phosphatidylserine-positive platelets compared with the control group (4.62+/-3.51% and 2.58+/-1.19% versus 2.73+/-1.08% and 1.54+/-0.68%, respectively). In vitro response of CD62 expression to thrombin was also greater in the patients than in the controls (92.51+/-6.00% versus 89.63+/-10.72%, p<0.05). Atorvastatin therapy normalized platelet hyperfunction in the patients studied and reduced GPIIb/IIIa response to ADP (from 82.65+/-6.43% to 75.84+/-4.89%, p<0.01). A significant correlation can be seen between such normalization and the decrease in plasma levels of total and LDL cholesterol.
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