Gemma Chiva-Blanch1, Rosa Suades1, Teresa Padró1, Gemma Vilahur1, Esther Peña1, Juan Ybarra2, Jose M Pou3, Lina Badimon4. 1. Institut Català de Ciències Cardiovasculars (ICCC), Barcelona, Spain. 2. Centro Médico Teknon, Barcelona, Spain. 3. Servicio de Endocrinología, Hospital de la Santa Creu i de Sant Pau, Universitat Autònoma de Barcelona, Barcelona, Spain. 4. Institut Català de Ciències Cardiovasculars (ICCC), Barcelona, Spain. Electronic address: lbadimon@csic-iccc.org.
Abstract
INTRODUCTION AND OBJECTIVES: Diabetes mellitus is associated with an enhanced risk for cardiovascular disease and its prevalence is increasing. Diabetes induces metabolic stress on blood and vascular cells, promoting platelet activation and vascular dysfunction. The level of vascular cell activation can be measured by the number and phenotype of microparticles found in the circulation. The aim of this study was to investigate the effect of a platelet-inhibitory dose of aspirin on the number and type of microparticles shed to the circulation. METHODS: Forty-three diabetic patients were enrolled in the study and received a daily dose of 100mg of aspirin for 10 days to cover the average platelet life-span in the circulation. Before and after the intervention period, circulating microparticles were characterized and quantified by flow cytometry. RESULTS: Type 1 diabetic patients had about twice the number of tissue factor-positive circulating microparticles (derived both from platelets and monocytes) and endothelial-derived E-selectin positive microparticles than type 2 diabetic patients. Aspirin therapy significantly inhibited platelets since cyclooxygenase 1 derived thromboxane generation levels were reduced by 99%. Microparticles derived from erythrocytes, activated monocytes, and smooth muscle cells were significantly reduced after 10 days of aspirin administration. CONCLUSIONS: These results indicate that: a) vascular and blood cells in type 1 diabetic patients are exposed to more sustained stress shown by their specific microparticle origin and levels; b) aspirin therapy inhibits vascular wall cell activation and microparticle shedding, and c) the effects of aspirin are similar in type 1 and 2 diabetes.
INTRODUCTION AND OBJECTIVES:Diabetes mellitus is associated with an enhanced risk for cardiovascular disease and its prevalence is increasing. Diabetes induces metabolic stress on blood and vascular cells, promoting platelet activation and vascular dysfunction. The level of vascular cell activation can be measured by the number and phenotype of microparticles found in the circulation. The aim of this study was to investigate the effect of a platelet-inhibitory dose of aspirin on the number and type of microparticles shed to the circulation. METHODS: Forty-three diabeticpatients were enrolled in the study and received a daily dose of 100mg of aspirin for 10 days to cover the average platelet life-span in the circulation. Before and after the intervention period, circulating microparticles were characterized and quantified by flow cytometry. RESULTS: Type 1 diabeticpatients had about twice the number of tissue factor-positive circulating microparticles (derived both from platelets and monocytes) and endothelial-derived E-selectin positive microparticles than type 2 diabeticpatients. Aspirin therapy significantly inhibited platelets since cyclooxygenase 1 derived thromboxane generation levels were reduced by 99%. Microparticles derived from erythrocytes, activated monocytes, and smooth muscle cells were significantly reduced after 10 days of aspirin administration. CONCLUSIONS: These results indicate that: a) vascular and blood cells in type 1 diabeticpatients are exposed to more sustained stress shown by their specific microparticle origin and levels; b) aspirin therapy inhibits vascular wall cell activation and microparticle shedding, and c) the effects of aspirin are similar in type 1 and 2 diabetes.
Authors: Daniela Cesselli; Pietro Parisse; Aneta Aleksova; Claudia Veneziano; Celeste Cervellin; Andrea Zanello; Antonio Paolo Beltrami Journal: Front Physiol Date: 2018-10-01 Impact factor: 4.566