[Procoagulant membranous microparticles and atherothrombotic complications in diabetics].
Endothelial apoptosis and platelet activation play a key role in atherothrombotic event. These two mechanisms resulting membrane thickening leading to procoagulant microparticle (MP) liberation into the blood stream. In the vascular compartment, MP contribute to increased thrombin formation, to platelet activation, and prolong inflammation of the arterial wall by inducing the synthesis of cytokines and adhesion of glycoproteins by the endothelial cells. In diabetic patients, increased endothelial apoptosis associated with intense platelet and monocytic activation could contribute to accelerated atherothrombosis. Endothelial, platelet and monocytic derived MP, found in high concentrations in these patients, induce a prothrombotic, proadhesive and proinflammatory tendency in the vascular comportment which could directly impact on the vascular prognosis. In diabetes, increased platelet or monocytic MP is a marker for microvascular disease. Likewise, in acute coronary syndromes of diabetic patients, high concentrations of procoagulant MP could be associated with a poor cardiovascular prognosis. In these diabetic patients, many treatments (antioxidant, antiplatelet, lipid lowering, antihypertensive) significantly reduce the levels of MP and parameters associated with inflammation. MP are one of the key factors linking inflammation, oxidative stress, apoptosis and thrombosis in accelerated atherothrombotic disease of the diabetic. In future, the measurement of MP should help evaluate the efficacy of antioxidant and antiplatelet therapy, especially in diabetic patients.
Morel
O
O
Fédération de cardiologie des hôpitaux universitaires de Strasbourg, Hôpital de Hautepierre. Olivier.Morel@chru-strasbourg.fr
Hugel
B
B
Jesel
L
L
Zobairi
F
F
Bareiss
P
P
Freyssinet
J M
JM
Toti
F
F
D000975:Antioxidants / Q000627:therapeutic use; D017209:Apoptosis; D001161:Arteriosclerosis / Q000503:physiopathology*; D048909:Diabetes Complications; D004727:Endothelium / Q000473:pathology; D006801:Humans; D007249:Inflammation; D018384:Oxidative Stress; D010316:Particle Size; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D013927:Thrombosis / Q000503:physiopathology*
D000975:Antioxidants; D010975:Platelet Aggregation Inhibitors