Because MV are procoagulant owing to PhtdSer exposure and the eventual presence of TF when shed from monocytes, neutrophils and endothelial cells, their impact as pathogenic effectors in acute or chronic cardiovascular diseases and associated disorders such as myocardial infarction, atrial fibrillation, unstable angina, type-2 diabetes and their accumulation in the arteriosclerotic plaque has been extensively studied in relationship with the vascular inflammatory responses27. This evidence concerns the gene TF and myocardial infarction.