Glucemia posprandial y riesgo cardiovascular

Atherosclerosis is the most frequent cause of the increased cardiovascular morbidity and mortality observed in type 2 diabetic patients. Over the past few years, epidemiological and preliminary intervention studies have identified that the posprandial state, characterized by a rapid and large increase in blood glucose levels, is a direct and independent risk factor for atherosclerosis and a contributing factor to the development of cardiovascular disease. Posprandial hyperglycemia may have a direct toxic effect on the vascular endothelium, mediated by oxidative stress, which favors the development of endothelial dysfunction, a prothrombotic and proinflammatory condition, through the production of free radicals. This effect is independent of other cardiovascular risk factors such as hyperlipidemia. The control and correction of posprandial glucose levels is an important strategy in the prevention of diabetes-related cardiovascular disease. In this review, epidemiological and intervention studies that associate posprandial hyperglycemia with cardiovascular risk, the mechanisms involved in this effect, and the distinct therapeutic strategies to control posprandial hyperglycemia are reviewed. These therapeutic strategies include lifestyle changes, drugs such as short-acting secretagogues, alpha-glucosidase inhibitors, fast-acting insulin analogues, and new agents under development, such as the synthetic human amylin analogue pramlintide, the insulinotropic hormone GLP-1, a homologue of GLP-1-exendin, dipeptidylpeptidase IV inhibitors (DPPIV) and inhaled insulin formulations.