Cerebrovascular disease in type 2 diabetes mellitus.

摘要: Incidence of CVD in diabetic men was reported to be twice as that non-diabetics and almost three times greater women the Framingham Study. It is postulated excessive glycation oxidation, endothelial dysfunction increased platelet aggregation may responsible for proliferation thickening plasmatic membrane small blood vessels ('lipohyalinosis') leading lacunar infarction. Prothrombotic state precipitate a stroke, however, aggregability, elevated fibrinopeptide A (FPA) D-dimer were not significantly related stroke mellitus (DM), whereas suppressed fibrinolytic activity common finding. Of many unknown factors pathogenesis, deficient insulin secretion, resistance action at level 'insulin receptors', changes counter regulatory hormones (e.g. glucagon, pancreatic polypetides, growth hormone, catecholamines, etc.) decrease hepatic sensitivity suppressing glucose output have received more attention. Hyperosmolar can simulate syndromes. Early recognition treatment risk such hypertension or better glycemic control, correction hyperlipidemia obesity population are important. In subjects already showing recurrent transient cerebral ischemic attacks (TIAs) minor strokes, benefit antiplatelet agents antithrombotic therapy prevention major strokes well established. Ramipril has been found effective reducing by 33% patinets HOPE study.