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