Ischemic stroke among patients with metabolic syndrome with or without type 2 diabetes mellitus

Abstract

T2DM represents an independent risk factor for vascular cerebral pathology, with a (2-3) times greater probability of stroke. The number of diabetic patients with stroke increased substantially from (6.2% to 11.3%) during (1996-2006). Ischemic stroke, small or large vessels occlusion, is the main subtype of cerebrovascular disease, while a smaller percentage is attributed to cerebral hemorrhage. From the total number of deaths caused by acute cerebrovascular events 16% for men and 33% for women are due to T2DM.

The pathophysiology of T2DM is complex, with many different elements acting to cause the disease. It seems certain that a genetic predisposition is needed although little was known about specific genetic mutations. The diabetes phenotype depends on a large number of environmental factors that share an ability to stress the glucose homeostasis system by promoting insulin resistance or worsening beta-cell function. This pathogenesis provides insight into prevention and treatment of T2DM and its major complications cardiovascular events.

Hyperglycemia has several deleterious effects on the risk of atherothrombosis. Glucose toxicity further impairs insulin signaling, glucose metabolism and endothelial function. Furthermore, hyperglycemia stimulates the MAP kinase pathway leading to elevated synthesis of adhesion molecules and endothelin-1, as well as to the stimulation of vascular smooth muscle cell proliferation, and changes in the arterial wall. Finally, in diabetes there are abnormalities in platelet function and coagulation. These abnormalities increase intrinsic platelet activation and decrease endogenous inhibitors of platelet activity, and augment blood coagulation.