Glycaemic control is essential for effective cardiovascular risk reduction across the type 2 diabetes continuum.

The growing prevalence of diabetes, an established risk factor for cardiovascular disease, threatens to significantly increase the global burden of cardiovascular morbidity and mortality. The risk of cardiovascular mortality is substantially higher in individuals with early glucose intolerance than in those with normal glucose levels and the pathological changes in vascular function begin many years before the diagnosis of overt type 2 diabetes. Postprandial hyperglycaemia is particularly deleterious to vascular function, and impaired glucose tolerance (IGT) - but not impaired fasting glucose - and may be an independent risk factor for cardiovascular disease throughout the glucose intolerance continuum. Evidence that molecular mechanisms induced by postprandial hyperglycaemia contribute to vascular damage has further highlighted the importance of targeting this component of the metabolic syndrome. Indeed, clinical trials have failed to convincingly show that interventions targeting fasting hyperglycaemia significantly reduce diabetes-associated cardiovascular risk. It may be necessary to refocus therapy to target postprandial hyperglycaemia to effectively reduce cardiovascular risk in the diabetic population. There is now direct evidence that pharmacological intervention, in the form of acarbose, to reduce postprandial hyperglycaemia, can significantly decrease the risk of cardiovascular events in individuals with IGT or type 2 diabetes.