Key result
Impaired glucose tolerance contributes to CVD via endothelial damage and apoptosis independent of overt diabetes.
Understanding the pathophysiological mechanisms of vascular damage in impaired glucose tolerance may facilitate the implementation of appropriate therapeutic measures to reduce cardiovascular risk.
IGT may warrant inclusion in CVD risk assessment beyond diabetes; leaves open whether targeting it improves outcomes.
Impaired glucose tolerance (IGT) is an independent risk predictor for cardiovascular morbidity and mortality, as well as for total mortality, independent of the subsequent development of overt diabetes mellitus. Increased rates of major adverse cardiac event and shorter survival in subjects with IGT who are post acute myocardial infarction have also been observed. The aim of this review article is to provide an overview of the pathophysiological basis of IGT and the actual mechanism(s) of vascular damage, accounting for its impact in cardiovascular disease (CVD). We focus on endothelial damage, aberrant angiogenesis and apoptosis-the three important pathophysiological mechanisms responsible for most long term complications in frank diabetes. However, on this occasion we evaluate these mechanisms in the milieu of IGT (post prandial hyperglycaemia or post challenge hyperglycaemia) rather than frank diabetes per se. A better understanding of the actual mechanisms of vascular damage in IGT may not only enhance our understanding about the disease process but may also facilitate implementation of appropriate therapeutic measures.
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Jessani et al. (2009) conducted a review in Impaired glucose tolerance. Impaired glucose tolerance was evaluated. Impaired glucose tolerance contributes to cardiovascular disease through endothelial damage, aberrant angiogenesis, and apoptosis, independent of overt diabetes.
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