Impaired glucose tolerance and cardiovascular disease: the possible role of post-prandial hyperglycemia

Am Heart J. 2004 May;147(5):803-7. doi: 10.1016/j.ahj.2003.11.020.


There is increasing evidence that the post-prandial state is an important contributing factor in the development of atherosclerosis. In subjects with impaired glucose tolerance, whereas fasting glycemia is in reference range, the post-prandial phase is characterized by a rapid and large increase in blood glucose levels. The possibility that this post-prandial "hyperglycemic spike" may be relevant to the development of cardiovascular disease in these subjects has received recently much attention. The oral glucose tolerance test, although highly non-physiological, has been used largely as model of the post-prandial state, and epidemiological studies have shown that impaired oral glucose tolerance is associated with an increased risk of cardiovascular disease, because the glycemia level after 2 hours of the glucose challenge is a direct and independent risk factor. Most of the cardiovascular risk factors are modified in the post-prandial phase and are directly affected by an acute increase of glycemia. The mechanisms through which acute hyperglycemia exerts its effects may be identified in the production of free radicals, which favours the development of an endothelial dysfunction, a prothrombotic and proinflammatory condition. Future studies may evaluate whether correcting the post-prandial hyperglycemia in the impaired glucose tolerance state can form part of the strategy for the prevention and management of cardiovascular diseases in these subjects.

Publication types

  • Review

MeSH terms

  • Blood Glucose / metabolism*
  • Cardiovascular Diseases / etiology*
  • Cell Adhesion Molecules / metabolism
  • Coronary Artery Disease / etiology
  • Endothelium, Vascular / physiopathology
  • Glucose Intolerance / diagnosis
  • Glucose Tolerance Test
  • Humans
  • Postprandial Period / physiology*
  • Thrombosis / etiology


  • Blood Glucose
  • Cell Adhesion Molecules