Postprandial dysmetabolism and large-vessel disease.
The increased cardiovascular disease morbidity and mortality in people with Type 2 diabetes mellitus (T2DM) is not explained by the prevalence of cardiovascular disease risk factors and is often attributed to poor glycaemic control. Epidemiological studies have shown fasting and especially postprandial or post-challenge hyperglycaemia to be strong predictors of cardiovascular disease morbidity and mortality in people with either T2DM or prediabetic states. Post-challenge hyperglycaemia in people with impaired glucose tolerance has been associated with increased cardiovascular disease mortality, regardless of the fasting blood glucose (FBG) concentration, but the relationship between FBG and cardiovascular disease was dependent on post-challenge glycaemia. Improving blood glucose and HbA1c concentrations by intensive insulin treatment reduced the risk of cardiovascular disease in a small group of Japanese patients with T2DM and, in another study, improved the outcome in patients with T2DM who had suffered a myocardial infarction. However, on the basis of currently available data, there is no evidence that improved glycaemic control results in a significant reduction of cardiovascular disease risk in people with T2DM. The aim in the present article is to review existing information on the relationship between glycaemia, particularly postprandial glucose concentrations, and cardiovascular disease in people with T2DM or impaired glucose tolerance, and to point at possible mechanisms by which postprandial hyperglycaemia could lead to cardiovascular disease.
Segal
P
P
Diabetes Unit, Chaim Sheba Medical Center, Tel-Hashomer, Israel. psegal@post.tau.ac.il
D001786:Blood Glucose / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology / Q000378:metabolism / Q000401:mortality*; D003924:Diabetes Mellitus, Type 2 / Q000150:complications / Q000188:drug therapy / Q000378:metabolism*; D005215:Fasting; D006442:Glycated Hemoglobin / Q000032:analysis; D006943:Hyperglycemia / Q000378:metabolism / Q000503:physiopathology*; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D019518:Postprandial Period; D012307:Risk Factors
D001786:Blood Glucose; D006442:Glycated Hemoglobin; D007004:Hypoglycemic Agents