TY - JOUR
T1 - Glycaemic control is essential for effective cardiovascular risk reduction across the type 2 diabetes continuum
AU - Karasik, Avraham
N1 - Funding Information:
This review was supported by Bayer HealthCare. The author would like to acknowledge the editorial support of Thomson Gardiner-Caldwell London in the preparation of this manuscript.
PY - 2005
Y1 - 2005
N2 - 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.
AB - 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.
KW - Acarbose
KW - Cardiovascular disease
KW - Glucose intolerance
KW - Postprandial hyperglycaemia
KW - Type 2 diabetes
UR - http://www.scopus.com/inward/record.url?scp=21344433452&partnerID=8YFLogxK
U2 - 10.1080/07853890510037365
DO - 10.1080/07853890510037365
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C2 - 16019723
AN - SCOPUS:21344433452
VL - 37
SP - 250
EP - 258
JO - Annales medicinae experimentalis et biologiae Fenniae
JF - Annales medicinae experimentalis et biologiae Fenniae
SN - 0785-3890
IS - 4
ER -