Abstract

Introduction In recent years, much attention has been given to the evidence that the concomitant occurrence of hyperglycaemia in patients admitted to intensive care units with an acute myocardial infarction (AMI) enhances the risk of mortality and morbidity, whether the patient was diagnosed with having diabetes or not .1 In some cases, the elevation of glucose levels could simply be a marker of preexisting, but not yet detected, type 2 diabetes or impaired glucose tolerance (IGT). 2 This may mean that besides being causal, elevated glucose also could be a marker of existing insulin resistance and/or beta-cell failure that may contribute to the poor prognosis through other mechanisms. However, a positive association between hyperglycaemia at the time of the event and subsequent mortality from AMI has frequently been reported .3,4,5,6 A strong correlation between glycaemia and shock or development of heart failure has also been reported. 7 Consequently, understanding the possible mechanisms through which hyperglycaemia worsens the prognosis of AMI, as well the effectiveness of its control during AMI, seems to be of great relevance. It is now accepted worldwide that the most important factor influencing atherosclerotic plaque instability is inflammation. Elevated blood glucose levels per se adversely affect outcome through the cumulative effects of several mechanisms, including induction of endothelial dysfunction, oxidative stress, hyper coagulability and impaired fibrinolysis. 7,8 Acute hyperglycaemia in healthy subjects and in patients with impaired glucose tolerance or overt diabetes produces a rise in inflammatory markers. Following this line of thought, it might be speculated that the detrimental effect of stress hyperglycaemia in acute MI might also stem from its ability to increase inflammation. This study aims at exploring the association between the admission glycemic status and 30-day mortality in acute myocardial infarction in non diabetic patients.

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