Abstract

BackgroundInflammation plays an important role in the pathophysiology of both atherosclerosis and type 2 diabetes and some inflammatory markers may also predict the risk of developing type 2 diabetes. The aims of the present study were to assess a potential association between circulating levels of inflammatory markers and hyperglycaemia measured during an acute ST-elevation myocardial infarction (STEMI) in patients without known diabetes, and to determine whether circulating levels of inflammatory markers measured early after an acute STEMI, were associated with the presence of abnormal glucose regulation classified by an oral glucose tolerance test (OGTT) at three-month follow-up in the same cohort.MethodsInflammatory markers were measured in fasting blood samples from 201 stable patients at a median time of 16.5 hours after a primary percutanous coronary intervention (PCI). Three months later the patients performed a standardised OGTT. The term abnormal glucose regulation was defined as the sum of the three pathological glucose categories classified according to the WHO criteria (patients with abnormal glucose regulation, n = 50).ResultsNo association was found between inflammatory markers and hyperglycaemia measured during the acute STEMI. However, the levels of C-reactive protein (CRP) and monocyte chemoattractant protein-1 (MCP-1) measured in-hospital were higher in patients classified three months later as having abnormal compared to normal glucose regulation (p = 0.031 and p = 0.016, respectively). High levels of CRP (≥ 75 percentiles (33.13 mg/L)) and MCP-1 (≥ 25 percentiles (190 ug/mL)) were associated with abnormal glucose regulation with an adjusted OR of 3.2 (95% CI 1.5, 6.8) and 7.6 (95% CI 1.7, 34.2), respectively.ConclusionElevated levels of CRP and MCP-1 measured in patients early after an acute STEMI were associated with abnormal glucose regulation classified by an OGTT at three-month follow-up. No significant associations were observed between inflammatory markers and hyperglycaemia measured during the acute STEMI.

Highlights

  • Inflammation plays an important role in the pathophysiology of both atherosclerosis and type 2 diabetes and some inflammatory markers may predict the risk of developing type 2 diabetes

  • We have recently shown that high levels of HbA1c, admission glucose, and fasting plasma glucose measured early in-hospital in patients with an acute ST-elevation myocardial infarction (STEMI) were predictive to identify patients with abnormal glucose regulation at three-month follow-up [4]

  • The aims of the study were 1) to assess a potential association between circulating levels of inflammatory markers and hyperglycaemia measured during an acute STEMI in patients without known diabetes and 2) to identify a possible association between circulating levels of inflammatory markers measured acutely and abnormal glucose regulation classified by an oral glucose tolerance test (OGTT) at threemonth follow-up in the same cohort

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Summary

Introduction

Inflammation plays an important role in the pathophysiology of both atherosclerosis and type 2 diabetes and some inflammatory markers may predict the risk of developing type 2 diabetes. The aims of the present study were to assess a potential association between circulating levels of inflammatory markers and hyperglycaemia measured during an acute ST-elevation myocardial infarction (STEMI) in patients without known diabetes, and to determine whether circulating levels of inflammatory markers measured early after an acute STEMI, were associated with the presence of abnormal glucose regulation classified by an oral glucose tolerance test (OGTT) at three-month follow-up in the same cohort. Increased prevalence of unknown impaired glucose tolerance and type 2 diabetes has been shown in patients suffering an acute myocardial infarction (AMI) [1] Both the short- and long-term prognoses after an AMI are worse among individuals with abnormal compared to. We hypothesized that STEMI patients having abnormal glucose regulation would present with an increased pro-inflammatory profile

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