Shahirose Jessani

Should oral glucose tolerance testing be mandatory following acute myocardial infarction

A high prevalence of newly detected diabetes mellitus (DM) and impaired glucose tolerance (IGT) has been reported in patients with acute myocardial infarction (AMI) and no previous diagnosis of DM. However, the prevalence of newly detected DM is grossly underestimated by using fasting plasma glucose (FPG). We determined the prevalence of DM and IGT in patients post‐AMI from our local mixed ethnicity population, and evaluated the usefulness of oral glucose tolerance testing in such patients. All non‐diabetic subjects admitted with AMI underwent a standardised oral glucose tolerance test (OGTT) with 75 g glucose load predischarge in our institution. Fasting and 2‐h postchallenge plasma glucose levels were recorded, in addition to admission plasma glucose, serum cholesterol, triglycerides, HDL cholesterol and haemoglobin A1Clevels. We studied 61 patients [38 (62%) male; mean (SD) age, 64 (12.5) years], of whom 70% were white European and 30% South Asians. Mean (SD) plasma glucose concentration on admission was 6.9 (1.7; range, 5.8–8.1) mmol/l. Newly diagnosed DM and IGT were detected in 31% (95% CI 10–52) and 33% (95% CI 12–53) of patients respectively. Of those with newly detected diabetes only 32% (95% CI 0–69) had FPG > 6.1 mmol/l. The 12 month major adverse cardiac event rate was 4.5%, 15% and 32% in those with normal glucose tolerance, IGT and DM respectively. Previously undiagnosed DM and IGT in patients with AMI is common. The false reassurance of a normal FPG denies a significant proportion of undiagnosed diabetics the chance of early treatment. The importance of OGTT in the diagnostic work up of this vulnerable high‐risk group cannot be over‐emphasised.

Impaired glucose tolerance and endothelial damage, as assessed by levels of von Willebrand factor and circulating endothelial cells, following acute myocardial infarction

Background. Impaired glucose tolerance (IGT) following acute myocardial infarction (AMI) increases the incidence of major adverse cardiac events. We hypothesized that endothelial damage following AMI, as assessed by levels of von Willebrand factor (vWF) and circulating endothelial cells (CECs), would be more pronounced in patients with IGT compared to those with normal glucose tolerance (NGT). Methods. We studied non-diabetic patients with AMI (n=125; 107 (86%) male; mean age 59 years (SD 12.5)) who underwent oral glucose tolerance testing 3–5 days after admission. We measured vWF (enzyme-linked immunosorbent assay) and CECs (CD146 immunobead capture) in the fasting state and at 2 h post glucose load. Results. Base-line vWF and CEC levels were higher in IGT patients versus those with NGT and healthy controls (HC) (P<0.001). The acute increase in vWF and CECs in response to the glucose load was significantly higher in the IGT group compared to those with NGT and HC (P<0.01)—an increase on a par with that seen in newly diagnosed diabetics. Conclusion. The degree of endothelial damage post AMI in patients with IGT is greater than NGT, and comparable to that seen in frank diabetes mellitus. Subjects with IGT therefore need to be as actively sought and managed.

Vascular Damage in Impaired Glucose Tolerance: An Unappreciated Phenomenon?

Impaired glucose tolerance (IGT) is an independent risk predictor for cardiovascular morbidity and mortality, as well as for total mortality, independent of the subsequent development of overt diabetes mellitus. Increased rates of major adverse cardiac event and shorter survival in subjects with IGT who are post acute myocardial infarction have also been observed. The aim of this review article is to provide an overview of the pathophysiological basis of IGT and the actual mechanism(s) of vascular damage, accounting for its impact in cardiovascular disease (CVD). We focus on endothelial damage, aberrant angiogenesis and apoptosis-the three important pathophysiological mechanisms responsible for most long term complications in frank diabetes. However, on this occasion we evaluate these mechanisms in the milieu of IGT (post prandial hyperglycaemia or post challenge hyperglycaemia) rather than frank diabetes per se. A better understanding of the actual mechanisms of vascular damage in IGT may not only enhance our understanding about the disease process but may also facilitate implementation of appropriate therapeutic measures.

Is it the post-challenge hyperglycaemic spike or arterial stiffness we should be screening for?

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