Glycaemic variability is associated with severity of coronary artery disease in patients with poorly controlled type 2 diabetes and acute myocardial infarction

Background. - In patients with type 2 diabetes (T2D), glycaemic variability (GV), another component of glycaemic abnormalities, is a novel potentially aggravating factor for coronary artery disease (CAD). Objectives: The aim of our study was to identify interactions between GV and severity of CAD in diabetes patients admitted for acute myocardial infarction (AMI). Methods. - All patients with T2D admitted to our university hospital for AMI from March 2015 to February 2017 who received intravenous (IV) insulin therapy and underwent coronary angiography were included. GV was assessed by mean amplitude of blood glucose excursion (MACE) values taken within 2 days of admission. Patients with higher GV (highest MACE tertile) were compared with those with lower GV (first and second MACE tertiles). Results. - A total of 204 patients were included: median age was 72 (61-81) years; 32% were female; HbA(1c), was 7.3% (6.4-8.2%); diabetes duration was 10 (2-17.5) years; and MACE value was 0.65 (0.43-0.92) g/L. Compared with those with lower GV, patients with the highest GV were more often women, treated with previous insulin, and had higher blood glucose and HbA(1c) levels. In addition, patients with elevated GV had significantly higher SYNTAX scores: 17 (10-28) vs. 12 (6-22) (P = 0.009). Indeed, SYNTAX scores (OR: 1.05, 95% CI: 1.02-1.08; P = 0.001) remained independently associated with high GV beyond HbA(1c) levels (OR: 1.51, 95% CI: 1.2-1.89; P < 0.001). Conclusion. - In AMI patients with poorly controlled diabetes, GV is associated with CAD severity beyond chronic hyperglycaemia. Although no causality can be determined from our observational study, the results suggest that, in AMI, early evaluation of GV might contribute to the identification of those diabetes patients at high risk, and serve as a therapeutic target for both primary and secondary prevention. (C) 2019 Published by Elsevier Masson SAS.