A decrease in glucose variability does not reduce cardiovascular event rates in type 2 diabetic patients after acute myocardial infarction: a reanalysis of the HEART2D study

Sarah E Siegelaar, Lisa Kerr, Scott J Jacober, J Hans Devries, Sarah E Siegelaar, Lisa Kerr, Scott J Jacober, J Hans Devries

Abstract

Objective: To assess the effect of intraday glucose variability (GV) on cardiovascular outcomes in a reanalysis of Hyperglycemia and Its Effect After Acute Myocardial Infarction on Cardiovascular Outcomes in Patients With Type 2 Diabetes Mellitus (HEART2D) study data.

Research design and methods: Type 2 diabetic patients after acute myocardial infarction were randomized to an insulin treatment strategy targeting postprandial (PRANDIAL; n = 557) or fasting/interprandial (BASAL; n = 558) hyperglycemia. GV was calculated as mean amplitude of glycemic excursions (MAGE), mean absolute glucose (MAG) change, and SD.

Results: The PRANDIAL strategy resulted in an 18% lower MAG than BASAL (mean [SEM] difference 0.09 [0.04] mmol/L/h, P = 0.02). In addition, MAGE and SD were lower in the PRANDIAL group, however, not significantly. HbA(1c) levels and cardiovascular event rates were comparable between groups.

Conclusions: A PRANDIAL strategy demonstrated lower intraday GV vs. a BASAL strategy with similar overall glycemic control but did not result in a reduction in cardiovascular outcomes. This does not support the hypothesis that targeting GV would be beneficial in reducing subsequent secondary cardiovascular events.

Figures

References

1. 1. Borg R, Kuenen JC, Carstensen B, et al. ADAG Study Group HbA1(c) and mean blood glucose show stronger associations with cardiovascular disease risk factors than do postprandial glycaemia or glucose variability in persons with diabetes: the A1C-Derived Average Glucose (ADAG) study. Diabetologia 2011;54:69–72
2. 1. Nalysnyk L, Hernandez-Medina M, Krishnarajah G. Glycaemic variability and complications in patients with diabetes mellitus: evidence from a systematic review of the literature. Diabetes Obes Metab 2010;12:288–298
3. 1. Monnier L, Colette C, Mas E, et al. Regulation of oxidative stress by glycaemic control: evidence for an independent inhibitory effect of insulin therapy. Diabetologia 2010;53:562–571
4. 1. Kilpatrick ES, Rigby AS, Atkin SL. The effect of glucose variability on the risk of microvascular complications in type 1 diabetes. Diabetes Care 2006;29:1486–1490
5. 1. Siegelaar SE, Kilpatrick ES, Rigby AS, Atkin SL, Hoekstra JB, Devries JH. Glucose variability does not contribute to the development of peripheral and autonomic neuropathy in type 1 diabetes: data from the DCCT. Diabetologia 2009;52:2229–2232
6. 1. Kilpatrick ES, Rigby AS, Atkin SL. Effect of glucose variability on the long-term risk of microvascular complications in type 1 diabetes. Diabetes Care 2009;32:1901–1903
7. 1. Siegelaar SE, Holleman F, Hoekstra JB, DeVries JH. Glucose variability: does it matter? Endocr Rev 2010;31:171–182
8. 1. Siegelaar SE, Kulik W, van Lenthe H, Mukherjee R, Hoekstra JB, Devries JH. A randomized clinical trial comparing the effect of basal insulin and inhaled mealtime insulin on glucose variability and oxidative stress. Diabetes Obes Metab 2009;11:709–714
9. 1. Raz I, Wilson PW, Strojek K, et al. Effects of prandial versus fasting glycemia on cardiovascular outcomes in type 2 diabetes: the HEART2D trial. Diabetes Care 2009;32:381–386
10. 1. Hermanides J, Vriesendorp TM, Bosman RJ, Zandstra DF, Hoekstra JB, Devries JH. Glucose variability is associated with intensive care unit mortality. Crit Care Med 2010;38:838–842
11. 1. Service FJ, Molnar GD, Rosevear JW, Ackerman E, Gatewood LC, Taylor WF. Mean amplitude of glycemic excursions, a measure of diabetic instability. Diabetes 1970;19:644–655

Source: PubMed