Department of Cardiology, University Hospital Groningen, Hanzeplein 1, Postbus 30.001, 9700 RB Groningen, The Netherlands
American College of Cardiology Foundation
Dr. Iwakura and colleagues in a recent issue of the Journal(1) conclude that, from a retrospective analysis of 146 patients, hyperglycemia might be associated with impaired microvascular function after acute myocardial infarction. The investigators describe an independent relation between elevated blood glucose levels on admission and no-reflow phenomenon after primary angioplasty of the infarct-related artery. They also state that this relation was independent of HbA1c level or diabetes mellitus (DM), because no differences existed in HbA1c levels or in the incidence of DM in both the no-reflow group and the reflow group.
We have some considerations about these results. First, the investigators defined hyperglycemia by the optimal cutoff to differentiate the patients showing no reflow with a receiver-operating characteristic curve analysis. By using this cutoff in the same cohort they found a relation between hyperglycemic patients and no-reflow phenomenon. The researchers have generated an interesting hypothesis, but new studies in another patient population still have to prove the validity of this cutoff. Furthermore, we are interested in details with regard to the methods used to determine blood glucose and HbA1c levels. No information was reported as to whether the blood glucose level was measured with point-of-care of laboratry measurements or whether their method has been validated in critically ill patients. Clinically relevant differences in blood glucose levels have been observed in patients with shock (2), and there may be an influence of acidosis and hematocrit values (3). Finally, the absolute differences of 0.3% in HbA1c and 13% in incidence of DM were not statistically related to the no-reflow phenomenon, but this may be due to the small number of patients. The investigators found that 45.3% of the patients with hyperglycemia were diabetic versus 9.9% in patients without hyperglycemia (p < 0.0001).
The hypothesis that acute hyperglycemia (i.e., hyperglycemia at admission) is associated with the no-reflow phenomenon is intriguing. We, however, hypothesize that this relation is not independent of chronic hyperglycemia (i.e., elevated HbA1c level and/or DM). Therefore, new clinical studies have to determine the effect of hyperglycemia on no-reflow and the impact of metabolic regulation.
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