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We thank Dr. Zijlstra and colleagues for their interest in our work and for their comments. We agree with them that further study is preferable to prove the validity of the present cutoff point of blood glucose for prediction of the no-reflow phenomenon. We measured blood glucose in whole arterial blood samples with reflectance glucometer at the bedside. The measurements of glucose in whole blood are predictably 10% to 15% less than those in plasma, and arterial blood glucose is higher than venous glucose. Although capillary blood glucose measurement could be inaccurate in patients with severe hypotension, whole-blood glucose measurement has been reported to be accurate even in critically ill patients (1)(also see Ref. 1 in Dr. van der Horst’s letter). Moreover, only 7 (4.8%) of 146 patients had blood pressure <100 mm Hg. Hematocrit might also affect blood glucose measurement, especially in the whole-blood sample. However, the effects of hematocrit could be important only at high hematocrit levels, such as >55% (2), and no patients in our study had such a high hematocrit. Thus, we believe that the effects of blood pressure or hematocrit on blood glucose measurement could be negligible in our study.
It is important to question whether chronic hyperglycemia also affects the development of the no-reflow phenomenon. In our previous report based on the 199 patients with anterior acute myocardial infarction, none of whom were enrolled in our recent study, we did not find that diabetes mellitus predicts the no-reflow phenomenon independently (3), as in our recent study. We also performed multivariate logistic analysis again and found that blood glucose level could be an independent predictor of the no-reflow phenomenon (p = 0.008, odds ratio [95% confidence interval] = 1.03 [1.01 to 1.06]) even among the 105 patients without diabetes. Thus, we concluded that acutehyperglycemia in itself is related with the no-reflow phenomenon independently from chronic hyperglycemia. Akbari et al. (4)also reported that acute hyperglycemia impairs vasodilation in microcirculation even in healthy subjects.
- American College of Cardiology Foundation