Dithering over the treatment of diabetics with acute myocardial infarction

tion. In a recent review of over 80 000 patients given thrombolytic therapy for acute myocardial infarction, the 1-month mortality rate was 1·7 times higher in diabetics than in non-diabetics, and this difference persisted throughout the first year. As was the case in the TRACE Registry, insulin-treated diabetics had the worst prognosis, with a mortality rate 1·3 times higher than that of non-insulin-treated diabetics. Apart from a longer delay to treatment in diabetic patients (even under clinical trial conditions), other possible explanations for the excess mortality include reduced efficacy of thrombolytic regimens, more extensive underlying coronary disease, and worse left ventricular function due to diabetes and its metabolic derangement. These issues were partly addressed by the GUSTO-I Angiographic Substudy, but it should be noted that high-risk patients (who are more likely to die before angiography can be performed) were under-represented in the analysis. Although microvascular blood flow may be impaired in diabetics, their rates of infarct artery blood flow were found to be no different from those of nondiabetics. The rates of angiographic reocclusion and global systolic ejection fractions were also no different between diabetics and non-diabetics, although diabetics had an attenuated hyperkinetic response in the non-infarct zones. This finding is consistent with the Thrombolysis and Angioplasty in Myocardial Infarction (TAMI) Study results, and may have been due to concomitant multivessel disease or microcirculatory and cellular dysfunction caused by diabetes. In the GUSTO-I Angiographic Substudy, the difference in wall motion in the non-infarct zones of diabetics was no longer apparent after the acute phase of myocardial infarction. Metabolic derangement occurs during the acute stress of myocardial infarction. There is anaerobic metabolism of glucose and free fatty-acid accumulation, and insulin deficiency or resistance reduces cellular glucose uptake even further. Stress hyperglycaemia during myocardial infarction increases the risk of in-hospital mortality in both diabetics and non-diabetics. The benefit of metabolic modulation may depend on restoration of cellular perfusion in the infarct zone and the degree of metabolic derangement in the non-infarct zone, both of which may be affected by concomitant multivessel coronary artery disease. See page 1937 for the article to which this Editorial refers