Determinants and importance of stress hyperglycaemia in non-diabetic patients with myocardial infarctionDeterminants of plasma glucose concentrations were studied in patients on admission to hospital with confirmed acute myocardial infarction but without previous glucose intolerance as evidenced by raised concentrations of glycosylated haemoglobin (HbA&,). Mortality in hospital increased significantly with increasing plasma concentrations ofglucose in patients with both normal (p<0O0001, n=311) and borderline (p<0-02, n=70) concentrations of HbA1c. There was a weak relation between plasma glucose concentrations and infarct size as estimated by peak aspartate transaminase activity in both HbA,1 groups (rs= 0-26, n=101 and r,=041, n=35 respectively). A correlation was found between adrenaline and plasma glucose concentrations (r=047, n=27) and cortisol and plasma glucose concentrations (r=0*75, n=19), but the relation of plasma noradrenaline and plasma glucose suggested a threshold effect. Concentrations of adrenaline, but not those of noradrenaline or cortisol, correlated with infarct size as measured both by peak aspartate transaminase activity and cumulative release of creatine kinase MB isoenzyme. Multiple regression analysis showed that concentrations of cortisol, adrenaline, and noradrenaline (but not the concentration of-HbAc, infarct size, or age) are the main determinants of plasma glucose concentration measured in non-diabetic patients when admitted to hospital after acute myocardial infarction.

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We compare the clinical features and hospital outcomes in 83 diabetic patients admitted with acute myocardial infarction and 380 nondiabetic patients with levels of glycosylated hemoglobin (HbA1c) low enough to exclude undiagnosed diabetes. The hospital mortality was 42.2% in diabetic and 24.7% in nondiabetic patients, an odds ratio of 2.22 (CI 1.37-3.60, P less than .002). The excess mortality was due to cardiogenic shock and left ventricular failure (pump failure). There was no difference in peak levels of aspartate transaminase between the groups. Among the diabetic patients, the admission levels of plasma glucose and peak levels of aspartate transaminase were higher among those who developed pump failure or died, but there was no relationship between outcome and gender, disease duration, or treatment. Prior blood glucose control, as judged by levels of HbA1c, was not related to hospital outcome (P greater than .5). In a further study, the 83 diabetic patients were compared with 249 age- and sex-matched diabetic subjects without myocardial infarction for treatment, disease duration, and control. There was an increased risk of admission with myocardial infarction of 2.35 (CI 1.41-3.92, P less than .005) within the first 5 yr of diagnosis of diabetes. Infarct patients had significantly lower levels of HbA1c than control subjects (P less than .005), but treatment did not differ between groups. Neither incidence nor case fatality of myocardial infarction in diabetic patients is positively associated with cumulative glycemic exposure.