Key result
Streptozotocin-induced diabetes increases 20-minute mortality after acute coronary ligation by ~47%.
Why the study?
Does diabetes increase early mortality after acute myocardial infarction in a rat model?
Does diabetes increase early mortality after acute myocardial infarction in a rat model?
Absolute Event Rate: 78% vs 53%
p-value: p=<0.05
In a rat model of acute myocardial infarction, diabetes significantly increased early mortality, which was associated with worse metabolic control (higher glucose and lower insulin).
Warrants caution against clinical extrapolation; leaves open metabolic effects on early human post-MI mortality.
Diabetes mellitus is well known to increase the death rate after acute myocardial infarction in humans. The mechanisms of this adverse effect of diabetes, however, remain unknown. In the present study an animal model was developed in which the influence of diabetes on the survival rate after acute myocardial infarction could be studied in more detail. Male Wistar rats were rendered diabetic with streptozotocin (45 mg·kg−1 intravenously) and kept in the study if one week later their tail blood glucose concentration was between 13.9 and 22.2 mmol·litre−1 after a four hour fast. Ten weeks later they underwent acute left coronary artery ligation. In comparison with control rats (n=30), diabetic rats (n=32) had a higher mortality in the first 20 minutes after acute coronary artery ligation (78% vs 53%; p<0.05 by x2 test). Creatine kinase-MB isoenzyme activity tended to increase less in surviving diabetic rats than in their non-diabetic counterparts. Moreover, blood samples collected a few minutes before the surgical procedure showed that diabetic rats dying within the first 20 minutes (n=25) had higher mean(SEM) plasma glucose concentrations (26.9(0.5) vs 23.4(1.2) mmol·litre−1; p<0.01) and lower mean(SEM) plasma insulin concentrations (20(1) vs 26(2) mU·litre−1; p<0.05) than those (n=7) that survived that critical period. It is suggested that (a) acute ligation of the left coronary artery in streptozotocin diabetic rats may be a good model for evaluating some of the deleterious effects of diabetes on the survival rate of subjects who sustain acute myocardial infarction and (b) the increased death rate of diabetics experiencing acute myocardial infarction is possibly partly related to acute disturbances in their metabolic control.
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Nadeau et al. (1986) studied Acute myocardial infarction (n=62). Streptozotocin-induced diabetes vs. Control (non-diabetic) rats was evaluated on Mortality in the first 20 minutes after acute coronary artery ligation (p=<0.05). Streptozotocin-induced diabetes significantly increased mortality in the first 20 minutes after acute coronary artery ligation compared to non-diabetic controls (78% vs 53%; p<0.05).
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