ACUTE MYOCARDIAL-INFARCTION IN DOGS WITH EXPERIMENTAL DIABETES

Objective: The aim was to examine whether diabetes interferes with the development of myocardial injury in a canine ischaemia-reperfusion mo del. Methods: Non-insulin-requiring diabetes was induced in dogs by th e streptozotocin-alloxan method. After 75 d, the dogs were anaesthetis ed and myocardial infarction was provoked by occluding the left anteri or descending coronary artery for 2 h followed by 6 h reperfusion. Res ults: Diabetic dogs had higher blood glucose [9.4(SEM 1) mmol.litre-1] , fructosamine [417(57) mumol.litre-1], and glycated haemoglobin [3.3( 0.7)%], than control dogs [5.5(0.6), p = 0.04, 243(15), p = 0.01, and 0.7(0.2), p = 0.003, respectively], and they also had higher serum lip ids (p = 0.00 1) and platelet aggregation (p = 0.03). Area at risk was similar in diabetic and control dogs but in contrast to controls (r = 0.78, p = 0.007), area at risk and infarct size were not correlated i n diabetics (r = 0.08). In both groups, collateral flow was the major determinant of infarct size: r = A.73 in controls (p = 0.02) and -0.97 in diabetics (p = 0.00 1). In spite of higher subendocardial collater al flow in diabetics [representing 21.6(6)% of the flow in the corresp onding non-ischaemic zone] than in controls [11.2(6)%], infarct size w as similar in both groups. However, the mean observed infarct size in the diabetic group [7.5(2.8)% of the left ventricle] was significantly (p < 0.03) larger than the mean predicted infarct size [5.2(2)%]. Mul tivariate analysis confirmed that diabetes, as well as collateral flow , is an independent (p = 0.03) predictor of infarct size. Conclusions: For a given collateral flow, diabetic dogs develop larger infarcts th an controls. Further studies are required to investigate the biochemic al mechanism(s) underlying this deleterious effect. However, this may partly explain the poor prognosis of myocardial infarction in diabetic