Abstract

During myocardial infarction (MI), a transient decrease of both insulin sensitivity and secretion triggers stress hyperglycemia which is followed by a substantial increase in mortality. Recent data indicate that HDL modulates insulin sensitivity and secretion. To date, however the role of HDL on stress hyperglycemia remains unknown. We explored the influence of HDL on stress hyperglycemia during acute phase of MI. Consecutive non-diabetic patients with ST-elevation MI (n=183) were selected from the Brasilia Heart Study for this investigation. Blood glucose and plasma insulin and C-peptide were measured in the first 24 hours and at the fifth day after MI onset. Patients were divided into HDL-C quartiles for the analyses (Q1:<31, Q2:31-38, Q3:38-47 and Q4:>47 mg/dL). On admission, no difference was found between the quartiles in blood glucose (p=0.6), plasma insulin (p=0.6), plasma C-peptide (p=0.5), HOMA2S (p=0.9) and HOMA2B (p=1.0). On the fifth day there was a reduction in blood glucose whose intensity was directly proportional to HDL-C quartile (-1±32, -13±46, -19±25, -27±21; respectively, p<0.001). In parallel, there was a reduction in plasma insulin [-7.1(-25,1), -5.5(-22,-1), -9.9(-26,-1), -17.7(-32,-9); respectively, p<0.001] and C-peptide [0(-3,1), -1.2(-3,1), -1.7(-3,0), -2.4(-4,0); respectively, p<0.001] whose magnitude was inversely proportional to HDL-C quartile. Consistently, the change in HOMA2S [1(-11,15), 7(-15,17), 10(-5,30), 15(-8,28); respectively, p<0.001] and HOMA2B [-11(-43,31), 16(-45,48), 22(-8,44), 24(-23,61); respectively, p=0.01] and disposition index (DI) [159(-1693,1988), 1104(-1561,3329), 2444(1099,3899), 2447(1052,4856); respectively, p<0.001] were also proportional to HDL-C quartiles. Furthermore, in a multivariate analysis model, HDL-C levels were positively and independently associated with a higher change in DI (B=0.068; Exp(B)=1.071; p<0.001). This study provides the first evidence that patients with higher HDL plasma levels may be more protected against stress hyperglycemia during MI via acceleration of the improvement in insulin secretion and sensitivity.

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