Abstract

Purpose: To access the insulin resistance markers dynamics in ST-segment elevation patients with MI with presented and non-presented T2DM in acute and post-acute rehabilitation periods. Methods: 95 patients with myocardial infarction and 60 patients with MI and associated T2DM were included in the study; the control group consisted of 30 healthy subjects. The concentration of serum FFA, glucose, C-peptide and insulin were measured on the 1st and 12th days of the study. MI was diagnosed according to the 2007 National Scientific Cardiology Society. The study design was approved by the Institutional Review Board. The insulin resistance level was estimated using a mathematical model incorporating fasting serum insulin and glucose measurement with the QUICKI calculation. The results were statistically processed using non-parametric criteria; differences were considered to be statistically significant in p < 0.05. Results: Blood glucose level increased in the Group 1 and on the 1st day after MI onset. An elevation of glucose level was noticed in the Group 2 during the whole follow-up period, whereas in the Group 1 blood glucose level decreased on the 12th day. Postprandial glucose level increased in the Group 2 in comparison with the control values on the 12th day from the MI onset. In contrast, fasting serum insulin and C-peptide level tended to increase in both groups on the 1st and 12th days from the MI onset. Postprandial insulin level raised equally in both groups compared to the control group. In the Group 1, the QUICKI indices were 0,316±0.005 and 0,319±0.005 on the 1st and 12th days after the MI onset, respectively, and they were interpreted as breakpoint values between severe and moderate IR. In the Group 2, the QUICKI indices were 0,296±0.009 and 0,300±0.005, that verified a pronounced tissue insulin resistance. FFA levels in the Group 1 and in the Group 2 exceeded the control group values. PAI-1 concentration was higher in the Group 1 and higher in the Group 2 compared to the control group on the 1st day. In addition, PAI-1 concentration significantly reduced in both groups on the 12th day. Postprandial insulin positively correlated to FFA levels (R=0,47, p=0.02) and QUICKI index negatively correlated to FFA levels (R=-0,229, p=0,006). Moreover, a negative correlation between PAI-1 concentration and QUICKI index was reported in Group 2 and in Group 1 (R= -0,77, p=0,005; R= -0,47, p=0,005, respectively). Conclusion: Elevated FFA and PAI-1 levels are significant indicators of impaired insulin sensitivity under the conditions of acute MI compared to the postprandial glycemia and insulinemia.

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