Assessment of the dynamic parameters of the inflammatory response in acute myocardial infarction in patients with type 2 diabetes mellitus

BACKGROUND: The development of myocardial infarction is accompanied by an inflammatory reaction involving various immune cells that influence the monocyte response. An adequate inflammatory response has to ensure healing of the necrotic area in myocardium to approach the maximum possible restoration of left ventricular function, which directly affects the prognosis of patients with acute myocardial infarction. Patients with type 2 diabetes mellitus are a special group of patients with chronic low-grade inflammation and a high risk of complications. The features of changes in inflammatory response indicators and, above all, the monocyte response in patients with diabetes mellitus during the development of myocardial infarction have not been sufficiently studied.

AIM: To evaluate the dynamics of inflammatory response indicators in myocardial infarction in patients with type 2 diabetes mellitus.

MATERIALS AND METHODS: The study included 121 patients with myocardial infarction and type 2 diabetes mellitus. In addition to the standard study, the number of cells of different leukocyte subpopulations was evaluated on days 1, 3, 5 and 12 using flow cytometry with the CytoDiff® panel. Nonparametric methods of statistical analysis were used (STATISTICA 10). Quantitative data are presented as Median (Q25; Q75). Wilcoxon test was used to compare related groups, Spearman coefficient (R) was calculated to assess correlation dependencies. Differences were considered significant at p <0.05.

RESULTS: In patients with acute myocardial infarction and type 2 diabetes mellitus, the inflammatory reaction in the early stages was characterized by the development of neutrophilia: on 1^st day — up to 7310 (5304; 10,018) cells/μl, with subsequent normalization of their number by day 12: 4343 (3564; 5496) cells/μl, p <0.001. There was also a lower count of CD16(–) T-lymphocytes and natural killer cells on day 1: 1373 (1007; 1815) cells/μl, with their subsequent increase up to 1571 (1180; 1915) cells/μl, p=0.004. The development of a biphasic monocytic response with proinflammatory phase lasting up to 5 days was observed: on the 5^th day of myocardial infarction, the values of the CD16(–) monocytes reached a maximum in the peripheral blood and amounted to 692 (514; 791) cells/μl, decreasing to 505 (405; 626) cells/μl, p <0.001, by day 12. CD16(+) monocytes count on day 5 was 61 (40; 75) cells/μl with a further decrease in their number to 45 (30; 77) cells/μl (p=0,012) by the 12^th day. A direct correlation was revealed between neutrophils and CD16(–) monocytes on the 1st and 12^th days of myocardial infarction (R=0.650, R=0.573, respectively; p <0.05). Similar correlation was found between CD16(–) and CD16(+) monocytes determined on day 3 and the number of platelets determined on day 1 (R=0.632 and R=0.735, respectively; p <0.05), as well as between B-lymphocytes on day 3 and the percentage of CD16(+) monocytes on day 5 (R=0.786, p <0.05).

CONCLUSION: In patients with type 2 diabetes mellitus, a biphasic monocytic response is observed in acute myocardial infarction with signs of pronounced proinflammatory phase. The revealed correlations between the monocytes and other leukocyte subpopulations count, as well as platelets, indicate the presence of mutual influences between cells and complex regulation of the inflammatory response in myocardial infarction.