Relationship between local and systemic inflammatory response in the early postinfarction period

Introduction. Radionuclide imaging of somatostatin receptor type 2 (SSTR-2) shows great promise as a novel marker of cardiovascular inflammation. However, it is still unclear whether local inflammation and high levels of macrophages in the infarct area that overexpress SSTR-2 are positive or negative factors for myocardial healing. Aim. To evaluate the relationship between inflammatory biomarkers as indicators of the systemic response to ischemic injury and the local inflammatory response in the myocardium, as measured by SSTR-2-targeted imaging, during the early post- infarction period. Material and methods. Twenty-three patients with acute primary anterior wall myocardial infarction and ST-segment elevation myocardial infarction (STEMI) were included in the study. On the first day (before PCI) and on the fifth day after AMI, venous blood was collected from all patients to determine hsCRP and IL-6 levels. Five to six days after the acute coronary event, all patients underwent SPECT/CT with 99m Tc-Tektrotyd. Seven days after the acute coronary event, they underwent myocardial perfusion scintigraphy with 99m Tc-MIBI at rest. Results. The results of the study indicated a negative correlation between hs-CRP and IL-6 levels on days 1 and 5 with left ventricular ejection fraction (LVEF) and a positive correlation with the summed rest score (SRS). Concurrently, SUVmax exhibited no correlation with hsCRP and IL-6 levels. Concurrently, SUVmax exhibited a moderate correlation with SRS (r = 0.517, p = 0.011). In the context of univariate linear regression, SUVmax demonstrated no statistically significant impact on hs-CRP and IL-6 levels. Concurrently, the total resting perfusion defect score (SRS) exerted an influence on the alteration in the levels of inflammatory biomarkers. It is also noteworthy that no regression relationship was identified between SUVmax and SRS. Conclusion. The findings indicated that the intensity of accumulation of somatostatin analog 99m Tc-Tectrotyd in the left ventricular myocardium during the early postinfarction period is not associated with the levels of inflammatory biomarkers. Our findings indicate the activation of cellular and biochemical pathways of the inflammatory cascade. Conversely, the study identified a potential anti-inflammatory function of somatostatin receptor type 2 hyperexpression.