The relationship between overexpression of somatostatin receptor type 2 in the infarcted myocardium and serum biomarkers of inflammation in the early post-infarction 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 assess 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 percutaneous intervention) and on the fifth day after acute myocardial infarction (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 single-photon emission computed tomography (SPECT)/computed tomography (CT) with 99mTc-Tektrotyd. Seven days after the acute coronary event, they underwent myocardial perfusion scintigraphy with 99mTcMIBI 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. At the same time 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 99mTc-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 antiinflammatory function of somatostatin receptor type 2 hyperexpression.