Key result
Early somatostatin inversely correlates with post-MI IL-1β, but not myocardial tracer uptake.
Why the study?
The dynamics of endogenous somatostatin and its association with myocardial 99mTc-Tektrotyd uptake intensity and cytokine profiles in the early post-infarction period required evaluation.
Cohort (n=22)
No
In the early post-infarction period following primary anterior STEMI, endogenous somatostatin levels inversely correlate with pro-inflammatory IL-1β levels and Day 5 left ventricular remodeling parameters (LVEDV and WMSI), but do not directly correlate with myocardial 99mTc-Tektrotyd uptake on SPECT/CT.
Hypothesis-generating for somatostatin's role in post-STEMI inflammation; leaves open any link to SSTR2 uptake or remodeling.
The aim of the study was to evaluate the dynamics of endogenous somatostatin (SST) and its association with the intensity of 99mTc-Tektrotyd uptake and the cytokine profile in patients with primary anterior ST-segment elevation myocardial infarction during the early post-infarction period. Materials and Methods. The study included 22 patients admitted within the first 24 h from disease onset with a diagnosis of primary anterior ST-segment elevation myocardial infarction. The median age was 60.0 (53.0–65.5) years. All patients underwent percutaneous coronary intervention, echocardiography, and measurement of serum SST, high-sensitivity C-reactive protein, and interleukins (IL-1β, IL-6, IL-10) on days 1 and 5. On days 5–6, SPECT/CT with 99mTc-Tektrotyd was performed, with calculation of the maximum standardized uptake value of 99mTc-Tektrotyd (SUVmax) in the myocardium. Results. Myocardial 99mTc-Tektrotyd uptake was found in 18 patients (SUVmax — 2.8 [1.8–3.1] g/ml). The SST level on day 1 was 20.2 [11.2–40.8] pg/ml, and on day 5 — 23.2 [15.8–42.4] pg/ml (p=0.874); the dynamics were multidirectional. A negative correlation was found between SST concentration on day 1 and IL-1β level on day 1 (ρ=−0.645; p=0.001) and day 5 (ρ=−0.655; p=0.0001), as well as with left ventricular end-diastolic volume (ρ=−0.453; p=0.036) and the wall motion score index of the left ventricle (ρ=−0.484; p=0.023) on day 5. There was no correlation between SST level and SUVmax (ρ=−0.078; p=0.728). Regression analysis confirmed a significant effect of SST on IL-1β concentration (R2=0.526; p=0.0001 for day 1; R2=0.476; p=0.001 for day 5). Conclusion. In the early post-infarction period, endogenous SST demonstrates a negative relationship with the level of the proinflammatory cytokine IL-1β and left ventricular remodeling parameters, which emphasizes its important anti-inflammatory role. The absence of a direct association between SST concentration and SUVmax of 99mTc-Tektrotyd indicates the complex nature of peptide-receptor interaction and requires further investigation. The obtained data substantiate the potential of studying the somatostatinergic system as a promising therapeutic target in acute myocardial infarction.
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Ilyushenkova et al. (2026) conducted a cohort in Primary anterior ST-segment elevation myocardial infarction (STEMI) (n=22). Endogenous serum somatostatin (SST) concentration and 99mTc-Tektrotyd SPECT/CT imaging was evaluated on Association of endogenous somatostatin (SST) dynamics with IL-1β levels and myocardial 99mTc-Tektrotyd uptake (SUVmax) (ρ = -0.645 (day 1 IL-1β); ρ = -0.655 (day 5 IL-1β), p=0.001 (day 1); 0.0001 (day 5)).
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