Evaluation of the adipose-dependent proinflammatory markers level in patients with acute coronary syndrome
DOI:
https://doi.org/10.63341/ijmmr/2.2025.81Keywords:
obesity, troponin I, leptin, caspase-9, apoptosis, adipokines, myocardial necrosis, myocardial infarctionAbstract
Obesity is a predictor of the development of acute coronary syndrome with ST segment elevation and is realised through increased apoptotic processes. The objective of the study was to evaluate the relationship between body mass index, troponin I as a specific marker of myocardial necrosis and adipose-dependent non-specific markers in patients with acute coronary syndrome with ST segment elevation affected by obesity. An open-label longitudinal comparative cohort study was conducted involving 120 patients with acute coronary syndrome with ST segment elevation, stratified by body mass index into three groups. The levels of troponin I, leptin and caspase-9 (ELISA method) were determined, followed by the use of statistical research methods. In obese patients, a significant increase in the levels of caspase-9 (62.40 ± 3.8 ng/mL) and leptin (57.27 ± 4.1 ng/mL) was found compared to the overweight groups (45.27 ± 2.26 ng/mL and 36.60 ± 2.9 ng/mL) and controls (38.08 ± 2.1 ng/mL and 28.92 ± 2.5 ng/mL; p < 0.001). In group 2, there was a nearly linear relationship between leptin and caspase-9 (r=0.999; p<0.001) and a moderate correlation of troponin I with body
mass index (r = 0.632; p < 0.001) and with leptin (r = 0.316; p < 0.05). With increasing body mass index in patients with ST-elevation myocardial infarction, there is an increased correlation between leptin, caspase-9, and troponin I, which promotes the activation of the adipokine-apoptosis-necrosis sequential cascade. Leptin-dependent activation of apoptosis may be one of the key mechanisms of metabolically mediated myocardial damage. The obtained results support the use of leptin and caspase-9 as additional risk stratification markers in acute coronary syndrome
Received: 12.08.2025 | Revised: 21.11.2025 | Accepted: 30.12.2025
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