Objective To analyze the relationships of serum systemic immune-inflammation index (SII) and triglyceride-glucose index (TyG) levels with the occurrence of major adverse cardiovascular events (MACE) in patients with acute coronary syndrome (ACS) undergoing emergency percutaneous coronary intervention (PCI). Methods A total of 918 ACS patients who underwent emergency PCI at The First Affiliated Hospital of Xinjiang Medical University between June 2013 and June 2023 were selected. Clinical information and admission laboratory data were collected. SII was calculated based on routine blood tests, and TyG was calculated based on biochemical tests. Patients were followed up and divided into a MACE group and a non-MACE group based on the occurrence of MACE. Univariable and multivariable logistic regression analyses were performed to identify factors associated with MACE after emergency PCI in ACS patients. Receiver operating characteristic curves were constructed to evaluate the predictive value of serum SII and TyG levels for postoperative MACE in this population． Results The incidence of MACE at 1 year after emergency PCI in the 918 ACS patients was 22.77% (209/918). SII and TyG levels in the non-MACE group were lower than those in the MACE group [SII: 851.23 (576.39, 1305.27) vs 1409.42 (911.48, 1955.90); TyG: 8.82 (8.44, 9.23) vs 9.37 (8.85, 9.83)], with statistically significant differences (P<0.05). Advanced age and elevated SII and TyG levels were identified as independent risk factors for MACE after emergency PCI in ACS patients (P<0.05). The areas under the receiver operating characteristic curves for predicting MACE using serum SII and TyG alone were 0.691 and 0.699, respectively. The area under the curve for the prediction of MACE using both SII and TyG was 0.737, which was higher than that of either index alone. Conclusion Elevated serum SII and TyG levels are associated with an increased risk of MACE after emergency PCI in ACS patients. Combined detection of these two indices demonstrates superior predictive value for postoperative MACE．

Objective To investigate the impact of the sonic hedgehog (SHH) signaling pathway on angiogenesis in a rabbit model of acute myocardial infarction (AMI) by administering exogenous SHH agonists or inhibitors to activate or inhibit the pathway. Methods A rabbit AMI model was established by ligating the left anterior descending coronary artery in New Zealand white rabbits using silk thread. Rabbits were randomly divided into a control group (sham operation), a model group (AMI induced by ligation of the left anterior descending coronary artery), an agonist group (ligation of the left anterior descending coronary artery and SHH pathway activation using purmorphamine), and an inhibitor group (ligation of the left anterior descending coronary artery and SHH pathway inhibition using cyclopamine). Animals were euthanized 24 h postoperatively, and venous blood and myocardial tissue samples were collected. Serum levels of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) were measured using enzyme-linked immunosorbent assay at 24 h postoperatively. Immunohistochemistry was employed to detect VEGF and bFGF protein expression in myocardial tissues across groups. Real-time fluorescence quantitative PCR was used to assess the mRNA expression levels of SHH, smoothened (SMO), and glioma-associated oncogene homolog 1 (Gli-1) associated with the SHH signaling pathway within myocardial tissues. Results Compared with the control group, serum VEGF and bFGF levels in the AMI model group, as measured by enzyme-linked immunosorbent assay, were significantly elevated (228.03±9.62 pg/mL vs 306.59±12.42 pg/mL; 78.25±8.35 pg/mL vs 141.80±5.58 pg/mL; P<0.05). Relative to the model group, the agonist group exhibited increased VEGF and bFGF levels (306.59±12.42 pg/mL vs 374.68±17.52 pg/mL; 141.80±5.58 pg/mL vs 167.00±9.57 pg/mL; P<0.05), while the inhibitor group showed decreased levels (306.59±12.42 pg/mL vs 266.12±13.69 pg/mL; 141.80±5.58 pg/mL vs 106.53±7.23 pg/mL; P<0.05). Compared with the control group, VEGF and bFGF protein expression levels in infarcted myocardial tissue from the model group were significantly higher (0.0951±0.0080 vs 0.1732±0.0068; 0.0636±0.0047 vs 0.1921±0.0063; P<0.05). Relative to the model group, the agonist group showed elevated VEGF and bFGF expression (0.1732±0.0068 vs 0.1963±0.0127; 0.1921±0.0063 vs 0.2320±0.0120; P<0.05), whereas the inhibitor group showed reduced expression (0.1732±0.0068 vs 0.1472±0.0416; 0.1921±0.0063 vs 0.1645±0.0048; P<0.05). Compared with the control group, mRNA expression levels of SHH, SMO, and Gli-1 in the model group were significantly increased (1±0.058 vs 1.376±0.171; 1±0.067 vs 1.202±0.877; 1±0.105 vs 1.028±0.083; P<0.05). Relative to the model group, the agonist group exhibited significantly higher expression of SHH, SMO, and Gli-1 (1.376±0.171 vs 2.165±0.267; 1.202±0.877 vs 1.990±0.152; 1.028±0.083 vs 1.619±0.174; P<0.05), while the inhibitor group showed significantly lower expression of SHH, SMO, and Gli-1 (1.376±0.171 vs 0.911±0.15; 1.202±0.877 vs 0.536±0.389; 1.028±0.083 vs 0.583±0.053; P<0.05). Conclusion Activation of the SHH signaling pathway increases the expression of angiogenic factors, thereby promoting angiogenesis following myocardial infarction. These findings suggest that the activation of SHH signaling pathway is associated with vascular regeneration in AMI.