Assessment of the Relationship Between C-Reactive Protein-to-Albumin Ratio and Culprit Lesion Location in Patients With ST-Segment Elevation Myocardial Infarction.

Aims/Background The C-reactive protein to albumin ratio (CAR) has traditionally been employed to assess inflammatory status in non-cardiac diseases. Recent clinical studies suggest that CAR is a valuable indicator of inflammation in atherosclerotic coronary artery diseases. However, its relationship with ST-segment elevation myocardial infarction (STEMI) remains unclear. This study aimed to investigate the relationship between CAR and the exact location of the culprit lesion in STEMI patients and its potential clinical implications. Methods A retrospective analysis was conducted on patients who presented with STEMI and were treated with primary percutaneous coronary intervention (PCI) within 12 hours of symptom onset between November 2018 and November 2023. Based on coronary angiography (CAG) findings, patients were categorized into three groups according to the culprit vessel: left anterior descending artery (LAD) (n = 218), left circumflex artery (LCX) (n = 31), and right coronary artery (RCA) (n = 153). Three patients with ramus occlusion were excluded from the subgroup analysis. Furthermore, based on the lesion location within the culprit vessel, patients were divided into proximal (n = 122), middle (n = 222), and distal (n = 61) segment groups. Clinical baseline characteristics and laboratory results were recorded. Statistical analyses, including analysis of variance (ANOVA), the Kruskal-Wallis H-test, Fisher's exact test, and the chi-square test, were performed based on variable types and distribution. Correlation analysis was conducted using Spearman's rank correlation coefficient. The receiver operating characteristic (ROC) curve was applied to determine the optimal cut-off value for CAR. A p-value < 0.05 was considered statistically significant. Results A total of 405 patients were included in the study. CAR and left ventricular ejection fraction (LVEF) showed significant differences across groups stratified by culprit vessels (p = 0.001 for CAR; p < 0.001 for LVEF) and lesion location within the vessels (p < 0.001 for CAR and LVEF). CAR values were higher in more proximally located lesions (r = 0.218, p < 0.001), while LVEF showed an inverse relationship (r = -0.203, p < 0.001). ROC curve analysis showed that CAR could predict proximal- and mid-vessel lesions in STEMI patients, with a cut-off value of 26.16 (area under the curve [AUC]: 0.662, 95% confidence interval [CI]: 0.59-0.74, p < 0.001). Conclusion CAR is an easily calculable and reliable biomarker associated with culprit lesion location in STEMI patients, providing potential clinical utility in risk stratification and disease assessment.