COMPARATIVE EVALUATION OF LP-PLA2 AND MANNOSE BINDING LECTIN AS INFLAMMATORY AND COMPLEMENT RELATED BIOMARKERS IN EARLY MYOCARDIAL INFARCTION: A CASE-CONTROL STUDY

Abstract

Background: Early myocardial infarction involves plaque disruption, lipid-mediated inflammation, sterile inflammatory signaling and myocardial injury. Lp-PLA2 is associated with oxidized lipoproteins and plaque inflammation, whereas mannose-binding lectin (MBL) contributes to lectin complement pathway activation. Their circulating concentrations may not fully represent local pathway activity, but they can provide useful information about early inflammatory and complement-related responses. Objective: To compare serum Lp-PLA2 and MBL concentrations in early MI and evaluate their diagnostic performance for differentiating MI from healthy controls and STEMI from NSTEMI. Methods: This case-control study included 132 participants: 90 patients with MI (58 STEMI and 32 NSTEMI) and 42 healthy controls. Serum Lp-PLA2 concentration and MBL concentration were measured by ELISA. Group differences were analyzed using non-parametric statistics, and diagnostic discrimination was assessed by ROC analysis. Results: Lp-PLA2 concentration was significantly lower in both MI subgroups compared with controls (Kruskal-Wallis H = 15.65, p < 0.001). Median Lp-PLA2 was 10.59 ng/mL in controls, 10.06 ng/mL in NSTEMI and 9.95 ng/mL in STEMI. MBL showed no significant difference across groups (H = 1.99, p = 0.369), with medians of 69.34, 68.79 and 70.03 ug/L in controls, NSTEMI and STEMI, respectively. For total MI versus controls, Lp-PLA2 showed moderate discrimination (AUC = 0.714; 95% CI 0.611-0.809; cutoff <=10.56 ng/mL; sensitivity 80.0%; specificity 54.8%), whereas MBL was non discriminatory (AUC = 0.516; 95% CI 0.397-0.633). Conclusion: Serum Lp-PLA2 concentration was reduced in early MI and showed moderate diagnostic performance, while serum MBL concentration was not diagnostically useful in this cohort. The findings emphasize the need to distinguish circulating biomarker concentration from local inflammatory or complement pathway activity.