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Presentation Details
Relevance of Annexin V with Coagulation Factors X and V in Pulmonary Embolism Patients

Aryan Mathur, Mira Nigudkar, Martin Lundy, Fakiha Siddiqui, Debra Hoppensteadt, Amir Darki, Jeanine Walenga, Jawed Fareed.

Loyola University Stritch School of Medicine, Maywood, IL, USA

Abstract


Background: Pulmonary embolism (PE) is a life-threatening condition resulting from the thrombotic occlusion of pulmonary arteries, where early diagnosis and risk stratification are critical. However, current clinical biomarkers lack specificity and have limited utility in assessing disease severity. Annexin V is a calcium-dependent phospholipid-binding protein indicative of endothelial cell apoptosis, and coagulation Factors X and V are biologically linked to thrombosis and coagulation. Despite their well-characterized individual functions, the interplay between Annexin V and these coagulation factors in PE remains unclear.  Objective: To quantify and compare plasma levels of Annexin V, Factor X, and Factor V in patients with acute PE versus healthy controls, and to evaluate correlations between these biomarkers. Methods: Plasma samples were collected from patients with confirmed acute PE (n = 65) under a pre-approved IRB protocol at Loyola University Medical Center, with healthy adults as controls (n = 15). Biomarkers were measured by enzyme-linked immunosorbent assays (ELISAs). Results were reported as medians and interquartile ranges (IQR) and compared using nonparametric tests via Prism GraphPad software. Pearson correlation analysis assessed associations among the biomarkers. Levels were also examined across PE risk stratification categories (high, intermediate, low risk per AHA guidelines) and by BMI category (≥ 30 vs <30). Results: All three biomarkers were markedly elevated in PE patients compared to controls. Median Annexin V concentration was 18.5 ng/mL in the PE group (IQR 11.7-31.0) versus 0.8 ng/mL (IQR 0.45-1.05) in controls ( p <0.001, Figure 1). Factor X levels were also higher in PE patients (median 71.3% [59.3-89.9] vs 65.3% [46.7-70.2] in controls), and similarly Factor V (68.4% [57.3-81.4] vs 50.7% [45.5-67.0]), with both differences reaching statistical significance (p <0.05; Figure 1). No significant correlations were observed among biomarkers (Pearson r = 0.05-0.19, p > 0.1; Figure 2), suggesting independent variation. Subgroup analyses showed no significant differences across PE risk severity or BMI categories, though Annexin V trended higher in more severe PE and obese individuals. Conclusion: Acute PE patients demonstrated significantly elevated Annexin V, Factor X, and Factor V levels, highlighting a pronounced prothrombotic and endothelial injury profile. Among the markers, Annexin V showed the most dramatic increase, consistent with extensive endothelial cell apoptosis in acute PE. The lack of correlation suggests distinct pathophysiological roles, despite biochemical links between Factors X and V. Further investigation in larger cohorts is warranted to determine their potential utility in patient risk stratification and as targets for therapeutic monitoring as independent yet complementary markers of pulmonary embolisms.   

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