The Association of Elevated Factor VIII and von Willebrand Factor (vWF) Levels with SYNTAX Score in Patients with Chronic Coronary Syndrome.

Factor VIII (FVIII) and the von Willebrand factor (vWF) are key components of hemostatic balance. Disruption of the vWF-ADAMTS13 axis, characterized by elevated vWF and reduced ADAMTS13 activity has been implicated in thrombotic disorders, including COVID-19-asscoiated coagulopathy, where this imbalance correlates with disease severity and mortality. This study evaluated the relationship between plasma FVIII and vWF levels and the severity of coronary artery disease (CAD), as assessed by the SYNTAX score. We enrolled 82 patients with chronic coronary syndrome (CCS) and a positive treadmill test who underwent elective coronary angiography. Based on the SYNTAX score, patients were divided into three groups: Group I (≤22), Group II (23-32), and Group III (≥33). FVIII levels varied significantly (Group I: 2.25 ± 0.75; Group III: 2.97 ± 0.95; = 0.007), with an OR of 3.632 (95% CI: 1.116-11.826; = 0.03). vWF levels differed significantly across SYNTAX groups (Group I: 1.16 ± 0.59; Group II: 1.52 ± 0.62; Group III: 1.49 ± 0.80; = 0.040). vWF > 1.75 was more frequent in Groups II and III, with an odds ratio (OR) of 4.909 (95% CI: 1.429-16.864; = 0.01) for Group III vs. Group I. Fibrinogen and C-reactive protein (CRP) were elevated in patients with SYNTAX scores ≥33. In multinomial logistic regression analysis, FVIII emerged as the sole independent predictor of CAD complexity ( = 0.004), while the vWF showed significance in pairwise comparison (Group II vs. Group I; OR = 3.433, = 0.049). This study demonstrated significant differences in hemostatic and inflammatory biomarkers across SYNTAX score categories reflecting CAD severity in CCS patients. FVIII emerged as an independent predictor of CAD complexity, while the vWF demonstrated significant associations in specific subgroup comparisons. The observed vWF-ADAMTS13 axis dysregulation supports the rationale for investigating vWF-targeted therapeutics, including agents such as caplacizumab, in cardiovascular disease management. These findings require validation in larger studies.