Functional activity of platelets and platelet-leukocyte interaction in rheumatoid arthritis: association with subclinical cardiac involvement

Platelet activation plays a crucial role in the pathogenesis of rheumatoid arthritis (RA) and its associated cardiovascular complications. Assessing platelet functional activity and platelet-leukocyte complexes (PLCs) may help elucidate mechanisms of subclinical myocardial involvement in RA. The purpose was to evaluate platelet activation and PLCs in RA patients and investigate their relationship with disease activity and cardiac dysfunction compared to patients with ischemic heart disease (IHD) and healthy controls. A total of 124 subjects were examined: 57 with RA, 55 with IHD, and 12 healthy subjects. Flow cytometry was used to assess CD41+/CD62p+ platelets, CD14+/CD41+ (platelet — monocyte), and CD45+/CD41+ (platelet — neutrophil) aggregates. Echocardiography, speckle-tracking echocardiography (STE), Modified DAS28 (Disease Activity Score), C-reactive protein (CRP), Rheumatoid factor (RF), Anti-citrullinated protein antibodies (ACPA), and N-terminal pro-brain natriuretic peptide (NT-proBNP) were evaluated. RA patients exhibited significantly reduced CD41+/CD62p+ levels (0.3 % vs. 1.0 % in IHD; p = 0.002) and lower CD45+/CD41+ aggregates (p < 0.01), suggesting impaired platelet activation and interaction with neutrophils. CD14+/CD41+ levels remained stable. CD41+/CD62p+ levels positively correlated with DAS28, CRP, RF, NT-proBNP (r = 0.32–0.48), and inversely with GLS (r = –0.45). Similar correlations were found for CD14+/CD41+ and CD45+/CD41+, indicating their role in diastolic dysfunction and myocardial strain abnormalities. Regression analysis revealed that CD41+/CD62p+ was an independent predictor of elevated NT-proBNP (β = 0.43; p = 0.01), and CD14+/CD41+ was linked to reduced GLS (β = 0.36; p = 0.02). These associations were absent in IHD. A distinct myocardial impairment pattern was identified in RA, predominantly affecting basal segments. Impaired platelet activation and altered PLCs are characteristic of RA and associated with subclinical myocardial dysfunction. These parameters may serve as early prognostic markers of cardiovascular risk in RA and support the development of personalized monitoring strategies.