Evaluation of the relationship between thrombus burden, inflammation indices, and prognosis in central and peripheral...

Early risk stratification is critical to clinical management of acute pulmonary embolism (APE). We aimed to evaluate the relationships among thrombus localization, thrombus burden, and inflammatory indices in patients with APE, and to assess the prognostic value of these parameters.

This retrospective, single-center study included adult patients with computed tomography pulmonary angiography (CTPA)-confirmed APE. Patients with active infection, hematologic or active solid organ malignancy, or immunosuppressive therapy were excluded. The cohort comprised 821 patients. Thrombus localization was assessed by CTPA and classified as central or peripheral. Thrombus burden was quantified using the Qanadli score. The Systemic Immune-Inflammation Index (SII), Systemic Inflammatory Response Index (SIRI), and Aggregate Index of Systemic Inflammation (AISI) were calculated from hematologic parameters at admission. Clinical, laboratory, and echocardiographic data were analyzed to assess 28-day mortality.

In patients with central thrombus location, the Qanadli score, right heart overload findings, pulmonary artery pressure, troponin, and B-type natriuretic peptide (pro-BNP) levels were significantly higher (p < 0.05). However, no significant relationship was found between thrombus localization and 28-day mortality, and the Qanadli score was also not associated with mortality (p > 0.05). SII, SIRI, and AISI values were significantly higher among patients who died (p < 0.05). In multivariate analyses, age, pro-BNP, C-reactive protein (CRP), red cell distribution width (RDW), and SII were identified as independent predictors of mortality (p < 0.05). In the receiver operating characteristics (ROC) analysis, SII showed the highest discriminatory power for predicting mortality (AUC = 0.748; p < 0.001).

In APE, although thrombus burden and localization may correlate with clinical severity, mortality appears to be primarily driven by systemic inflammation. SII can serve as a practical, complementary biomarker for early risk stratification.