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  3. The interaction of fibrinolysis and the complement system in patients with acute pulmonary embolism, treated with ultrasound-assisted catheter-directed thrombolysis.

The interaction of fibrinolysis and the complement system in patients with acute pulmonary embolism, treated with ultrasound-assisted catheter-directed thrombolysis.

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DOI
10.48620/94324
Publisher DOI
10.1186/s12959-026-00830-3
PubMed ID
41612339
Abstract
Ultrasound-assisted catheter-directed thrombolysis (USAT) with recombinant tissue-type plasminogen activator (rt-PA) is widely used as a reperfusion approach for acute pulmonary embolism (PE). The fibrinolytic effector protease plasmin is known to be a potent activator of the complement system. The aim of this study was to better characterize the extent of complement activation during USAT, and its relationship with the fibrinolytic system. In this single-center cohort study of USAT for PE, pulmonary-arterial hemodynamic measurements were performed, and plasma samples obtained from 35 patients before treatment start and at 6 h (during infusion of rt-PA). Hemostatic properties were evaluated with thromboelastometry and assessment of fibrinolytic markers. In addition, levels of the complement components C3a, C4a, C5a, soluble C5b-9 (sC5b-9), Ba, Bb, factor H and factor I at these time points were determined. Several complement components, including the anaphylatoxin C3a, showed a reduction during USAT. We found a positive correlation of the plasmin-antiplasmin complex (plap complex) with factor H, yet a negative correlation with both Ba and Bb, C5a and sC5b-9. The potent plasmin-inhibitor, α2-antiplasmin, displayed a positive correlation with Ba and Bb, factor I and factor H. In addition, the anaphylatoxin C5a negatively, and Ba positively predicted treatment responsiveness to USAT. In conclusion, in the setting of acute PE and reperfusion therapy with USAT, there appears to be a competing effect between plasmin-mediated complement activation and a reduction of the inflammatory trigger by resolution of obstruction and ischemia. Complement activation in PE is downregulated during USAT, an effect exceeding the complement-activating properties of plasmin.
Date Issued
2026-01-29
Publication Type
Article
Subject(s)
600 Technology > 610 Medicine & health
Subjects
Catheter-directed thrombolysis
•
Complement
•
Fibrinolysis
•
Fibrinolytic capacity
•
Fibrinolytic potential
•
Inflammation
•
Pulmonary embolism
Language(s)
en
Author(s)
Draxler, Dominik F.  
Clinic of Cardiology  
Department for BioMedical Research (DBMR)  
Barrett, Christopher D
Brodard, Justine  
Clinic of Haematology and Central Haematological Laboratory  
Maginot, Elizabeth R
Chalkou, Konstantina  
Department of Clinical Research (DCR) - Statistics & Methodology (Heg)  
Ho, Heidi
Keragala, Charithani B
Heg, Dik  
Department of Clinical Research (DCR) - Statistics & Methodology (Heg)  
Kremer Hovinga, Johanna A.  
Clinic of Haematology and Central Haematological Laboratory  
Moore, Ernest E
Medcalf, Robert L
Angelillo-Scherrer, Anne  
Clinic of Haematology and Central Haematological Laboratory  
Stortecky, Stefan  
Clinic of Cardiology  
Additional Credits
Clinic of Cardiology  
Clinic of Haematology and Central Haematological Laboratory  
Department for BioMedical Research (DBMR)  
Department of Clinical Research (DCR) - Statistics & Methodology (Heg)  
Journal
Thrombosis Journal
Publisher
BioMed Central
ISSN
1477-9560
Access(Rights)
open.access
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