Key result
Balloon pulmonary angioplasty in CTEPH is linked to ~18-mmHg lower mPAP and improved hemodynamics.
Why the study?
Balloon pulmonary angioplasty improves hemodynamics and functional status in CTEPH, but whether these improvements are accompanied by measurable shifts in coagulation–fibrinolysis biomarkers during the treatment course remained incompletely defined.
Does balloon pulmonary angioplasty improve hemodynamic parameters and shift coagulation–fibrinolysis biomarkers in patients with chronic thromboembolic pulmonary hypertension?
Observational (n=16)
Does balloon pulmonary angioplasty improve hemodynamic parameters and shift coagulation–fibrinolysis biomarkers in patients with chronic thromboembolic pulmonary hypertension?
Hemodynamic and clinical improvements during balloon pulmonary angioplasty in CTEPH are accompanied by significant shifts in coagulation–fibrinolysis biomarkers (PI, TFPI, and TAFI), suggesting treatment-related biological adaptation beyond hemodynamic relief.
Background Balloon pulmonary angioplasty (BPA) improves hemodynamics and functional status in chronic thromboembolic pulmonary hypertension (CTEPH). Whether these changes are accompanied by measurable shifts in coagulation–fibrinolysis biomarkers during the BPA treatment course remains incompletely defined. Purpose To assess paired changes in hemodynamic/clinical parameters and coagulation–fibrinolysis biomarkers during the BPA course in CTEPH, and to explore whether selected biomarker changes relate to hemodynamic response. Methods Sixteen CTEPH patients with paired data were analyzed between protocol entry and interim reassessment during treatment. Hemodynamics included right atrial pressure (RAP), mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), and cardiac index (CI); clinical assessment included WHO functional class, SaO2, and NT-proBNP. Biomarkers included TFPI, TAFI antigen, α2-antiplasmin (plasmin inhibitor; PI), and other coagulation/fibrinolysis parameters. Baseline represented the first available protocol assessment and not necessarily a true pre-treatment state, as some patients had already undergone BPA sessions before enrollment. The second timepoint was the nearest available clinically stable interim reassessment. Results Significant improvements were observed in mPAP [48 (41–55) to 30 (26–41), adjusted p<0.001], PVR [9.4 (6.6–11) to 4.0 (3.2–6.9), adjusted p=0.004], SaO2 [92% (88–94) to 97% (93–98), adjusted p=0.013], and WHO functional class (adjusted p=0.012). In parallel, α2-antiplasmin (PI)decreased [88 (83–101) to 75 (63–88), adjusted p=0.012], TFPI increased [9.4 (6.1–14) to 25 (22–37), adjusted p=0.004], with a shift toward normal categorical distribution, and TAFI antigen increased markedly [6993 (5305–10391) to 35455 (20423–41088) ng/mL, adjusted p=0.001]. Exploratory analysis showed an inverse correlation between %ΔPI and %ΔmPAP (rs=−0.54, p=0.029). Patients with >4 BPA sessions before study entry showed a greater % increase in TAFI than those with ≤4 sessions (p=0.037). Conclusions In this paired pre–interim CTEPH analysis, improvement in hemodynamic and clinical status during the BPA course was accompanied by significant changes in coagulation–fibrinolysis and endothelial-related biomarkers. The association between PI change and mPAP response suggests that selected biomarker shifts may reflect treatment-related biological adaptation, while TAFI dynamics may vary according to prior BPA exposure. These findings support the concept that response to BPA extends beyond hemodynamic improvement alone.
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Kostelidou et al. (2026) conducted an observational in Chronic thromboembolic pulmonary hypertension (CTEPH) (n=16). Balloon pulmonary angioplasty (BPA) vs. Baseline protocol entry (pre-interim assessment) was evaluated on Paired changes in hemodynamic/clinical parameters (including mPAP and PVR) and coagulation–fibrinolysis biomarkers (including PI, TFPI, and TAFI antigen) (p=<0.001). Balloon pulmonary angioplasty in CTEPH significantly reduced mPAP from 48 to 30 mmHg (p<0.001) and PVR from 9.4 to 4.0 (p=0.004) alongside significant shifts in PI, TFPI, and TAFI.
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