Procoagulant membrane microparticles correlate with the severity of pulmonary arterial hypertension
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Updated: Jul 10, 2026
Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)
Published on: August 4, 2023
Babe Bakouboula1, Olivier Morel, Antoine Faure
1Hôpitaux Universitaires de Strasbourg, Fédération de Cardiologie, Strasbourg, France.
Rationale:
Procoagulant microparticles constitute valuable hallmarks of cell damage. Microparticles also behave as cellular effectors.
Objectives:
We hypothesized that the extent of the vascular cell damage measured by circulating microparticles could be related to the severity of pulmonary arterial hypertension (PAH).
Methods:
Circulating biomarkers of vascular damage and cell activation were measured in blood samples from 20 patients with PAH. Samples were withdrawn from occluded pulmonary artery and jugular vein. Peripheral venous blood samples were obtained in 23 control subjects. The microparticle procoagulant abilities were quantified by functional prothrombinase and tissue factor assays and their cellular origin was determined.
Measurements And Main Results:
Soluble vascular cellular adhesion molecule-1 and proinflammatory markers, such as monocyte chemoattractant protein-1 and highly specific C-reactive protein, were elevated in patients with PAH compared with control subjects. Microparticles bearing active tissue factor and CD105 (endoglin) were also elevated in patients with PAH compared with control subjects (29 +/- 13 vs. 16 +/- 6 fmol/L, P < 0.001, and 1.10 +/- 0.46 vs. 0.49 +/- 0.33 nmol/L phosphatidylserine equivalent, P < 0.001, respectively). A further increase in endothelium-derived CD105 microparticles was observed in pulmonary arterial blood compared with venous blood in patients with PAH (1.73 +/- 0.77, P = 0.038). Microparticles bearing active tissue factor were at a higher level in patients in functional class III and IV and who were walking fewer than 380 m with the six-minute-walk test.
Conclusions:
Circulating markers of endothelium damage, proinflammatory markers, and cell stimulation estimated with circulating microparticles appear to be valuable tools in determining the severity of PAH.
Insights
Circulating microparticles indicate vascular cell damage and inflammation in pulmonary arterial hypertension (PAH). Elevated levels of specific microparticles correlate with PAH severity, suggesting their use as biomarkers.
Area of Science:
- Cardiovascular Research
- Biomarker Discovery
- Pulmonary Hypertension Research
Background:
- Procoagulant microparticles are indicators of cellular damage and function as cellular effectors.
- Assessing microparticle levels may reveal insights into vascular health and disease processes.
Purpose of the Study:
- To investigate the relationship between circulating microparticles, reflecting vascular cell damage, and the severity of pulmonary arterial hypertension (PAH).
- To determine if microparticle levels can serve as biomarkers for PAH severity.
Main Methods:
- Blood samples were collected from 20 PAH patients and 23 controls.
- Functional assays quantified procoagulant abilities and cellular origins of microparticles.
- Biomarkers for vascular damage and cell activation were measured.
Main Results:
- PAH patients showed elevated levels of soluble vascular cellular adhesion molecule-1, monocyte chemoattractant protein-1, and C-reactive protein compared to controls.
- Microparticles with active tissue factor and CD105 (endoglin) were significantly higher in PAH patients.
- Endothelium-derived CD105 microparticles were further increased in pulmonary arterial blood versus venous blood in PAH patients.
- Higher levels of microparticles with active tissue factor were observed in patients with advanced functional class and reduced exercise capacity.
Conclusions:
- Circulating microparticles, alongside endothelium damage and proinflammatory markers, are valuable indicators of PAH severity.
- These microparticle-based markers show potential for clinical application in assessing and managing PAH.
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