Abstract Number: LPB0036
Meeting: ISTH 2021 Congress
Background: In-stent stenosis following intervention for post-thrombotic syndrome (PTS) occurs in ~30% of cases, despite therapeutic anticoagulation.
Aims: The aim of this study was to investigate whether platelets have a role in this process.
Methods: Case-matched patients undergoing venous stenting were prospectively recruited. Venous in-stent thrombus specimens were excised and immunohistochemical analysis was performed to detect collagen I, collagen III, CD68 and CD41. Blood samples were taken before and after venous stent placement, and platelet activation markers (P-selectin and phosphatidylserine) and reactivity were determined by flow cytometry and plate-based aggregation, respectively. Soluble glycoprotein VI (sGPVI), shed during activation, was measured in plasma. Patients with in-stent stenosis requiring reintervention (>50% diameter reduction) were compared with those who did not during follow-up.
Results: Forty-five patients were recruited (median age: 43yrs, range: 33-55yrs; 65% female). Re-intervention was required in 19/45 (42%; median time: 3wks, range: 1day-3mths). Immunohistochemical analysis of in-stent thrombosis demonstrated a rich network of platelets, both early (collagen III) and late (collagen I) forms of collagen, and inflammatory cell infiltrates. There was no significant difference in platelet activation or reactivity after stenting, but P-selectin exposure pre-stent was significantly higher in patients who developed in-stent stenosis (2.7%±0.4 vs 1.7%±0.2; P<0.05). sGPVI levels before stent insertion were increased in patients who developed in-stent stenosis (18.9±3.6ng/mL vs. 7.4±0.9ng/mL; P<0.01). Platelet reactivity to collagen-related peptide, a GPVI-specific platelet agonist, was reduced in patients who developed in-stent stenosis (logEC50 = -6.5M±0.3 vs -7.2M±0.2; P<0.01; n=33).
Conclusions: Venous stenting does not activate platelets or alter platelet function, but patients who developed in-stent stenosis exhibited greater levels of pre-stent platelet activation, greater loss of platelet surface GPVI in the form of sGPVI and consequent reduction in reactivity to GPVI activation. sGPVI may have potential to risk-stratify patients undergoing deep venous reconstruction and predict who requires closer surveillance.
To cite this abstract in AMA style:Gwozdz AM, Black SA, Morris R, Messiha S, Ikram M, Bye AP, Gibbins JM, Rand ML, Patel AS, Modarai B, Smith A, Saha P. Elevated Platelet-derived sGPVI Is a Biomarker of Venous In-stent Stenosis in Patients with Post-thrombotic Syndrome [abstract]. Res Pract Thromb Haemost. 2021; 5 (Suppl 2). https://abstracts.isth.org/abstract/elevated-platelet-derived-sgpvi-is-a-biomarker-of-venous-in-stent-stenosis-in-patients-with-post-thrombotic-syndrome/. Accessed June 25, 2022.
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