Abstract Number: PB0054
Meeting: ISTH 2022 Congress
Background: Acute COVID-19 is associated with marked endotheliopathy, VWF-ADAMTS13 axis imbalance and abnormal pulmonary angiogenesis. Persistent endotheliopathy and elevated VWF levels have also been reported in convalescent COVID-19 patients.
Aims: We investigated the hypothesis that altered pulmonary microvascular architecture may persist in COVID-19 convalescence, resulting in ongoing endothelial cell (EC) activation and VWF-ADAMTS13 axis imbalance, possibly contributing to Long COVID pathogenesis.
Methods: 50 patients (median age 50 years, 60% male, median 68 days post acute COVID-19) were reviewed. Six-minute-walk tests (6MWT) were performed (median 6MWT distance 430m) and plasma samples collected. Plasma VWF:Ag and ADAMTS13 levels were measured by ELISA, and angiogenesis markers assessed by membrane-based antibody array.
Results: Plasma VWF:Ag levels were significantly elevated in convalescent COVID-19 patients compared to controls (1.1 versus 0.84 IU/ml; p=0.004), with 30% (15/50) having VWF:Ag levels above the upper limit of normal. In contrast, plasma ADAMTS13 was significantly reduced in convalescent COVID-19 (median 467ng/ml vs 636ng/ml p < 0.001). ADAMTS13 levels were significantly lower in those who required hospitalization for acute COVID-19 compared with those managed as outpatients (median 454ng/ml v 513ng/ml, p=0.04). Overall, the VWF/ADAMTS13 ratio was significantly elevated in convalescent COVID-19 compared with controls (2.1 vs 1.1 p=0.0002) and interestingly was elevated in patients with reduced 6MWT distance (distance ≥430m or < 430m: 1.8 v 2.4, p=0.02). In total, 15 angiogenesis markers were elevated in convalescent COVID-19 compared to controls. An additional 17 angiogenesis markers were unique to convalescent COVID-19 and were not found in control plasma (Table 1).
Conclusion(s): Collectively, these novel findings demonstrate that endotheliopathy is sustained for months following acute COVID-19 in some patients. As a result, plasma VWF levels are significantly increased; ADAMTS13 levels reduced, and there is ongoing dysregulation of angiogenesis. Further studies will be required to define whether these alterations play a role in Long COVID pathogenesis.
To cite this abstract in AMA style:Fogarty H, Ward S, Townsend L, Karampini E, Elliott S, Byrne M, Bergin C, O'Sullivan J, Martin-Loeches I, Nadarajan P, Bannon C, Preston R, Rehill A, Ni Cheallaigh C, O'Donnell J. A role for Von Willebrand Factor-ADAMTS13 axis imbalance and abnormal angiogenesis in Long COVID syndrome [abstract]. https://abstracts.isth.org/abstract/a-role-for-von-willebrand-factor-adamts13-axis-imbalance-and-abnormal-angiogenesis-in-long-covid-syndrome/. Accessed September 24, 2023.
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