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Dysregulated platelet function in patients with postacute sequelae of COVID-19.
Aggarwal, Anu; Singh, Tamanna K; Pham, Michael; Godwin, Matthew; Chen, Rui; McIntyre, Thomas M; Scalise, Alliefair; Chung, Mina K; Jennings, Courtney; Ali, Mariya; Park, Hiijun; Englund, Kristin; Khorana, Alok A; Svensson, Lars G; Kapadia, Samir; McCrae, Keith R; Cameron, Scott J.
Afiliação
  • Aggarwal A; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Singh TK; Section of Vascular Medicine, Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Pham M; Section of Vascular Medicine, Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Godwin M; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Chen R; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • McIntyre TM; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Scalise A; Section of Vascular Medicine, Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Chung MK; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Jennings C; Section of Vascular Medicine, Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Ali M; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Park H; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Englund K; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Khorana AA; Department of Infectious Disease, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Svensson LG; Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic Lerner Research Institute, Cleveland, OH, USA.
  • Kapadia S; Department of Hematology and Oncology, Taussig Cancer Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • McCrae KR; Department of Cardiac Surgery, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
  • Cameron SJ; Section of Vascular Medicine, Department of Cardiovascular Medicine, Heart Vascular and Thoracic Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
Vasc Med ; 29(2): 125-134, 2024 04.
Article em En | MEDLINE | ID: mdl-38334067
ABSTRACT

BACKGROUND:

Postacute sequelae of COVID-19 (PASC), also referred to as "Long COVID", sometimes follows COVID-19, a disease caused by SARS-CoV-2. Although SARS-CoV-2 is well known to promote a prothrombotic state, less is known about the thrombosis risk in PASC. Our objective was to evaluate platelet function and thrombotic potential in patients following recovery from SARS-CoV-2, but with clear symptoms of patients with PASC.

METHODS:

patients with PASC and matched healthy controls were enrolled in the study on average 15 months after documented SARS-CoV-2 infection. Platelet activation was evaluated by light transmission aggregometry (LTA) and flow cytometry in response to platelet surface receptor agonists. Thrombosis in platelet-deplete plasma was evaluated by Factor Xa activity. A microfluidics system assessed thrombosis in whole blood under shear stress conditions.

RESULTS:

A mild increase in platelet aggregation in patients with PASC through the thromboxane receptor was observed, and platelet activation through the glycoprotein VI (GPVI) receptor was decreased in patients with PASC compared to age- and sex-matched healthy controls. Thrombosis under shear conditions as well as Factor Xa activity were reduced in patients with PASC. Plasma from patients with PASC was an extremely potent activator of washed, healthy platelets - a phenomenon not observed when stimulating healthy platelets after incubation with plasma from healthy individuals.

CONCLUSIONS:

patients with PASC show dysregulated responses in platelets and coagulation in plasma, likely caused by a circulating molecule that promotes thrombosis. A hitherto undescribed protective response appears to exist in patients with PASC to counterbalance ongoing thrombosis that is common to SARS-CoV-2 infection.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Trombose / COVID-19 Idioma: En Ano de publicação: 2024 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Trombose / COVID-19 Idioma: En Ano de publicação: 2024 Tipo de documento: Article