PB0087 - Hyperresponsive platelets and a reduced platelet granule release capacity is associated with severity of COVID-19 symptoms and with increased mortality.

Sunday, July 10, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Co-Author(s)

FG

Fadel Muhammad Garishah

PhD student
Radboud University Medical Center
Nijmegen, Gelderland, Netherlands
Dana Huskens, PhD

PhD, Research Project Leader
Synapse research insitute
MAASTRICHT, Limburg, Netherlands
SP

Setyo Gundi Pramudo

Investigator
Diponegoro University
Semarang, Jawa Barat, Indonesia
DA

Dessy Andriani

Investigator
KRMT Wongsonegoro Hospital
semarang, Jawa Barat, Indonesia
mA

mila Astrilia

Investigator
KRMT Wongsonegoro Hospital
samarang, Jawa Barat, Indonesia
RS

Rizki Akbar Sentosa

Investigator
Diponegoro University, Dr. Kariadi Hospital
Semarang, Jawa Barat, Indonesia
Av

Andre van der Ven

Investigator
Radboud University Medical Center
Nijmegen, Gelderland, Netherlands
Bd

Bas de Laat, MD, PhD

General Director
Department of Functional Coagulation, Synapse Research Institute, Maastricht, the Netherlands
Maastricht, Limburg, Netherlands
MG

Muhammad Hussein Gasem

Investigator
Diponegoro University, Dr. Kariadi Hospital
Semarang, Jawa Barat, Indonesia
Qd

Quirijn de Mast

.
Department of Internal Medicine, Radboud Center for Infectious Diseases, Radboud University Medical Centre, Nijmegen, the Netherlands
Nijmegen, Gelderland, Netherlands

Presenting Author(s)

Mark Roest, PhD

Clinical Director
Department of Platelet pathophysiology, Synapse Research Institute, Maastricht, the Netherlands
Maastricht, Limburg, Netherlands

Background: COVID-19 is often associated with mild thrombocytopenia and increased platelet reactivity. The aim of the current study was to investigate if platelets of COVID-19 patients were primed to hyper-reactive platelets and if the circulating platelets become exhausted during COVID-19 disease.

Aims: To investigate if platelets of COVID-19 patients were primed to hyper-reactive platelets and if the circulating platelets become exhausted during COVID-19 disease.

Methods: Time dependent platelet activation is studied in whole blood by monitoring the ATP release kinetics from platelets upon stimulation with PAR1 receptor agonist in 41 critical ill COVID-19 patients, 47 COVID-19 patients who were hospitalized but were not critically ill and 30 healthy controls.

Results: Our study demonstrated that platelets of critical ill COVID-19 patients were hyper-responsive and had a reduced platelet granule release capacity, probably due to exhaustion. The platelet reactivity time of COVID-19 patients admitted to the critical care unit was 2-fold reduced if compared with the response time of healthy controls and 1.6-fold reduced if compared with non-critical COVID-19 patients. Platelet responsiveness was also associated (spearman r; P-value) with D-dimer (0.5; < 001), CRP (0.57; < 001) and neutrophil-lymphocyte ratio (0.54; < 001). Moreover, an increased platelet responsiveness and reduced platelet granule release capacity were associated with an increased mortality (OR; 95% CI: 18.8; 6.1-57.9 and 4.9; 1.5-16.3, respectively). These relationships remained significant after adjustment for age, sex, D-dimer, CRP and neutrophil-lymphocyte ratio.

Conclusion(s): Our findings show that platelet hyper-reactivity and reduced platelet granule release capacity were associated with increased critical illness and increased mortality of COVID-19 patients.