Antiplatelet Therapy for Acute Respiratory Distress Syndrome.

Chuan-Mu Chen,Wei Chen,Hsiao-Ching Lu,Yu-Tang Tung

doi:10.3390/biomedicines8070230

Abstract

Acute respiratory distress syndrome (ARDS) is a common and devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. No known pharmacologic therapy is beneficial in the treatment of ARDS, and the only effective management is through a protective lung strategy. Platelets play a crucial role in the pathogenesis of ARDS, and antiplatelet therapy may be a potential medication for ARDS. In this review, we introduce the overall pathogenesis of ARDS, and then focus on platelet-related mechanisms underlying the development of ARDS, including platelet adhesion to the injured vessel wall, platelet-leukocyte-endothelium interactions, platelet-related lipid mediators, and neutrophil extracellular traps. We further summarize antiplatelet therapy, including aspirin, glycoprotein IIb/IIIa receptor antagonists, and P2Y12 inhibitors for ARDS in experimental and clinical studies and a meta-analysis. Novel aspirin-derived agents, aspirin-triggered lipoxin, and aspirin-triggered resolvin D1 are also described here. In this narrative review, we summarize the current knowledge of the role of platelets in the pathogenesis of ARDS, and the potential benefits of antiplatelet therapy for the prevention and treatment of ARDS.

Highlights

Our study showed that pretreatment with aspirin reduced nuclear factor-κB (NF-κB) activation, active oxygen species expression, the number of macrophages, neutrophil infiltration, and lung edema compared with hyperoxia-only treatment in NF-κB-luciferase transgenic mice [95]
Platelets play a crucial role in the pathogenesis of Acute respiratory distress syndrome (ARDS) in a number of experimental studies, and antiplatelet therapy exerts a potential therapeutic benefit for ARDS
The main effects of antiplatelet therapy to reduce the severity of ARDS are possibly based on four directions: (1) reducing platelet adhesion to the injured vessel wall; (2) inhibiting platelet-leukocyte-endothelium interactions; (3) modulating lipid mediator related platelet aggregation, and (4) inhibiting Neutrophil Extracellular Traps (NETs) formation

Summary

Introduction

Acute respiratory distress syndrome (ARDS), or acute lung injury, is a devastating syndrome that contributes to serious morbidities and mortality in critically ill patients. The definition of this syndrome includes the acute onset of respiratory failure, bilateral infiltrates observed on chest radiographs, hypoxemia with a PaO2 /FiO2 ratio ≤ 300 mmHg with at least positive end-expiratory pressure of. Biomedicines 2020, 8, 230 mortality rate is high (approaching 40%) [4]. The only effective management to date to improve the survival rate of this syndrome is a protective lung strategy, with lower tidal volume ventilation [6]

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Results

Conclusion