Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation.
Thrombocytopathy and endotheliopathy: crucial contributors to COVID-19 thromboinflammation.
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DOI：
10.1038/s41569-020-00469-1
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发表时间：
2021-03
期刊：
影响因子：
--
通讯作者：
Hwa J
中科院分区：
文献类型：
--
作者：
Gu SX;Tyagi T;Jain K;Gu VW;Lee SH;Hwa JM;Kwan JM;Krause DS;Lee AI;Halene S;Martin KA;Chun HJ;Hwa J
冠状病毒病2019(新冠肺炎)的核心病理是严重急性呼吸综合征冠状病毒2(SARS-CoV-2)感染呼吸道细胞，导致过度炎症和呼吸系统疾病，最严重的病例涉及细胞因子风暴和急性呼吸窘迫综合征。血栓并发症是新冠肺炎患者发病率和死亡率的主要原因。既往有心血管疾病和/或传统心血管危险因素(包括肥胖、糖尿病、高血压和高龄)的患者死于新冠肺炎的风险最高。在这篇综述中，我们总结了新的证据，指出血小板和内皮功能障碍都是新冠肺炎病理的重要组成部分，并描述了可能解释心血管危险因素对新冠肺炎最严重预后的影响的机制。我们将强调凝血障碍、血小板增多和血管内皮细胞病变在新冠肺炎发病机制中的不同贡献，并讨论在治疗心血管疾病-19患者方面的潜在治疗策略。利用生物医学和临床界的专业知识，必须将现有的治疗药物扩大到抗凝剂之外，并针对血小板减少症和内皮病变。只有通过这种合作努力，我们才能更好地为进一步的浪潮和未来与冠状病毒有关的大流行做好准备。本文综述了血小板和内皮功能障碍是新冠肺炎发病的重要因素的最新证据，介绍了心血管危险因素导致新冠肺炎最严重预后的潜在机制，并重点介绍了凝血障碍、血小板病变和内皮病变在新冠肺炎发病中的作用。静脉血栓栓塞症、动脉血栓形成和血栓性微血管病是新冠肺炎患者发病率和死亡率增加的重要原因。凝血紊乱、血小板增多和内皮病变之间的复杂相互作用导致新冠肺炎相关的血栓性炎症。凝血障碍、血小板增多和血管内皮细胞病变是糖尿病、肥胖和老龄化等心血管危险因素的特征。心血管危险因素和感染SARS-CoV-2导致血栓形成加剧和死亡率增加。年龄在新冠肺炎的发病机制中起着重要作用；没有凝血障碍、血小板增多和血管内皮细胞病变倾向的年轻患者可能会出现明显的多系统炎症综合征，其中包括非常年轻的患者的川崎病样综合征。在治疗新冠肺炎相关血栓并发症方面，针对炎症、凝血障碍、血小板增多和内皮病变的联合治疗可能比单一药物更成功。
The core pathology of coronavirus disease 2019 (COVID-19) is infection of airway cells by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that results in excessive inflammation and respiratory disease, with cytokine storm and acute respiratory distress syndrome implicated in the most severe cases. Thrombotic complications are a major cause of morbidity and mortality in patients with COVID-19. Patients with pre-existing cardiovascular disease and/or traditional cardiovascular risk factors, including obesity, diabetes mellitus, hypertension and advanced age, are at the highest risk of death from COVID-19. In this Review, we summarize new lines of evidence that point to both platelet and endothelial dysfunction as essential components of COVID-19 pathology and describe the mechanisms that might account for the contribution of cardiovascular risk factors to the most severe outcomes in COVID-19. We highlight the distinct contributions of coagulopathy, thrombocytopathy and endotheliopathy to the pathogenesis of COVID-19 and discuss potential therapeutic strategies in the management of patients with COVD-19. Harnessing the expertise of the biomedical and clinical communities is imperative to expand the available therapeutics beyond anticoagulants and to target both thrombocytopathy and endotheliopathy. Only with such collaborative efforts can we better prepare for further waves and for future coronavirus-related pandemics. This Review summarizes the latest evidence indicating that platelet and endothelial dysfunction are essential components of COVID-19 pathology, describes the potential mechanisms underlying the contribution of cardiovascular risk factors to the most severe outcomes in COVID-19, and highlights the roles of coagulopathy, thrombocytopathy and endotheliopathy in COVID-19 pathogenesis. Venous thromboembolism, arterial thrombosis and thrombotic microangiopathy substantially contribute to increased morbidity and mortality in patients with COVID-19. A complex interaction between coagulopathy, thrombocytopathy and endotheliopathy contributes to COVID-19-associated thromboinflammation. Coagulopathy, thrombocytopathy and endotheliopathy are characteristic features associated with cardiovascular risk factors such as diabetes mellitus, obesity and ageing. The combination of cardiovascular risk factors and infection with SARS-CoV-2 leads to exacerbated thrombosis and increased mortality. Age has an important role in COVID-19 pathogenesis; young patients without a predisposition to coagulopathy, thrombocytopathy and endotheliopathy can have a distinct multisystem inflammatory syndrome that includes a Kawasaki disease-like syndrome in very young individuals. Combination therapies targeting inflammation, coagulopathy, thrombocytopathy and endotheliopathy are likely to be more successful than a single agent in tackling the COVID-19-associated thrombotic complications.
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