The Science Underlying COVID-19 Implications for the Cardiovascular System
The Science Underlying COVID-19 Implications for the Cardiovascular System
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DOI：
10.1161/circulationaha.120.047549
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发表时间：
2020-07-07
期刊：
影响因子：
37.8
通讯作者：
Li, Hongliang
中科院分区：
文献类型：
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作者：
Liu, Peter P.;Blet, Alice;Li, Hongliang
2019冠状病毒病（COVID-19）大流行以前所未有的规模影响了全球的健康和经济。患者有不同的临床结果，但那些既往存在心血管疾病、高血压和相关疾病的患者会产生不成比例的更差的结果。严重急性呼吸综合征冠状病毒2型的高传染性部分与受体结合域的新突变和s刺突蛋白中furin切割位点的获得有关。在无症状和有症状前个体中持续的病毒脱落增强了其社区传播。病毒利用血管紧张素转换酶2受体内化，并借助跨膜蛋白酶丝氨酸2蛋白酶。受体的组织定位与COVID-19出现症状和器官功能障碍相关。病毒诱导的血管紧张素转换酶2下调可能减弱其功能，降低其抗炎作用，并在易感患者中增强血管紧张素II的作用。淋巴细胞减少发生于早期，具有预后意义，可能与CD4+和一些CD8+ T细胞的减少有关。这导致先天/获得性免疫反应失衡，病毒清除延迟，巨噬细胞和中性粒细胞过度刺激。适当的I型干扰素通路激活对于病毒衰减和平衡免疫反应至关重要。易感患者（如老年人和有心血管风险的患者）的持续免疫激活可导致噬血细胞病样综合征，细胞因子产生不受控制的扩增，导致多器官衰竭和死亡。除了呼吸道和肺部外，心血管系统通常也参与COVID-19的早期发病，这反映在高度敏感的肌钙蛋白和利钠肽的释放上，这些蛋白和利钠肽都具有极好的预后作用，特别是在那些持续升高的肌钙蛋白和利钠肽以及白细胞介素-6等细胞因子的释放上。血管系统的炎症可导致弥漫性微血管病变伴血栓形成。心肌炎症可导致心肌炎、心力衰竭、心律失常、急性冠状动脉综合征、迅速恶化和猝死。基于早期预后指标的积极支持与期望管理可以潜在地改善恢复。心衰、心律失常、急性冠状动脉综合征和血栓形成的适当治疗仍然很重要。将制定针对COVID-19的具体循证治疗战略，并对多种方法的持续全球合作进行评估。为了保护更广泛的人群，将需要抗体检测和有效的疫苗来创造COVID-19的历史。
The coronavirus disease 2019 (COVID-19) pandemic has affected health and economy worldwide on an unprecedented scale. Patients have diverse clinical outcomes, but those with preexisting cardiovascular disease, hypertension, and related conditions incur disproportionately worse outcome. The high infectivity of severe acute respiratory syndrome coronavirus 2 is in part related to new mutations in the receptor binding domain, and acquisition of a furin cleavage site in the S-spike protein. The continued viral shedding in the asymptomatic and presymptomatic individuals enhances its community transmission. The virus uses the angiotensin converting enzyme 2 receptor for internalization, aided by transmembrane protease serine 2 protease. The tissue localization of the receptors correlates with COVID-19 presenting symptoms and organ dysfunction. Virus-induced angiotensin converting enzyme 2 downregulation may attenuate its function, diminish its anti-inflammatory role, and heighten angiotensin II effects in the predisposed patients. Lymphopenia occurs early and is prognostic, potentially associated with reduction of the CD4+ and some CD8+ T cells. This leads to imbalance of the innate/acquired immune response, delayed viral clearance, and hyperstimulated macrophages and neutrophils. Appropriate type I interferon pathway activation is critical for virus attenuation and balanced immune response. Persistent immune activation in predisposed patients, such as elderly adults and those with cardiovascular risk, can lead to hemophagocytosis-like syndrome, with uncontrolled amplification of cytokine production, leading to multiorgan failure and death. In addition to the airways and lungs, the cardiovascular system is often involved in COVID-19 early, reflected in the release of highly sensitive troponin and natriuretic peptides, which are all extremely prognostic, in particular, in those showing continued rise, along with cytokines such as interleukin-6. Inflammation in the vascular system can result in diffuse microangiopathy with thrombosis. Inflammation in the myocardium can result in myocarditis, heart failure, cardiac arrhythmias, acute coronary syndrome, rapid deterioration, and sudden death. Aggressive support based on early prognostic indicators with expectant management can potentially improve recovery. Appropriate treatment for heart failure, arrhythmias, acute coronary syndrome, and thrombosis remain important. Specific evidence-based treatment strategies for COVID-19 will emerge with ongoing global collaboration on multiple approaches being evaluated. To protect the wider population, antibody testing and effective vaccine will be needed to make COVID-19 history.