JAMA Cardiol: 新冠肺炎合并心血管病者病死率超10%!天坛医院金泽宁等发文认为原因有六

2020-03-28 循环 中国循环杂志

之前一项对44672例新型冠状病毒肺炎(COVID-19)患者进行的研究表明,合并心血管病病死率高达10.5%,合并高血压病死率高达6.0%,而无合并症病死率为0.9%。

之前一项对44672例新型冠状病毒肺炎(COVID-19)患者进行的研究表明,合并心血管病病死率高达10.5%,合并高血压病死率高达6.0%,而无合并症病死率为0.9%。

为什么心血管病患者会如此“雪上加霜”?

3月25日,首都医科大学附属北京天坛医院心脏及大血管病中心金泽宁等在JAMA Cardiology发文剖析了其中原因。

首先,急性肺部感染可能会影响心力衰竭和冠心病等患者心脏功能的稳定性,而恶化的心脏功能将反过来加剧COVID-19。

其次,研究者认为,对于COVID-19患者合并心血管疾病的关注不够。有关COVID-19临床特征的研究多数并没有对心血管疾病进行明确的分类,例如没有提供患有特定心血管疾病(包括缺血性心脏病、心力衰竭、心律失常等)的患者人数。

而这些心血管疾病可能对COVID-19的预后有不同的影响。

比如呼吸困难和疲劳是心力衰竭的两个主要症状,而这在COVID-19患者中也非常常见,尤其是在重症阶段。这使得COVID-19在慢性心力衰竭患者中的诊断可能更为困难。

另外,COVID-19的全身炎症反应可能引发潜在冠心病患者冠状动脉斑块破裂或糜烂,这使得COVID-19患者很难从心肌梗死中存活下来。

此外,COVID-19引起的低氧血症则可导致老年患者发生心房颤动。心房颤动在肺功能改善之前可能是不可治愈的。心房颤动和全身炎症反应使抗凝治疗方案的选择变得非常棘手。

目前关于COVID-19的心血管并发症的数据很少。新冠肺炎可能引起急性心肌损伤,可能是病毒感染、低氧血症和潜在心脏疾病恶化所致,机制仍不明确。总体上,关于冠状病毒感染引起人类心肌炎的报道非常少见。

最后,值得一提的是,合并比例较高的高血压是心血管疾病之一而不是独立于心血管疾病之外。

新型冠状病毒(SARS-CoV-2)和SARS-CoV具有相同的宿主受体血管紧张素转换酶2(ACE2),而有研究显示,SARS-CoV-2与ACE2的结合亲和力比SARS-CoV高10~20倍,这说明SARS-CoV-2很容易在人与人之间传播。

ACE2可能对心血管疾病有许多保护作用,比如预防高血压、心肌纤维化、心肌肥厚、心律失常、动脉粥样硬化和水钠潴留。因此,ACE2可能在COVID-19患者中扮演两个相反的角色,特别是在心血管疾病患者中。

血管紧张素转换酶抑制剂(ACEI)和血管紧张素Ⅱ受体拮抗剂(ARB)可以上调ACE2的表达或阻止ACE2的丢失,这是ACEI/ARB活性的机制之一。在这一点上,ACEI/ARB治疗可能增加了SARS-CoV-2感染的风险。

然而,实验表明,ARB类药物氯沙坦和重组人ACE2可保护小鼠免受酸吸入或脓毒症引起的严重急性肺损伤。考虑到ACEI/ARB广泛应用于高血压、心力衰竭和缺血性心脏病患者,对COVID-19患者和密切接触者使用ACEI/ARB应给予额外关注。

目前大多数COVID-19患者仍在住院治疗。研究者认为,今后还有几方面工作需要开展:

1. 需要继续观察COVID-19的心血管并发症,进一步评估,以确定预后不良的危险因素。

2. COVID-19作为一种急性传染病,可能由于基因重组而成为一种慢性流行性疾病。应该为COVID-19或其他冠状病毒的再次出现做好准备。

3. 考虑到心血管疾病是最为常见的非传染性疾病,并且许多患者正在使用ACEI/ARB类药物,探索ACEI/ARB对COVID-19易感性和预后的潜在影响也很有必要。

原始出处:Chengzhi Yang, Zening Jin.  An Acute Respiratory Infection Runs Into the Most Common Noncommunicable Epidemic—COVID-19 and Cardiovascular Diseases. JAMA Cardiology. 2020 March 25.

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    2020-03-28 公卫新人

    新冠肺炎,疫情何时才能消失

    0

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    2020-03-28 旺医

    顶刊就是顶刊,谢谢梅斯带来这么高水平的研究报道,我们科里同事经常看梅斯,分享梅斯上的信息

    0

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