冠状病毒病-2019 年住院患者心房颤动的发生率和影响

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Haiming Niu, Jianwei Li, Catherine Teng, Xiaojia Lu, Chengyue Jin, Peng Cai, Ao Shi, Xiaoqing Shen, Qiqi Chen, Miaolian Chen, Yong Yuan, Pengyang Li
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引用次数: 0

摘要

感谢您就我们关于 COVID-19 患者心房颤动 (AF) 的临床影响的研究提出的富有见地的询问。我们的观察结果表明,COVID-19 和心房颤动患者的死亡率增加,主要心血管和脑部并发症的发生率较高。这种模式表明,房颤可能反映了 COVID-19 的严重程度。然而,正如我们在局限性中所指出的,全国住院病人样本(NIS)缺乏特定的实验室数据,如血沉和 CRP 水平,这限制了我们直接比较心房颤动患者和非心房颤动患者炎症状态的能力。虽然我们的研究强调了心房颤动与 COVID-19 住院患者较差的住院预后有关,但并不能确定因果关系。我们同意您的观点,即心房颤动的存在可能意味着 COVID-19 的炎症状态更加严重。将主要因 COVID-19 合并心房颤动住院的患者与以心房颤动为主要病症的患者进行比较,为了解心房颤动与 COVID-19 之间的相互作用提供了令人感兴趣的可能性。然而,我们的研究设计和数据来源给这种比较带来了巨大挑战。NIS 数据库根据主要诊断和次要诊断对病情进行分类,而不区分新发房颤和原有房颤。这一局限性使得区分因心房颤动本身的严重程度而住院的患者和因心房颤动合并 COVID-19 而住院的患者变得更加复杂。该组可能包括以心房颤动为主要诊断住院的患者,这通常表示需要立即干预的急性发作,也可能包括以心房颤动为次要诊断因各种其他原因住院的患者。这些群体的临床情况和患者特征明显不同,因此与我们的 COVID-19 和房颤队列进行直接比较具有挑战性。前者心房颤动的急性表现与 COVID-19 患者更广泛的心房颤动严重程度形成鲜明对比,而后者不同的住院原因也带来了混杂变量,阻碍了直接比较。考虑到这些因素,我们的分析侧重于在现有数据的限制下阐明心房颤动与 COVID-19 结果之间的关联。在我们的研究中,我们使用 ICD-10 室颤(VF)和扑动(I490)以及室性心动过速(VT)(I472)的代码来识别这些患者,但不包括室性早搏(见附表)。COVID-19 、房颤和心脏骤停之间的关系涉及多方面的机制。其中包括 COVID-19 患者的房颤有可能恶化为危及生命的室性心律失常,如 VF 和 VT [1,2]。导致这些严重后果的因素可能包括急性心肌损伤、电解质失衡以及与 COVID-19 相关的全身炎症反应,这可能会加重潜在的心血管疾病[3, 4]。我们的分析受限于 NIS 中可用数据的范围,因此强调需要进一步研究详细的临床数据,以全面探讨这些途径。我们希望本回复能让您更清楚地了解我们的研究结果以及分析房颤与 COVID-19 之间相互作用的复杂性。我们感谢您的询问所引发的对话,并期待着就这一重要话题展开进一步讨论。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Incidence and Impact of Atrial Fibrillation on Hospitalized Coronavirus Disease-2019 Patients

Thank you for your insightful inquiries regarding our study on the clinical implications of atrial fibrillation (AF) in patients with COVID-19. We appreciate the opportunity to further discuss and clarify our findings and methodologies.

Our observations reveal that the cohort with COVID-19 and AF demonstrated increased mortality and a higher incidence of major cardiovascular and cerebral complications. This pattern suggests that AF might reflect the severity of COVID-19. However, as noted in our limitations, the National Inpatient Sample (NIS) lacks specific laboratory data, such as ESR and CRP levels, which restricts our capacity to compare the inflammatory status between patients with and without AF directly. While our study underscores the association of AF with poorer in-hospital outcomes in hospitalized COVID-19 patients, it does not establish causality. We concur with your perspective that the presence of AF could signify a more severe inflammatory status of COVID-19.

The comparison between patients hospitalized primarily for COVID-19 with AF and those with AF as the primary condition presents intriguing possibilities for understanding the interplay between AF and COVID-19. However, our study design and data source posed significant challenges for such a comparison. The NIS database categorizes conditions based on primary and secondary diagnoses without distinguishing between new onset and pre-existing AF. This limitation complicates the differentiation between patients hospitalized due to the severity of AF itself and those for whom AF is a comorbid condition alongside COVID-19.

Moreover, conceptualizing a comparison group of “AF alone” encounters methodological hurdles. The group could potentially consist of patients hospitalized with AF as the primary diagnosis, which often indicates acute episodes requiring immediate intervention, or patients with AF as a secondary diagnosis hospitalized for various other reasons. The clinical scenarios and patient profiles in these groups are markedly diverse, making direct comparisons with our COVID-19 and AF cohort challenging. The acute presentation of AF in the former contrasts with the broader spectrum of AF severity in COVID-19 patients, while the latter's diverse hospitalization reasons introduce confounding variables that hinder a clean comparison.

Given these considerations, our analysis focused on elucidating the association between AF and COVID-19 outcomes within the limitations of available data. While we acknowledge the potential value that such a comparison might offer, technical and methodological constraints led us to focus our study scope on patients hospitalized with COVID-19, with and without AF as a comorbid condition.

In our study, we identified them using ICD-10 codes for ventricular fibrillation (VF) and flutter (I490) and ventricular tachycardia (VT) (I472), excluding premature ventricular contractions (see Supplement table). The relationship between COVID-19, AF, and cardiac arrest involves multifaceted mechanisms. These include the potential for AF in COVID-19 patients to degenerate into life-threatening ventricular arrhythmias such as VF and VT [1, 2]. Factors contributing to these severe outcomes may include acute myocardial injury, electrolyte imbalances, and the systemic inflammatory response associated with COVID-19, which could exacerbate underlying cardiovascular conditions [3, 4]. Our analysis, constrained by the scope of data available in the NIS, highlights the need for further studies with detailed clinical data to explore these pathways comprehensively.

We hope that this response offers a clearer understanding of our study's findings and the complexities involved in analyzing the interplay between AF and COVID-19. We appreciate the dialogue that your inquiries have sparked and look forward to further discussions on this vital topic.

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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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