COVID-19患者心率变异性降低。

Intensive care research Pub Date : 2023-01-01 Epub Date: 2022-12-01 DOI:10.1007/s44231-022-00024-1
Chengfen Yin, Jianguo Li, Zhiyong Wang, Yongle Zhi, Lei Xu
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摘要

目的:2019冠状病毒病(新冠肺炎)是由严重急性呼吸综合征冠状病毒2(SARS-CoV-2)引起的,该病毒主要感染下呼吸道,并与肺泡上皮细胞上的血管紧张素转化酶2(ACE2)结合。ACE2不仅在肺部广泛表达,而且在心血管系统中也广泛表达。因此,严重急性呼吸系统综合征冠状病毒2型也会损伤心肌。本报告旨在强调SARS-CoV-2引起的心率变异性(HRV)降低和心脏损伤。材料和方法:我们评估了三名新冠肺炎死亡患者。患者的数据是从电子医疗记录中收集的。我们收集了患者的信息,包括基线信息、实验室结果、体温、心率、临床结果和其他相关数据。我们计算了HRV以及随着体温升高预期和实际心率变化之间的差异。结果:截至2020年3月14日,天津市136例新冠肺炎患者中有3例(2.2%)在新冠肺炎疫情早期死亡。病例1、病例2和病例3的直接死亡原因分别为心源性休克、心脏骤停和心脏骤停。HRV在所有三个病例的整个过程中都显著降低。随着温度的升高,心率的实际增加分别为5次/分、13次/分和4次/分,低于预期。肌钙蛋白I和肌酸激酶MB同工酶(CK-MB)仅在病例3中显著增加,直到第7天才能诊断为病毒相关的心脏损伤。在所有三种情况下,HRV和HR变化的降低发生得早于心脏生物标志物(如肌钙蛋白I和CK-MB)的增加。结论:总之,新冠肺炎可能会影响HRV并抵消因体温升高而引起的心动过速。HRV和HR变化的降低早于心肌标志物(肌钙蛋白I和CK-MB)的增加。它表明,在新冠肺炎中,HRV和HR变化的降低可能有助于比心肌标志物更早地预测心脏损伤,因此其早期识别有助于改善患者预后。补充信息:在线版本包含补充材料,可访问10.1007/s44231-022-00024-1。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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Decreased Heart Rate Variability in COVID-19.

Purpose: Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which primarily infects the lower airways and binds to angiotensin-converting enzyme 2 (ACE2) on alveolar epithelial cells. ACE2 is widely expressed not only in the lungs but also in the cardiovascular system. Therefore, SARS-CoV-2 can also damage the myocardium. This report aimed to highlight decreased heart rate variability (HRV) and cardiac injury caused by SARS-CoV-2.

Materials and methods: We evaluated three COVID-19 patients who died. Patients' data were collected from electronic medical records. We collected patient's information, including baseline information, lab results, body temperature, heart rate (HR), clinical outcome and other related data. We calculated the HRV and the difference between the expected and actual heart rate changes as the body temperature increased.

Results: As of March 14, 2020, 3 (2.2%) of 136 patients with COVID-19 in Tianjin died in the early stage of the COVID-19 epidemic. The immediate cause of death for Case 1, Case 2, and Case 3 was cardiogenic shock, cardiac arrest and cardiac arrest, respectively. The HRV were substantially decreased in the whole course of all three cases. The actual increases in heart rate were 5 beats/min, 13 beats/min, and 4 beats/min, respectively, less than expected as their temperature increased. Troponin I and Creatine Kinase MB isoenzyme (CK-MB) were substantially increased only in Case 3, for whom the diagnosis of virus-related cardiac injury could not be made until day 7. In all three cases, decreased in HRV and HR changes occurred earlier than increases in cardiac biomarkers (e.g., troponin I and CK-MB).

Conclusions: In conclusion, COVID-19 could affect HRV and counteract tachycardia in response to increases in body temperature. The decreases of HRV and HR changes happened earlier than the increases of myocardial markers (troponin I and CK-MB). It suggested the decreases of HRV and HR changes might help predict cardiac injury earlier than myocardial markers in COVID-19, thus its early identification might help improve patient prognosis.

Supplementary information: The online version contains supplementary material available at 10.1007/s44231-022-00024-1.

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