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Letter to the Editor regarding article “Association between electrocardiographic features and mortality in COVID-19 patients”
Annals of Noninvasive Electrocardiology ( IF 1.9 ) Pub Date : 2021-07-17 , DOI: 10.1111/anec.12869
Elham Mahmoudi 1 , Mohammad Keykhaei 2 , Hirad Yarmohammadi 3 , Reza Mollazadeh 4
Affiliation  

With interest, we read the study recently published in Annals of Noninvasive Electrocardiology by Antwi-Amoabeng et al., (2021) describing electrocardiographic predictors of mortality in coronavirus diseases 2019 (COVID-19) patients. The authors also illustrated that the post-infection corrected QT interval was similar to the baseline value.

Corrected QT interval (QTc), as a marker of ventricular repolarization duration, has been used to assess the risk of developing cardiac arrhythmias and sudden cardiac death (SCD) since 1952. It has been a major concern throughout the pandemic due to the concomitant use of COVID-19 medications and reports of SCD in severe cases (Laleh Far et al., 2020; Shirazi et al., 2021). However, the current study has not reported the QTc interval values in different study groups and its correlation with QT-prolonging agents. Besides, in the following sentences, we like to suggest another marker of SCD to be assessed in severe cases of COVID-19 patients.

According to the predisposing role of regional repolarization heterogeneity in developing ventricular reentries, electrocardiographic indicators of repolarization disparity have been proposed to predict the risk of lethal cardiac arrhythmias.

QT interval dispersion (QTd) among 12 leads of standard surface ECG has been suggested to be a predictor of ventricular arrhythmias, as it described the lower risk of pro-arrhythmia seen with amiodarone usage comparing to other anti-arrhythmic agents. However, further studies rejected these findings and its predictive value is now under question.

The interval between peak of T-wave (Tp) to end of T-wave (Te) represents the termination of repolarization in epicardial and M cells, respectively, and it is a marker of transmural repolarization disparity (Figure 1). The main determinant of Tp-Te interval is the action potential duration of M cells, carrying the longest action potential duration and being highly susceptible to delayed afterdepolarizations induced by drugs and intrinsic/extrinsic mediators. Therefore, the changes in Tp-Te interval would assess cardiac electrical instability due to systemic inflammations and variable treatment protocols.

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FIGURE 1
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A schematic description of T-peak to T-end and QT dispersion: Indicators of transmural and regional disparity of repolarization, respectively. (a) The interval from the peak of T wave to the end of T wave represents the transmural temporal differences in repolarization termination between epicardial and M cells (b) The solid and the dashed lines simulate the repolarization duration of M cells recorded from two different regions of myocardium. Differences between the endings of the repolarization curves, concomitant with the end of T waves, represent on surface ECG as variable QT intervals

Tp-Te interval has been reported to be prolonged in a group of 120 COVID-19 patients, and Tp-Te duration was correlated with the severity of the infection, though QTc was similar to healthy controls (Koc et al., 2020). Also, in another study by Shaghee et al. (2021), COVID-19 pneumonia outcome was significantly correlated with both the QTc and Tp-Te interval, though the latter marker had more prominent changes as the Tp-Te to QTc ratio was also significantly increased in more severe cases.

Taken together, we suggest that Tp-Te interval should be examined as an available robust method to predict the risk of cardiac arrhythmia in COVID-19 patients, considering the existed limitations of performing cardiovascular imaging and bedside history taking in severe cases of COVID-19.

Eventually, we should mention that the indexed article by Amoabeng et al. contains a figure to represent the prevalence of electrocardiographic features in COVID-19 patients before and during the infection. Since the pre-infection ECGs are available for only half of the patients, comparing the raw values of two groups is not reasonable and it would be more sensible to report the prevalence of ECG features per total records in each group.



中文翻译:

关于“COVID-19 患者心电图特征与死亡率之间的关联”一文的给编辑的信

我们饶有兴趣地阅读了 Antwi-Amoabeng 等人最近在《无创心电学年鉴》上发表的研究(2021 年),该研究描述了 2019 年冠状病毒病(COVID-19)患者死亡率的心电图预测指标。作者还说明感染后校正的 QT 间期与基线值相似。

校正 QT 间期 (QTc) 作为心室复极持续时间的标志物,自 1952 年以来一直用于评估发生心律失常和心源性猝死 (SCD) 的风险。 COVID-19 药物和重症 SCD 报告(Laleh Far 等人,2020 年;Shirazi 等人,2021 年)。然而,目前的研究尚未报告不同研究组的 QTc 间期值及其与 QT 延长剂的相关性。此外,在以下句子中,我们建议在 COVID-19 患者的重症病例中评估另一种 SCD 标志物。

根据区域复极异质性在心室折返发生中的诱发作用,已提出复极差异的心电图指标来预测致死性心律失常的风险。

标准体表 ECG 的 12 个导联之间的 QT 间期离散度 (QTd) 被认为是室性心律失常的预测因子,因为它描述了与其他抗心律失常药物相比,使用胺碘酮所见的促心律失常风险较低。然而,进一步的研究拒绝了这些发现,其预测价值现在受到质疑。

T 波 (Tp) 峰值到 T 波结束 (Te) 之间的间隔分别代表心外膜和 M 细胞复极的终止,它是透壁复极差异的标志(图 1)。Tp-Te 间隔的主要决定因素是 M 细胞的动作电位持续时间,具有最长的动作电位持续时间,并且对药物和内在/外在介质引起的延迟后去极化高度敏感。因此,Tp-Te 间隔的变化将评估由于全身炎症和可变治疗方案引起的心脏电不稳定性。

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图1
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T 峰到 T 端和 QT 色散的示意图描述:分别指示复极的透壁和区域差异。(a) T 波峰值到 T 波结束的间隔代表心外膜和 M 细胞复极终止的透壁时间差异 (b) 实线和虚线模拟从两个不同的 M 细胞记录的 M 细胞复极持续时间心肌区域。复极曲线末端之间的差异,伴随着 T 波的末端,在体表 ECG 上表现为可变的 QT 间期

据报道,一组 120 名 COVID-19 患者的 Tp-Te 间期延长,Tp-Te 持续时间与感染的严重程度相关,但 QTc 与健康对照相似(Koc 等人,2020 年)。此外,在 Shaghee 等人的另一项研究中。(2021 年),COVID-19 肺炎结果与 QTc 和 Tp-Te 间期均显着相关,尽管后者标志物有更显着的变化,因为在更严重的病例中 Tp-Te 与 QTc 的比率也显着增加。

总之,考虑到在 COVID-19 重症病例中进行心血管成像和床边病史记录存在局限性,我们建议应检查 Tp-Te 间期作为预测 COVID-19 患者心律失常风险的可靠方法.

最后,我们应该提到 Amoabeng 等人的索引文章。包含一个数字来表示感染前和感染期间 COVID-19 患者的心电图特征的流行情况。由于只有一半患者的感染前 ECG 可用,因此比较两组的原始值是不合理的,报告每个组中每个总记录的 ECG 特征的流行率会更明智。

更新日期:2021-09-02
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