空气污染对心室复极的影响。

Robert L Lux, C Arden Pope
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Given this positive finding and the well-established sensitivity of cardiac repolarization to physiologic, pharmacologic, and neurologic interventions, and in light of emerging novel tools for assessing repolarization, we hypothesized that high levels of particulate air pollution would alter repolarization independent of changes in heart rate and, consequently, would increase arrhythmogenic risk. The likely mechanism of any deleterious effects on repolarization would be alteration of sodium, calcium, and potassium channels. The channel's structure, function, and kinetics are responsible for generating the cellular action potentials, which, when summed over the entire heart, result in the waves recorded by the ECG. A positive finding would provide evidence that increased levels of air pollution may be directly linked to increases in arrhythmogenic risk and, potentially, sudden cardiac death. 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The study findings did not support the original hypothesis and demonstrated a lack of sensitivity of repolarization to changes in PM2.5 concentrations. None of the repolarization variables showed a statistically significant change between days of low and high PM2.5 concentrations, although we observed statistically significant differences for some variables using fixed-effects modeling. However, we did find a significant decrease in the standard deviation of cycle length, in concert with findings in the original study that showed a decrease in HRV parameter values. There was a slight but statistically insignificant increase in the width of the TW between recordings from days of low and days of high PM2.5, suggesting that, in a setting of prolonged exposure to high levels of PM, the original hypothesis might be supported. We conclude that in this study the short-term (day-today) differences in air pollution, specifically PM2.5 concentration, did not affect ventricular repolarization. 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引用次数: 0

摘要

我们对一组先前发表的心电图数据进行了回顾性研究,以调查颗粒空气污染水平与心室复极变化之间可能的直接关联。心室复极是心脏电生理过程,表现为心电图(ECG)的T波*,与心律失常的增加有明确的联系。该数据集发表的研究结果显示了明显的心脏效应,即随着颗粒物空气污染水平的增加,心率变异性(HRV)参数值降低(Pope et al. 2004),这表明可能存在致心律失常作用。鉴于这一积极的发现和心脏复极对生理、药理学和神经学干预的公认敏感性,以及评估复极的新工具的出现,我们假设高水平的颗粒空气污染会改变复极而不依赖于心率的变化,因此会增加致心律失常的风险。对复极化产生有害影响的可能机制是钠、钙和钾通道的改变。通道的结构、功能和动力学负责产生细胞动作电位,当对整个心脏求和时,就会产生ECG记录的波。一个积极的发现将提供证据,表明空气污染水平的增加可能与致心律失常风险的增加和潜在的心源性猝死的增加直接相关。研究人群包括88名不吸烟的老年受试者,他们收集了多次、连续、24小时、2通道的心电图记录,并收集了血液样本来评估炎症机制(本研究未进行)。测量或估计每日样本中细颗粒物(PM2.5,空气动力学直径<或= 2.5微米的颗粒物)的浓度,并用于触发记录,记录PM2.5浓度“低”或“高”的天数。在研究期间,每个受试者都参与了一到五次录音,所有受试者都住在犹他州的大盐湖谷。我们使用定制软件重新分析了这些记录,该软件包含ECG的幅度函数-所有记录导联的均方根(RMS ECG) -以确定24小时记录中每个节拍的以下内容:周期长度(RR);RR分散;RMS R波和t波峰值之间的间隔(RT),是对心室动作电位平均持续时间的稳健估计;RMS T波宽度(TW),这是对复极化时间范围的可靠估计,与复极化弥散和心律失常有关;从QRS发作到RMS心电图t波偏移量的RMS QT间期(QT);以及RT相对于RR、QT相对于RR、TW相对于RR的回归斜率,这些斜率提供了所谓复极恢复的估计,或复极的速率依赖性,这也与心律失常有关。研究结果不支持最初的假设,并证明了复极化对PM2.5浓度变化缺乏敏感性。尽管我们使用固定效应模型观察到一些变量在统计上有显著差异,但在PM2.5浓度低和高的日子之间,没有一个复极化变量显示出统计学上的显著变化。然而,我们确实发现周期长度的标准差显著降低,这与原始研究中HRV参数值降低的结果一致。在PM2.5低值和高低值记录之间的TW宽度有轻微但统计上不显著的增加,这表明,在长时间暴露于高水平PM的情况下,最初的假设可能得到支持。我们得出结论,在本研究中,短期(每天)空气污染的差异,特别是PM2.5浓度,不影响心室复极。对负面结果的一个可能解释是,复极的日常变化(由自主影响、活动和心率引起)远远超过了可能由空气污染引起的变化(如果有的话)。此外,这项研究可能力度不足。这些发现并没有反驳PM有害复极化效应的可能性,特别是在长时间暴露的情况下,但建议需要进行暴露研究,以提供更好的控制。根据最近的研究,在高危人群中——例如,患有心脏病的患者——复极的变化可能更明显。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Air pollution effects on ventricular repolarization.

We conducted a retrospective study of a set of previously published electrocardiographic data to investigate the possible direct association between levels of particulate air pollution and changes in ventricular repolarization -- the cardiac electrophysiologic process that manifests itself as the T wave* of the electrocardiogram (ECG) and that is definitively linked to and responsible for increased arrhythmogenesis. The published findings from this data set demonstrated a clear cardiac effect, namely, a reduction in heart rate variability (HRV) parameter values with increased levels of particulate air pollution (Pope et al. 2004), suggesting possible arrhythmogenic effects. Given this positive finding and the well-established sensitivity of cardiac repolarization to physiologic, pharmacologic, and neurologic interventions, and in light of emerging novel tools for assessing repolarization, we hypothesized that high levels of particulate air pollution would alter repolarization independent of changes in heart rate and, consequently, would increase arrhythmogenic risk. The likely mechanism of any deleterious effects on repolarization would be alteration of sodium, calcium, and potassium channels. The channel's structure, function, and kinetics are responsible for generating the cellular action potentials, which, when summed over the entire heart, result in the waves recorded by the ECG. A positive finding would provide evidence that increased levels of air pollution may be directly linked to increases in arrhythmogenic risk and, potentially, sudden cardiac death. The study population consisted of 88 nonsmoking, elderly subjects in whom multiple, continuous, 24-hour, 2-channel ECG recordings were collected, along with blood samples to evaluate inflammatory mechanisms (not pursued in the current study). The concentration of fine particulate matter (PM2.5, particulate matter with an aerodynamic diameter < or = 2.5 microm) in daily samples was measured or estimated and used to trigger recording sessions for days considered to have "low" or "high" PM2.5 concentrations. Each subject participated in one to five recordings over the study period, and all subjects lived within the greater Salt Lake Valley in Utah. We reanalyzed these recordings using custom software that incorporated a magnitude function of the ECG -- the root mean square of all recorded leads (RMS ECG) -- to determine the following for each beat in the 24-hour recording: cycle length (RR); RR dispersion; the interval between the RMS R- and T-wave peaks (RT), a robust estimate of mean duration of ventricular action potential; the width of the RMS T wave (TW), a robust estimate of the range of repolarization times that relates to repolarization dispersion and arrhythmogenesis; the RMS QT interval (QT) measured from the QRS onset to T-wave offset of the RMS ECG; and the regression slopes of RT versus RR, QT versus RR, and TW versus RR, which provide estimates of so-called repolarization restitution, or rate dependency of repolarization, which also is associated with arrhythmogenesis. The study findings did not support the original hypothesis and demonstrated a lack of sensitivity of repolarization to changes in PM2.5 concentrations. None of the repolarization variables showed a statistically significant change between days of low and high PM2.5 concentrations, although we observed statistically significant differences for some variables using fixed-effects modeling. However, we did find a significant decrease in the standard deviation of cycle length, in concert with findings in the original study that showed a decrease in HRV parameter values. There was a slight but statistically insignificant increase in the width of the TW between recordings from days of low and days of high PM2.5, suggesting that, in a setting of prolonged exposure to high levels of PM, the original hypothesis might be supported. We conclude that in this study the short-term (day-today) differences in air pollution, specifically PM2.5 concentration, did not affect ventricular repolarization. A likely explanation for the negative result is that the day-today variability of repolarization (arising from autonomic influences, activity, and heart rate) far outweighs the changes that might be induced by air pollution, if any. In addition, the study may have been underpowered. The findings do not refute the possibility of the deleterious repolarization effects of PM, particularly over prolonged periods of exposure, but suggest the need for exposure studies that provide better controls. In light of recent studies, it is also likely that in an at-risk population -- for example, patients compromised with heart disease -- repolarization changes may be more apparent.

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