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Transient recovery of epicardial and torso ST-segment ischemic signals during cardiac stress tests: A possible physiological mechanism
Journal of Electrocardiology ( IF 1.3 ) Pub Date : 2021-07-21 , DOI: 10.1016/j.jelectrocard.2021.07.007
Brian Zenger 1 , Wilson W Good 2 , Jake A Bergquist 2 , Lindsay C Rupp 2 , Maura Perez 3 , Gregory J Stoddard 4 , Vikas Sharma 5 , Rob S MacLeod 2
Affiliation  

Background

Acute myocardial ischemia has several characteristic ECG findings, including clinically detectable ST-segment deviations. However, the sensitivity and specificity of diagnosis based on ST-segment changes are low. Furthermore, ST-segment deviations have been shown to be transient and spontaneously recover without any indication the ischemic event has subsided.

Objective

Assess the transient recovery of ST-segment deviations on remote recording electrodes during a partial occlusion cardiac stress test and compare them to intramyocardial ST-segment deviations.

Methods

We used a previously validated porcineBZ experimental model of acute myocardial ischemia with controllable ischemic load and simultaneous electrical measurements within the heart wall, on the epicardial surface, and on the torso surface. Simulated cardiac stress tests were induced by occluding a coronary artery while simultaneously pacing rapidly or infusing dobutamine to stimulate cardiac function. Postexperimental imaging created anatomical models for data visualization and quantification. Markers of ischemia were identified as deviations in the potentials measured at 40% of the ST-segment. Intramural cardiac conduction speed was also determined using the inverse gradient method. We assessed changes in intramyocardial ischemic volume proportion, conduction speed, clinical presence of ischemia on remote recording arrays, and regional changes to intramyocardial ischemia. We defined the peak deviation response time as the time interval after onset of ischemia at which maximum ST-segment deviation was achieved, and ST-recovery time was the interval when ST deviation returned to below thresholded of ST elevation.

Results

In both epicardial and torso recordings, the peak ST-segment deviation response time was 4.9±1.1 min and the ST-recovery time was approximately 7.9±2.5 min, both well before the termination of the ischemic stress. At peak response time, conduction speed was reduced by 50% and returned to near baseline at ST-recovery. The overall ischemic volume proportion initially increased, on average, to 37% at peak response time; however, it recovered only to 30% at the ST-recovery time. By contrast, the subepicardial region of the myocardial wall showed 40% ischemic volume at peak response time and recovered much more strongly to 25% as epicardial ST-segment deviations returned to baseline.

Conclusion

Our data show that remote ischemic signal recovery correlates with a recovery of the subepicardial myocardium, while subendocardial ischemic development persists.



中文翻译:

心脏负荷试验期间心外膜和躯干 ST 段缺血信号的瞬时恢复:一种可能的生理机制

背景

急性心肌缺血有几个特征性的心电图表现,包括临床上可检测到的 ST 段偏差。然而,基于ST段改变诊断的敏感性和特异性较低。此外,ST 段偏差已被证明是短暂的并且会自发恢复,而没有任何迹象表明缺血事件已经消退。

客观的

在部分闭塞心脏压力测试期间评估远程记录电极上 ST 段偏差的瞬时恢复,并将其与心肌内 ST 段偏差进行比较。

方法

我们使用了以前验证过的猪BZ急性心肌缺血的实验模型,具有可控的缺血负荷和心壁内、心外膜表面和躯干表面的同步电测量。通过阻塞冠状动脉同时快速起搏或注入多巴酚丁胺以刺激心脏功能来诱导模拟心脏压力测试。实验后成像创建了用于数据可视化和量化的解剖模型。缺血标志物被确定为在 ST 段 40% 处测量的电位偏差。还使用逆梯度法测定壁内心脏传导速度。我们评估了心肌内缺血体积比例的变化、传导速度、远程记录阵列上缺血的临床表现以及心肌内缺血的区域变化。

结果

在心外膜和躯干记录中,峰值 ST 段偏差响应时间为 4.9±1.1 分钟,ST 恢复时间约为 7.9±2.5 分钟,均早于缺血性应激终止。在峰值响应时间,传导速度降低了 50%,并在 ST 恢复时恢复到接近基线。总体缺血体积比例最初平均增加至峰值反应时间的 37%;然而,它在 ST 恢复时仅恢复到 30%。相比之下,心肌壁的心外膜下区域在峰值反应时间显示出 40% 的缺血体积,并且随着心外膜 ST 段偏差恢复到基线,恢复得更加强烈,达到 25%。

结论

我们的数据表明,远程缺血信号恢复与心外膜下心肌的恢复相关,而心内膜下缺血的发展持续存在。

更新日期:2021-07-22
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