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Pharmacological and simulated exercise cardiac stress tests produce different ischemic signatures in high-resolution experimental mapping studies
Journal of Electrocardiology ( IF 1.3 ) Pub Date : 2021-07-24 , DOI: 10.1016/j.jelectrocard.2021.07.009
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  

Objective

Test the hypothesis that exercise and pharmacological cardiac stressors create different electrical ischemic signatures.

Introduction

Current clinical stress tests for detecting ischemia lack sensitivity and specificity. One unexplored source of the poor detection is whether pharmacological stimulation and regulated exercise produce identical cardiac stress.

Methods

We used a porcine model of acute myocardial ischemia in which animals were instrumented with transmural plunge-needle electrodes, an epicardial sock array, and torso arrays to simultaneously measure cardiac electrical signals within the heart wall, the epicardial surface, and the torso surface, respectively. Ischemic stress via simulated exercise and pharmacological stimulation were created with rapid electrical pacing and dobutamine infusion, respectively, and mimicked clinical stress tests of five 3-minute stages. Perfusion to the myocardium was regulated by a hydraulic occluder around the left anterior descending coronary artery. Ischemia was measured as deflections to the ST-segment on ECGs and electrograms.

Results

Across eight experiments with 30 (14 simulated exercise and 16 dobutamine) ischemic interventions, the spatial correlations between exercise and pharmacological stress diverged at stage three or four during interventions (p < 0.05). We found more detectable ST-segment changes on the epicardial surface during simulated exercise than with dobutamine (p < 0.05). The intramyocardial ischemia formed during simulated exercise had larger ST40 potential gradient magnitudes (p < 0.05).

Conclusion

We found significant differences on the epicardium between cardiac stress types using our experimental model, which became more pronounced at the end stages of each test. A possible mechanism for these differences was the larger ST40 potential gradient magnitudes within the myocardium during exercise. The presence of microvascular dysfunction during exercise and its absence during dobutamine stress may explain these differences.



中文翻译:

药理学和模拟运动心脏压力测试在高分辨率实验映射研究中产生不同的缺血特征

客观的

检验运动和药理学心脏压力源产生不同的电缺血特征的假设。

介绍

目前用于检测缺血的临床压力测试缺乏敏感性和特异性。检测不佳的一个未探索来源是药理刺激和有规律的运动是否会产生相同的心脏压力。

方法

我们使用了猪的急性心肌缺血模型,在该模型中,动物被配备了透壁插针电极、心外膜袜式阵列和躯干阵列,以分别同时测量心壁、心外膜表面和躯干表面内的心脏电信号. 分别通过快速电起搏和多巴酚丁胺输注通过模拟运动和药物刺激产生缺血性压力,并模拟五个 3 分钟阶段的临床压力测试。心肌灌注由围绕左冠状动脉前降支的液压封堵器调节。缺血被测量为心电图和电图上 ST 段的偏转。

结果

在包含 30 次(14 次模拟运动和 16 次多巴酚丁胺)缺血干预的 8 项实验中,运动和药理压力之间的空间相关性在干预期间的第三或第四阶段出现分歧(p  <  0.05)。我们发现在模拟运动期间心外膜表面的 ST 段变化比多巴酚丁胺更可检测(p  <  0.05)。模拟运动过程中形成的心肌内缺血具有较大的 ST40 电位梯度幅度(p  <  0.05)。

结论

我们使用我们的实验模型发现心脏压力类型之间的心外膜存在显着差异,这在每次测试的最后阶段变得更加明显。这些差异的可能机制是运动期间心肌内较大的 ST40 电位梯度幅度。运动期间微血管功能障碍的存在和多巴酚丁胺应激期间微血管功能障碍的存在可以解释这些差异。

更新日期:2021-08-01
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