Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA; School of Medicine, University of Utah, SLC, UT, USA.
Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA; Nora Eccles Harrison Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA; Department of Biomedical Engineering, University of Utah, SLC, UT, USA.
J Electrocardiol. 2021 Sep-Oct;68:56-64. doi: 10.1016/j.jelectrocard.2021.07.009. Epub 2021 Jul 24.
Test the hypothesis that exercise and pharmacological cardiac stressors create different electrical ischemic signatures.
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.
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.
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).
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.
验证运动和药理学心脏应激源产生不同电缺血特征的假设。
目前用于检测缺血的临床应激测试缺乏敏感性和特异性。尚未探索的一个原因是,药理学刺激和调节运动是否产生相同的心脏应激。
我们使用了一种急性心肌缺血的猪模型,在该模型中,动物被植入了贯穿壁的 plunge-needle 电极、心外膜套阵列和体数组,分别用于同时测量心壁内、心外膜表面和体表面的心脏电信号。通过快速电起搏和多巴酚丁胺输注分别模拟运动和药理学刺激的缺血应激,并模拟了五个 3 分钟阶段的临床应激测试。通过左前降支冠状动脉周围的液压夹具调节心肌灌注。通过心电图和电图上的 ST 段偏移来测量缺血。
在八项有 30 次(14 次模拟运动和 16 次多巴酚丁胺)缺血干预的实验中,在干预的第三或第四阶段,运动和药理学应激之间的空间相关性出现分歧(p<0.05)。我们发现,在模拟运动期间,心外膜表面的 ST 段变化更易检测到(p<0.05)。在模拟运动期间形成的心肌内缺血具有更大的 ST40 电势梯度幅度(p<0.05)。
我们在实验模型中发现了心脏应激类型在心脏外膜上的显著差异,这些差异在每个测试的后期阶段变得更加明显。这些差异的一个可能机制是运动期间心肌内 ST40 电势梯度幅度较大。运动期间存在微血管功能障碍,而多巴酚丁胺应激期间不存在微血管功能障碍,这可能解释了这些差异。