Zenger Brian, Good Wilson W, Bergquist Jake, Tate Jess D, Sharma Vikas, MacLeod Rob S
Scientific Computing and Imaging Institute, University of Utah, SLC, UT, USA.
Nora Eccles Cardiovascular Research and Training Institute, University of Utah, SLC, UT, USA.
Comput Cardiol (2010). 2018 Sep;45. doi: 10.22489/CinC.2018.305. Epub 2019 Jun 24.
Clinical tests to detect acute myocardial ischemia induce transient cardiac stress by means of exercise or pharmaceutical stimulation and measure electrical changes of the heart on the body surface via an electrocardiogram (ECG). Such tests assume that both stress mechanisms induce identical-or at least similar-forms of ischemia. To improve electrocardiographic detection of myocardial ischemia, we must study how varied stressing agents (pharmacological or paced stressors) change electrocardiographic signatures. We simultaneously measured electrical recordings within the myocardium, on the epicardial surface, and on the body surface. We then induced acute, controlled ischemia and monitored the electrical response. To create the hemodynamic substrate for ischemia, we applied a hydraulic occlusion to the left anterior descending coronary artery. We varied the ischemic stress with two clinical protocols, the BRUCE and dobutamine stress tests. Our results suggest significant differences in the recorded electrical signal between stress mechanisms. Differences include the location, volume, and temporal development of ischemia throughout a stress episode. These results, and the experimental means used to obtain them, are a significant breakthrough in the field with simultaneous, high density electrical recordings within the myocardium and on the heart and torso surfaces.
检测急性心肌缺血的临床试验通过运动或药物刺激诱导短暂的心脏应激,并通过心电图(ECG)测量体表心脏的电变化。此类试验假定两种应激机制会诱发相同或至少相似形式的缺血。为了改善心肌缺血的心电图检测,我们必须研究不同的应激因素(药理学或起搏应激源)如何改变心电图特征。我们同时测量了心肌内、心外膜表面和体表的电记录。然后我们诱导急性、可控的缺血并监测电反应。为了创建缺血的血流动力学基础,我们对左前降支冠状动脉进行了液压闭塞。我们采用两种临床方案(布鲁斯和多巴酚丁胺应激试验)来改变缺血应激。我们的结果表明,应激机制之间记录的电信号存在显著差异。差异包括整个应激发作过程中缺血的位置、范围和时间发展。这些结果以及用于获得它们的实验方法,是该领域的一项重大突破,实现了心肌内以及心脏和躯干表面的同步、高密度电记录。