Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, UT, USA; Department of Biomedical Engineering, University of Utah, Salt Lake City, UT, USA; Nora Eccles Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT, USA.
Scientific Computing and Imaging Institute, University of Utah, Salt Lake City, UT, USA; Department of Biomedical Engineering, University of Utah, Salt Lake City, UT, USA; Nora Eccles Cardiovascular Research and Training Institute, University of Utah, Salt Lake City, UT, USA; School of Medicine, University of Utah, Salt Lake City, UT, USA.
J Electrocardiol. 2021 May-Jun;66:86-94. doi: 10.1016/j.jelectrocard.2021.03.004. Epub 2021 Mar 23.
Acute myocardial ischemia occurs when coronary perfusion to the heart is inadequate, which can perturb the highly organized electrical activation of the heart and can result in adverse cardiac events including sudden cardiac death. Ischemia is known to influence the ST and repolarization phases of the ECG, but it also has a marked effect on propagation (QRS); however, studies investigating propagation during ischemia have been limited.
We estimated conduction velocity (CV) and ischemic stress prior to and throughout 20 episodes of experimentally induced ischemia in order to quantify the progression and correlation of volumetric conduction changes during ischemia. To estimate volumetric CV, we 1) reconstructed the activation wavefront; 2) calculated the elementwise gradient to approximate propagation direction; and 3) estimated conduction speed (CS) with an inverse-gradient technique.
We found that acute ischemia induces significant conduction slowing, reducing the global median speed by 20 cm/s. We observed a biphasic response in CS (acceleration then deceleration) early in some ischemic episodes. Furthermore, we noted a high temporal correlation between ST-segment changes and CS slowing; however, when comparing these changes over space, we found only moderate correlation (corr. = 0.60).
This study is the first to report volumetric CS changes (acceleration and slowing) during episodes of acute ischemia in the whole heart. We showed that while CS changes progress in a similar time course to ischemic stress (measured by ST-segment shifts), the spatial overlap is complex and variable, showing extreme conduction slowing both in and around regions experiencing severe ischemia.
当冠状动脉对心脏的灌注不足时，就会发生急性心肌缺血，这可能会打乱心脏高度有序的电激活，并导致不良的心脏事件，包括心源性猝死。已知缺血会影响心电图的 ST 和复极阶段，但它对传播（QRS）也有明显的影响；然而，研究缺血期间传播的研究一直很有限。
我们在 20 次实验诱导缺血发作之前和期间估计了传导速度（CV）和缺血应激，以量化缺血过程中容积传导变化的进展和相关性。为了估计容积 CV，我们 1）重建激活波前；2）计算元素梯度以近似传播方向；3）用逆梯度技术估计传导速度（CS）。
我们发现急性缺血会导致明显的传导减慢，使全球中位数速度降低 20cm/s。我们观察到一些缺血发作早期 CS 出现双相反应（加速然后减速）。此外，我们注意到 ST 段变化与 CS 减慢之间存在高度的时间相关性；然而，当比较这些空间变化时，我们只发现了中度相关性（相关系数=0.60）。
这项研究首次报告了整个心脏在急性缺血发作期间的容积 CS 变化（加速和减慢）。我们表明，虽然 CS 变化与缺血应激（通过 ST 段移位测量）的时间进程相似，但空间重叠是复杂和多变的，在经历严重缺血的区域及其周围都表现出极端的传导减慢。
