UT-Heart Inc., 3-25-8 Nozawa, Setagaya, Tokyo, 154-0003, Japan.
Future Center Initiative, The University of Tokyo, 178-4-4 Wakashiba, Kashiwa, Chiba, 277-0871, Japan.
J Physiol Sci. 2020 Jul 13;70(1):36. doi: 10.1186/s12576-020-00760-3.
ST elevation on an electrocardiogram is a hallmark of acute transmural ischemia. However, the underlying mechanism remains unclear. We hypothesized that high ischemic sensitivities of epicardial adenosine triphosphate-sensitive potassium (IK) and sodium (INa) currents play key roles in the genesis of ST elevation. Using a multi-scale heart simulation under moderately ischemic conditions, transmural heterogeneities of IK and INa created a transmural gradient, opposite to that observed in subendocardial injury, leading to ST elevation. These heterogeneities also contributed to the genesis of hyper-acute T waves under mildly ischemic conditions. By contrast, under severely ischemic conditions, although action potentials were suppressed transmurally, the potential gradient at the boundary between the ischemic and normal regions caused ST elevation without a contribution from transmural heterogeneity. Thus, transmural heterogeneities of ion channel properties may contribute to the genesis of ST-T changes during mild or moderate transmural ischemia, while ST elevation may be induced without the contribution of heterogeneity under severe ischemic conditions.
心电图上的 ST 段抬高是急性透壁性缺血的标志。然而，其潜在机制尚不清楚。我们假设，心外膜三磷酸腺苷敏感性钾（IK）和钠（INa）电流的高缺血敏感性在 ST 段抬高的发生中起关键作用。在中度缺血条件下，使用多尺度心脏模拟，IK 和 INa 的跨壁异质性产生了与心内膜下损伤相反的跨壁梯度，导致 ST 段抬高。这些异质性也有助于在轻度缺血条件下产生超急性 T 波。相比之下，在严重缺血条件下，虽然动作电位被跨壁抑制，但缺血和正常区域之间边界的电位梯度导致 ST 段抬高，而没有跨壁异质性的贡献。因此，离子通道特性的跨壁异质性可能导致轻度或中度透壁性缺血期间 ST-T 变化的发生，而在严重缺血条件下，ST 段抬高可能在没有异质性贡献的情况下发生。
