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The role of reduced left ventricular, systolic blood volumes in ST segment potentials overlying diseased tissue of the ischemic heart

机译:降低左心室,收缩血量在缺血性心脏的患病组织潜在的左心室,收缩血量的作用

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Myocardial ischemia is the response of the heart to reduced coronary blood flow, leading to changes in ST segment potentials. ST segment depression is regarded as an indicator of nontransmural myocardial ischemia; however, not all nontransmural ischemia results in ST depression. This apparent discrepancy may be the result of many complex factors in cardiac response mechanisms to reduced blood flow. As a result, sophisticated computer models have emerged that have provided key insights into this complex phenomenon and the circumstances surrounding ST depression. Though these models have been able to produce ST depressions, many have neglected the effect of intracavitary blood volume, associated with different phases of the cardiac cycle. To explore the influence of the cardiac blood volume variability on epicardial potentials during nontransmural ischemia, we incorporated a thin, subendocardial ischemic zone geometry into an anatomically realistic, image-based ventricular model, and generated a finite element, static bidomain solution to determine the resulting epicardial surface potentials. It was first determined that, under baseline conditions (i.e., expanded left ventricular volumes corresponding to diastole), a predictable ST depression developed over the ischemic region. Left ventricular volume was then incrementally reduced, while maintaining the size and general shape of the is-chemic region, in order to reflect the systolic phase of the cardiac cycle. As blood volume geometries decreased, epicardial ST depression overlying the ischemic region first increased in surface area as blood volume was reduced and before dramatically reducing near 30% blood volume reduction — accentuating the role and importance of blood volume variation in computational models ofischemia.
机译:心肌缺血是心脏降低冠状动脉血流量的响应,导致ST段电位的变化。 ST段压低被视为非透壁心肌缺血的指示符;然而,并不是所有的非透壁缺血导致ST段压低。这种明显的差异可以是在心脏反应机制,血流量减少许多复杂的因素的结果。其结果是,先进的计算机模型已经出现,提供了关键洞察这个复杂的现象,周围的ST段压低的情况。虽然这些车型已经能够产生ST洼地,很多人忽视了腔内血量与心动周期的不同阶段相关联的效果。为了探讨非透壁缺血的心外膜电位的心脏血液量的变化的影响,我们引入一个薄的,心内膜下缺血区几何形状成在解剖学上现实的,基于图像的心室模型,并产生一个有限元,静态bidomain溶液来确定最终心外膜表面电位。这是第一次确定,在基线条件下(即,扩展对应于舒张左心室体积),开发了缺血区域可预测的ST段压低。左心室体积然后逐渐减小,同时保持尺寸和是-CHEMIC区域的总体形状,以反映该心动周期的收缩期。由于血容量减少的几何形状,心外膜ST段压低覆缺血区第一表面积增加血容量减少,之前大幅降低近30%血量减少 - 在加剧计算模型ofischemia血容量变化的作用和重要性。

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