患有法洛四联症的人类胎儿心脏改变了流体动力学和力,AJP Heart and Circulatory Physiology

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患有法洛四联症的人类胎儿心脏改变了流体动力学和力
AJP Heart and Circulatory Physiology Pub Date : 2018-09-14 , DOI: 10.1152/ajpheart.00235.2018
Hadi Wiputra ₁ , Ching Kit Chen ₂ , Elias Talbi ₁ , Guat Ling Lim ₃ , Sanah Merchant Soomar ₂ , Arijit Biswas ₃ , Citra Nurfarah Zaini Mattar ₃ , David Bark ₄ , Hwa Liang Leo ₁ , Choon Hwai Yap ₁

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研究表明血流力对某些先天性心脏畸形的发病机制和进展有影响。因此，研究畸形产前心脏（例如法洛四联症（TOF））的流体力学环境是很有意义的，特别是在对胎儿 TOF 知之甚少的情况下。在这项研究中，我们对三个 TOF 和七个正常人类胎儿心脏进行了基于患者特定超声的血流模拟。与正常心室相比，TOF 右心室 (RV) 的舒张末期容积 (EDV) 较小，但每搏输出量 (SV) 相似，而 TOF 左心室 (LV) 的 EDV 相似，但 SV 略有增加。模拟显示，TOF 心室的收缩期室内压力梯度 (IVPG) 升高，需要额外的能量进行射血，但 IVPG 升高相对于动脉压而言被认为是轻微的。由于通过室间隔缺损 (VSD) 实现平衡，TOF 右心室和左心室具有相似的压力。此外，相对于正常情况，TOF RV 的舒张期壁剪切应力 (WSS) 有所增加，但 TOF LV 则没有。这是由超过 RV SV 的高三尖瓣流入引起的，导致从右到左分流和混沌流，并增强与壁的涡度相互作用，从而提高 WSS。三个 TOF RV 中的两个但没有一个 LV 的厚度增加。由于压力升高程度轻微，我们假设压力和 WSS 升高可能在 RV 增厚以及其他致病因素中发挥作用。最后，由于右心室到左心室的血流分流和通过主动脉的高流速，VSD 周围的心内膜始终经历高 WSS。新的和值得注意的血流力被认为会导致先天性心脏畸形并影响疾病进展。我们对法洛四联症 (TOF) 人胎儿心脏的心内流体力学进行了新的研究，发现了与正常心脏的本质区别。TOF 右心室 (RV) 和左心室具有相似且升高的压力，但只有 TOF RV 由于三尖瓣流入量增加而具有升高的壁剪切应力，这可能导致观察到的 RV 增厚。TOF 心脏还需要消耗更多的能量来进行射血。

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Human fetal hearts with tetralogy of Fallot have altered fluid dynamics and forces

Studies have suggested the effect of blood flow forces in pathogenesis and progression of some congenital heart malformations. It is therefore of interest to study the fluid mechanic environment of the malformed prenatal heart, such as the tetralogy of Fallot (TOF), especially when little is known about fetal TOF. In this study, we performed patient-specific ultrasound-based flow simulations of three TOF and seven normal human fetal hearts. TOF right ventricles (RVs) had smaller end-diastolic volumes (EDVs) but similar stroke volumes (SVs), whereas TOF left ventricles (LVs) had similar EDVs but slightly increased SVs compared with normal ventricles. Simulations showed that TOF ventricles had elevated systolic intraventricular pressure gradient (IVPG) and required additional energy for ejection but IVPG elevations were considered to be mild relative to arterial pressure. TOF RVs and LVs had similar pressures because of equalization via ventricular septal defect (VSD). Furthermore, relative to normal, TOF RVs had increased diastolic wall shear stresses (WSS) but TOF LVs were not. This was caused by high tricuspid inflow that exceeded RV SV, leading to right-to-left shunting and chaotic flow with enhanced vorticity interaction with the wall to elevate WSS. Two of the three TOF RVs but none of the LVs had increased thickness. As pressure elevations were mild, we hypothesized that pressure and WSS elevation could play a role in the RV thickening, among other causative factors. Finally, the endocardium surrounding the VSD consistently experienced high WSS because of RV-to-LV flow shunt and high flow rate through the over-riding aorta.NEW & NOTEWORTHY Blood flow forces are thought to cause congenital heart malformations and influence disease progression. We performed novel investigations of intracardiac fluid mechanics of tetralogy of Fallot (TOF) human fetal hearts and found essential differences from normal hearts. The TOF right ventricle (RV) and left ventricle had similar and elevated pressure but only the TOF RV had elevated wall shear stress because of elevated tricuspid inflow, and this may contribute to the observed RV thickening. TOF hearts also expended more energy for ejection.

更新日期：2018-09-14

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