Thammavong Keooudone, Luewan Suchaya, Jatavan Phudit, Tongsong Theera
Department of Obstetrics and Gynecology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand.
ESC Heart Fail. 2020 Dec;7(6):3473-3482. doi: 10.1002/ehf2.12969. Epub 2020 Sep 10.
This study aims to update new knowledge regarding foetal cardiovascular response to anaemia, using foetal haemoglobin Bart's disease as a study model. Original research articles, review articles, and guidelines were narratively reviewed and comprehensively validated. The main foetal cardiovascular changes in response to anaemia are consequences of hypervolaemia and increased cardiac output to meet tissue oxygen requirement. New challenging insights are as follows: (i) the earliest morphological change is an increase in cardiac size and remodelling of the sphericity (an increase in diameter more pronounced than that in long axis) followed by several markers, such as placentomegaly and hepatosplenomegaly. (ii) The earliest functional change is increased peak systolic velocity of the red blood cells because of low viscosity, especially in the middle cerebral artery. (iii) The foetal heart has very high reserve potentials to cope with anaemia: increasing workload without increased central venous pressure and increased myocardial performance without compromising shortening fraction. This hard-working period with good performance lasts long, including most part of the second and third trimester. (iv) At the time cardiomegaly myocardial cellular damage has already occurred, in spite of good cardiac function. (v) Anaemic hydrops foetalis is mainly due to hypervolaemia, hypoalbuminaemia, and high vascular permeability, not heart failure. (vi) Foetal heart failure occurs only when the adaptive mechanism becomes exhausted or long after the development of anaemic hydrops foetalis. Heart failure is a very late result of a longstanding overworked heart. (vii) Ultrasound is highly effective in the detection of foetal response to anaemia. An increase in cardiac size and middle cerebral artery is very helpful in predicting the affected foetuses in pre-hydropic phase. (viii) Theoretically, intrauterine treatment of anaemic hydrops results in satisfactory outcomes as long as cardiac function is normal, but intrauterine intervention should be strongly considered in pre-hydropic phase because myocardial cell damage could have already occurred in this phase or early hydropic phase. Anaemic hydrops foetalis is not primarily caused by heart failure as commonly advocated, but it is rather a consequence of hypervolaemia, hypoalbuminaemia, and high vascular permeability while heart failure is a very late consequence of a longstanding overworked heart. New insights gained from this review may be useful to base clinical practice on which sonographic markers imply significant pathological changes, how ultrasound can be helpful in early detection of anaemic response, when intrauterine transfusion for anaemia due to non-lethal causes should be administered, etc.
本研究旨在以胎儿血红蛋白Bart病作为研究模型，更新有关胎儿心血管系统对贫血反应的新知识。对原始研究文章、综述文章和指南进行了叙述性综述并全面验证。胎儿心血管系统对贫血的主要变化是血容量过多和心输出量增加以满足组织氧需求的结果。新的具有挑战性的见解如下：（i）最早的形态学变化是心脏大小增加和球形重塑（直径增加比长轴更明显），随后出现一些指标，如胎盘肿大和肝脾肿大。（ii）最早的功能变化是由于低粘度导致红细胞收缩期峰值速度增加，尤其是在大脑中动脉。（iii）胎儿心脏具有非常高的储备潜力来应对贫血：增加工作量而不增加中心静脉压，增加心肌性能而不损害缩短分数。这种良好表现的高强度工作期持续很长时间，包括妊娠中期和晚期的大部分时间。（iv）尽管心脏功能良好，但在心脏肥大时心肌细胞损伤已经发生。（v）胎儿贫血性水肿主要是由于血容量过多、低白蛋白血症和高血管通透性，而非心力衰竭。（vi）胎儿心力衰竭仅在适应机制耗尽时或在胎儿贫血性水肿发展很久之后才会发生。心力衰竭是长期过度工作的心脏的非常晚期的结果。（vii）超声在检测胎儿对贫血的反应方面非常有效。心脏大小和大脑中动脉的增加对预测水肿前期受影响的胎儿非常有帮助。（viii）理论上，只要心脏功能正常，贫血性水肿的宫内治疗会产生令人满意的结果，但在水肿前期应强烈考虑宫内干预，因为在这个阶段或早期水肿阶段心肌细胞损伤可能已经发生。胎儿贫血性水肿并非如通常所主张的那样主要由心力衰竭引起，而是血容量过多、低白蛋白血症和高血管通透性的结果，而心力衰竭是长期过度工作的心脏的非常晚期的结果。从本综述中获得的新见解可能有助于为临床实践提供依据，例如哪些超声标志物意味着显著的病理变化、超声如何有助于早期检测贫血反应、对于非致死性原因引起的贫血何时应进行宫内输血等。
