A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations.
A mathematical model of twin-twin transfusion syndrome with pulsatile arterial circulations.
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具有脉动动脉循环的双胞胎输血综合征的数学模型。
DOI：
10.1152/ajpregu.00534.2006
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发表时间：
2007
期刊：
影响因子：
--
通讯作者：
vanGemert,MartinJC
中科院分区：
文献类型：
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作者：
vandenWijngaard,JeroenPHM;Westerhof,BerendE;Ross,MichaelG;vanGemert,MartinJC
双胎输血综合征（TTTS）是单绒毛膜双胞胎妊娠的一种严重并发症，由一对双胞胎（供体）的血液通过胎盘吻合口净输注到另一对双胞胎（受体）。为了研究TTTS在临床I至IV期的病理生理学演变，我们扩展了我们的数学模型，包括沿动脉树传播的脉动循环、胎盘和脑血管阻力、动脉壁厚度和刚度。该模型表明，供体双胞胎的脐带动脉血流异常（TTTS III期）是由胎盘阻力增加和脑动脉阻力降低引起的。相比之下，受体双胎脐带动脉异常血流需要胎盘阻力显著增加，这是由高羊水压力的压缩作用造成的。因此，模拟的供体脐动脉搏动异常在供体中比在受体中更常见和更早发生。“正常”分期顺序（I、II、III、IV）与补偿性胎盘吻合口的存在相关，补偿性吻合口构成了大多数单绒毛膜双胎胎盘。然而，在我们的模型中，TTTS III期可能发生在II期表现（缺乏供体膀胱填充）之前，这与单一动静脉吻合引起的严重TTTS相关，这是一种罕见的胎盘血管构筑。总之，该数学模型描述了TTTS的四个阶段的发生和发展，再现了各种临床表现，并可能有助于确定TTTS分期顺序的潜在病理生理学。
The twin-twin transfusion syndrome (TTTS) is a severe complication of monochorionic twin pregnancies caused by a net transfusion of blood from one twin (the donor) to the other (the recipient) through placental anastomoses. To examine the pathophysiology of TTTS evolving through clinical stages I to IV, we extended our mathematical model to include pulsating circulations propagating along the arterial tree as well as placental and cerebral vascular resistances, and arterial wall thickness and stiffness. The model demonstrates that abnormal umbilical arterial flow (TTTS stage III) in the donor twin results from increased placental resistance as well as reduced resistance in the cerebral arteries. In contrast, recipient twin abnormal umbilical arterial flow requires a significantly greater increase in placental resistance, resulting from the compressive effects of high amniotic fluid pressure. Thus simulated abnormalities of donor umbilical arterial pulsations occur in the donor more commonly and earlier than in the recipient. The “normal” staging sequence (I, II, III, IV) correlates with the presence of compensating placental anastomoses, constituting the majority of monochorionic twin placentas. However, TTTS stage III may occur before manifestations of stage II (lack of donor bladder filling), in our model correlating with severe TTTS from a single arteriovenous anastomosis, an infrequent occurring placental angioarchitecture. In conclusion, this mathematical model describes the onset and development of the four stages of TTTS, reproduces a variety of clinical manifestations, and may contribute to identifying the underlying pathophysiology of the staging sequence in TTTS.