Henriette Kühle, Steven K S Cho, Alex J Charest-Pekeski, Jessica S M Chow, Fu-Tsuen Lee, Tanroop Aujla, Brahmdeep S Saini, Jessie Mei Lim, Jack R T Darby, Dariusz Mroczek, Alejandro A Floh, Mark J McVey, Janna L Morrison, Mike Seed, Liqun Sun, Christoph Haller
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In utero scans were used as control data.</p><p><strong>Results: </strong>AP fetuses (n = 13; 102±4d gestational age [term 115d]; 616 ± 139 g [g]; survival 46.4 ± 46.8 h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24 h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24 h.</p><p><strong>Conclusions: </strong>Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.</p>","PeriodicalId":20387,"journal":{"name":"Prenatal Diagnosis","volume":null,"pages":null},"PeriodicalIF":2.7000,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Echocardiographic assessment of cardiovascular physiology of preterm miniature piglets supported with a pumped artificial placenta system.\",\"authors\":\"Henriette Kühle, Steven K S Cho, Alex J Charest-Pekeski, Jessica S M Chow, Fu-Tsuen Lee, Tanroop Aujla, Brahmdeep S Saini, Jessie Mei Lim, Jack R T Darby, Dariusz Mroczek, Alejandro A Floh, Mark J McVey, Janna L Morrison, Mike Seed, Liqun Sun, Christoph Haller\",\"doi\":\"10.1002/pd.6612\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objectives: </strong>We evaluated fetal cardiovascular physiology and mode of cardiac failure in premature miniature piglets on a pumped artificial placenta (AP) circuit.</p><p><strong>Methods: </strong>Fetal pigs were cannulated via the umbilical vessels and transitioned to an AP circuit composed of a centrifugal pump and neonatal oxygenator and maintained in a fluid-filled biobag. Echocardiographic studies were conducted to measure ventricular function, umbilical blood flow, and fluid status. In utero scans were used as control data.</p><p><strong>Results: </strong>AP fetuses (n = 13; 102±4d gestational age [term 115d]; 616 ± 139 g [g]; survival 46.4 ± 46.8 h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24 h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24 h.</p><p><strong>Conclusions: </strong>Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.</p>\",\"PeriodicalId\":20387,\"journal\":{\"name\":\"Prenatal Diagnosis\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2024-06-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Prenatal Diagnosis\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1002/pd.6612\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/5/29 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"Q2\",\"JCRName\":\"GENETICS & HEREDITY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Prenatal Diagnosis","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1002/pd.6612","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/5/29 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
引用次数: 0
摘要
目的我们评估了早产微型猪在人工胎盘(AP)回路中的胎儿心血管生理学和心脏衰竭模式:方法:通过脐带血管为胎儿插管,将其过渡到由离心泵和新生儿氧合器组成的人工胎盘回路,并将其保存在充满液体的生物袋中。进行超声心动图检查以测量心室功能、脐血流量和体液状态。宫内扫描结果作为对照数据:AP胎儿(n = 13;胎龄102±4d [足月115d];体重616±139 g[g];存活46.4±46.8 h)心动过速、高血压,最初血流超生理水平。观察到心肌壁厚度增加。所有仔猪都有胎儿水肿的迹象。过渡到回路后,左心室的整体纵向应变(GLS)测量值增加。与子宫内测量结果相比,右心室(RV)和左心室应变率在AP支持期间早期下降,但在实验结束时恢复。支持时间超过24小时的胎儿的RV GLS与子宫内对照组相似,而与仅存活24小时的仔猪相比,GLS明显更高:结论:使用泵支持 AP 循环的胎儿后负荷增加,AP 和全身循环之间的血流重新分配,这与舒张末期充盈压升高有关。这导致了心力衰竭和肾积水。这些早产儿无法承受与当前 AP 回路连接相关的血流动力学变化。为了更好地模拟原生胎盘的生理结构并保护胎儿正常的心血管生理结构,需要进一步优化该回路。
Echocardiographic assessment of cardiovascular physiology of preterm miniature piglets supported with a pumped artificial placenta system.
Objectives: We evaluated fetal cardiovascular physiology and mode of cardiac failure in premature miniature piglets on a pumped artificial placenta (AP) circuit.
Methods: Fetal pigs were cannulated via the umbilical vessels and transitioned to an AP circuit composed of a centrifugal pump and neonatal oxygenator and maintained in a fluid-filled biobag. Echocardiographic studies were conducted to measure ventricular function, umbilical blood flow, and fluid status. In utero scans were used as control data.
Results: AP fetuses (n = 13; 102±4d gestational age [term 115d]; 616 ± 139 g [g]; survival 46.4 ± 46.8 h) were tachycardic and hypertensive with initially supraphysiologic circuit flows. Increased myocardial wall thickness was observed. Signs of fetal hydrops were present in all piglets. Global longitudinal strain (GLS) measurements increased in the left ventricle (LV) after transition to the circuit. Right ventricle (RV) and LV strain rate decreased early during AP support compared with in utero measurements but recovered toward the end of the experiment. Fetuses supported for >24 h had similar RV GLS to in utero controls and significantly higher GLS compared to piglets surviving only up to 24 h.
Conclusions: Fetuses on a pump-supported AP circuit experienced an increase in afterload, and redistribution of blood flow between the AP and systemic circulations, associated with elevated end-diastolic filling pressures. This resulted in heart failure and hydrops. These preterm fetuses were unable to tolerate the hemodynamic changes associated with connection to the current AP circuit. To better mimic the physiology of the native placenta and preserve normal fetal cardiovascular physiology, further optimization of the circuit will be required.
期刊介绍:
Prenatal Diagnosis welcomes submissions in all aspects of prenatal diagnosis with a particular focus on areas in which molecular biology and genetics interface with prenatal care and therapy, encompassing: all aspects of fetal imaging, including sonography and magnetic resonance imaging; prenatal cytogenetics, including molecular studies and array CGH; prenatal screening studies; fetal cells and cell-free nucleic acids in maternal blood and other fluids; preimplantation genetic diagnosis (PGD); prenatal diagnosis of single gene disorders, including metabolic disorders; fetal therapy; fetal and placental development and pathology; development and evaluation of laboratory services for prenatal diagnosis; psychosocial, legal, ethical and economic aspects of prenatal diagnosis; prenatal genetic counseling