%0 Journal Article
%T Echocardiographic assessment of cardiovascular physiology of preterm miniature piglets supported with a pumped artificial placenta system.
%A Kühle H
%A Cho SKS
%A Charest-Pekeski AJ
%A Chow JSM
%A Lee FT
%A Aujla T
%A Saini BS
%A Lim JM
%A Darby JRT
%A Mroczek D
%A Floh AA
%A McVey MJ
%A Morrison JL
%A Seed M
%A Sun L
%A Haller C
%J Prenat Diagn
%V 44
%N 6
%D 2024 Jun 29
%M 38809178
%F 3.242
%R 10.1002/pd.6612
%X <B>OBJECTIVE: </B>We evaluated fetal cardiovascular physiology and mode of cardiac failure in premature miniature piglets on a pumped artificial placenta (AP) circuit.<BR><B>METHODS: </B>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.<BR><B>RESULTS: </B>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.<BR><B>CONCLUSIONS: </B>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.