Abstract
Disturbed fetal haemodynamics often affects cardiac development and leads to congenital cardiac defects. Reduced left ventricular (LV) preload in the fetus may result in hypoplastic LV, mitral and aortic valve, mimicking a moderate form of hypoplastic left heart complex. We aimed to induce LV hypoplasia by occluding the foramen ovale (FO) to reduce LV preload in the fetal sheep heart, using percutaneous trans-hepatic catheterisation. Under maternal anaesthesia and ultrasound guidance, hepatic venous puncture was performed in six fetal lambs (0.7–0.75 gestation). A coronary guidewire was advanced into the fetal inferior vena cava, right and left atrium. A self-expandable stent was positioned across the FO. An Amplatzer Duct Occluder was anchored within the stent for FO occlusion. Euthanasia and post-mortem examination was performed after 3 weeks. Nine fetuses were used as age-matched controls. Morphometric measurements and cardiac histopathology were performed. Compared with controls, fetal hearts with occluded FO had smaller LV chamber, smaller mitral and aortic valves, lower LV-to-RV ratio in ventricular weight and wall volume, and lower number of LV cardiomyocyte nuclei. We conclude that fetal FO occlusion leads to a phenotype simulating LV hypoplasia. This large animal model may be useful for understanding and devising therapies for LV hypoplasia.
Highlights
Disturbed fetal haemodynamics often affects cardiac development and leads to congenital cardiac defects
A similar effect was observed by Fishman et al 5 years later in fetal sheep when inserting a balloon in the left atrium (LA) obstructed left ventricular (LV) filling and produced the phenotype of hypoplastic left heart complex (HLHC), all of the fetal lambs died within a few days of the procedure[3]
LA and LV filling is almost completely dependent on right to left shunting of oxygenated blood from the placenta through the foramen ovale (FO) since the right ventricular (RV) output is mostly bypassing the lungs through the ductus arteriosus and LA filling by pulmonary venous return is only marginal
Summary
Disturbed fetal haemodynamics often affects cardiac development and leads to congenital cardiac defects. Others described induction of a HLHC by reducing LV filling due to LA ligation in the chick embryo[4,5] Such induced LV hypoplasia can be rescued by an increased volume loading of the left heart at a later timepoint[6]. We report the effects of in-utero occlusion of the FO in the fetal lamb in mid-gestation, using a novel fetal cardiac catheterisation method with trans-hepatic access that we have described previously[16,17]. We hypothesized that by reducing volume loading of the left sided heart structures, a fetus with obliterated or obstructed blood flow through the FO would develop the phenotype of HLHC
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