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Ann Thorac Surg 2007;83:631-639
© 2007 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

Revisiting Animal Models of Aortic Stenosis in the Early Gestation Fetus

^a Divisions of Pediatric Cardiac Surgery and Pediatric Cardiology, University of Cincinnati College of Medicine and Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
^b Department of Surgery, University of Cincinnati College of Medicine and Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
^c Department of Biostatistics and Epidemiology, University of Cincinnati College of Medicine and Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio
^d Department of Pediatric Pathology, University of Cincinnati College of Medicine and Cincinnati Children’s Hospital Medical Center, Cincinnati, Ohio

Accepted for publication September 6, 2006.

^_* Address correspondence to Dr Eghtesady, Division of Pediatric Cardiac Surgery, Cincinnati Children’s Hospital Medical Center, 3333 Burnet Ave, MLC 2004, Cincinnati, OH 45229-3039 (Email: pirooz.eghtesady{at}cchmc.org).

BACKGROUND: Mechanisms leading to left ventricular hypoplasia and endocardial fibroelastosis in the fetus remain unknown. Prevailing theory is that obstruction to blood flow through the left ventricle leads to elevated end-diastolic pressures, compromised myocardial perfusion, and endocardial ischemia. Fetal interventions are now being performed, based on the presumption that they would prevent such pathogenic mechanisms.

METHODS: Forty first-trimester fetal sheep (mean gestational age, 53 days) were studied. Severe fetal left ventricular outflow obstruction was created by banding the ascending aorta in 25 fetuses; 15 control fetuses underwent "sham" surgery with thoracotomy. Serial fetal echocardiography was used to assess left ventricular growth and fetal hemodynamics. Findings were correlated to morphologic and histopathologic changes, and intracardiac pressure measurements obtained from fetal cardiac catheterization.

RESULTS: Surviving banded fetuses (n = 13) had one of two phenotypes: compensatory left ventricular hypertrophy (n = 7) or noncompensatory left ventricular dilatation (n = 6) with hydrops and severe left ventricular dysfunction. All fetuses had elevated left ventricular end-diastolic pressures (mean, 21 mm Hg; range, 14 to 28 mm Hg), which correlated to the gradient across the ascending aorta (mean, 41 mm Hg; range, 28 to 73 mm Hg). In vivo echocardiography findings were incongruous with those at autopsy, and demonstrated preservation of left ventricular growth indices in all fetuses. Endocardial fibroelastosis and myocardial fibrosis were not observed in any banded fetus.

CONCLUSIONS: While early gestational obstruction to flow can compromise left ventricular function in the fetus, it does not retard normal growth. Similarly, an elevated left ventricular end-diastolic pressure is not sufficient to cause myocardial fibrosis or endocardial fibroelastosis in the fetus.