{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,13]],"date-time":"2026-03-13T19:28:56Z","timestamp":1773430136120,"version":"3.50.1"},"reference-count":41,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2013,6,26]],"date-time":"2013-06-26T00:00:00Z","timestamp":1372204800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["obgyn.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ultrasound in Obstet &amp; Gyne"],"published-print":{"date-parts":[[2013,8]]},"abstract":"ABSTRACT<\/jats:title>Objective<\/jats:title>To investigate the relationship between fetal heart defects and maternal serum placental growth factor (PlGF<\/jats:styled-content>), a marker of placental angiogenesis.<\/jats:p><\/jats:sec>Methods<\/jats:title>Maternal serum PlGF<\/jats:styled-content>, pregnancy\u2010associated plasma protein\u2010A (PAPP<\/jats:styled-content>\u2010A) and uterine artery pulsatility index (UtA\u2010PI<\/jats:styled-content>) at 11\u201313 weeks' gestation were compared in 68 cases of isolated fetal major heart defects and 340 normal controls. Variables were converted into multiples of the median (MoM<\/jats:styled-content>) after adjustment for gestational age, maternal age, racial origin, weight, parity and method of conception, and then compared between groups. The cardiac defects included 11 cases of obstruction of the left ventricular outflow tract (LVOT<\/jats:styled-content>), 25 conotruncal abnormalities and 32 valve defects.<\/jats:p><\/jats:sec>Results<\/jats:title>The median PlGF\u2010MoM<\/jats:styled-content> in the heart defect group was lower than in controls (0.80 (interquartile range (IQR<\/jats:styled-content>), 0.57\u20131.08) vs<\/jats:italic> 1.00 (IQR<\/jats:styled-content>, 0.79\u20131.32); P<\/jats:italic> < 0.0001). Low PlGF<\/jats:styled-content> levels were observed in the presence of conotruncal and valve defects but not in the presence of LVOT<\/jats:styled-content> defects. There was no significant difference between the group with fetal heart defects and controls in PAPP<\/jats:styled-content>\u2010A\u2010MoM<\/jats:styled-content> (0.95 (IQR<\/jats:styled-content>, 0.68\u20131.28) vs<\/jats:italic> 1.01 (IQR<\/jats:styled-content>, 0.70\u20131.39); P<\/jats:italic> = 0.292) or UtA\u2010PI\u2010MoM<\/jats:styled-content> (1.01 (IQR<\/jats:styled-content>, 0.84\u20131.28) vs<\/jats:italic> 0.99 (IQR<\/jats:styled-content>, 0.80\u20131.20); P<\/jats:italic> = 0.396).<\/jats:p><\/jats:sec>Conclusion<\/jats:title>In pregnancies with isolated fetal heart defects there is evidence of impaired placental angiogenesis in the absence of impaired placental perfusion and function. Copyright \u00a9 2012 ISUOG. 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