© 2005 by BMJ Publishing Group & British Cardiac Society
MINI-SYMPOSIUM
Response of the fetal heart to changes in load: from hyperplasia to heart failure
Correspondence to:
Correspondence to:
Dr Helena M Gardiner
Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College, Queen Charlottes and Chelsea Hospital, Du Cane Road, London, W12 ONN, UK; helena.gardiner@imperial.ac.uk
Keywords: fetal heart; hyperplasia; heart failure
| The first 150 words of the full text of this article appear below. |
The fetal circulation works in parallel with the dominant right ventricle, ejecting approximately 60% of the combined ventricular output. Three important communications exist between the two circulations (oval foramen and the arterial and venous ducts) that influence loading conditions. In particular, the determinants of fetal left ventricular filling differ considerably from those seen in the adult heart. Pulmonary venous return contributes only a small proportion to left ventricular preload because of the relatively low pulmonary blood flow in fetal life (rising from an estimated 11% to 25% of right ventricular output by the third trimester).1 Left ventricular filling depends predominantly on patency of the oval foramen to allow the relatively oxygen-rich blood returning from the placental circulation, via the umbilical vein and venous duct, to stream through the right atrium and enter the left side of the heart.2 The right ventricle fills from mostly upper body systemic venous return and
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