Editing Intrauterine growth restriction (section)

=== Cardiovascular ===
In IUGR, there is an increase in [[vascular resistance]] in the placental circulation, causing an increase in cardiac [[afterload]]. There is also increased [[vasoconstriction]] of the arteries in the periphery, which occurs in response to chronic [[Hypoxia (medical)|hypoxia]] in order to preserve adequate blood flow to the fetus' vital organs.<ref>{{Cite journal|last1=Cohen|first1=Emily|last2=Wong|first2=Flora Y.|last3=Horne|first3=Rosemary S. C.|last4=Yiallourou|first4=Stephanie R.|date=June 2016|title=Intrauterine growth restriction: impact on cardiovascular development and function throughout infancy|journal=Pediatric Research|volume=79|issue=6|pages=821–830|doi=10.1038/pr.2016.24|issn=1530-0447|pmid=26866903|doi-access=free}}</ref> This prolonged vasoconstriction leads to remodeling and stiffening of the arteries, which also contributes to the increase in cardiac afterload. Therefore, the fetal heart must work harder to contract during each heartbeat, which leads to an increase in wall stress and cardiac [[Ventricular hypertrophy|hypertrophy]].<ref name=":0">{{Cite journal|last1=Malhotra|first1=Atul|last2=Allison|first2=Beth J.|last3=Castillo-Melendez|first3=Margie|last4=Jenkin|first4=Graham|last5=Polglase|first5=Graeme R.|last6=Miller|first6=Suzanne L.|date=2019|title=Neonatal Morbidities of Fetal Growth Restriction: Pathophysiology and Impact|journal=Frontiers in Endocrinology|volume=10|pages=55|doi=10.3389/fendo.2019.00055|issn=1664-2392|pmc=6374308|pmid=30792696|doi-access=free}}</ref> These changes in the fetal heart lead to increased long-term risk of [[hypertension]], [[atherosclerosis]], cardiovascular disease, and [[stroke]].<ref name=":0" />