- Being born extremely early affects blood vessel cell development, and may explain why adults born pre-term are at increased risk of high blood pressure.
Embargoed until 4 p.m. ET, Thursday, Sept. 15
ORLANDO, Florida, Sept. 15, 2016 – Abnormalities in a type of cell involved in blood vessel development and healing may explain why adults who were born prematurely are at increased risk of high blood pressure and other heart alterations, according to new research presented at the American Heart Association’s Council on Hypertension 2016 Scientific Sessions.
Researchers at the University of Montreal compared the function of endothelial colony-forming cells (ECFCs) – which help maintain healthy blood vessels – taken from 30 young adults (21-28 years old) born very preterm (less than 29 weeks gestation) and 30 young adults born at term (37 or more weeks gestation). Among the findings:
- In lab tests, the cells from preterm adults were slower to form colonies, a key step in forming new capillaries;
- In preterm adults, slower colony formation was associated with two risk factors of heart disease, a higher systolic (top number) blood pressure and enlargement of the heart’s left pumping chamber.
Abnormal function of ECFCs has also been associated with early complications of preterm birth. For example, prolonged oxygen therapy exposure and consequent development of lung disease.
Co-authors include Mariane Bertagnolli, Ph.D.; Marie-Amelie Lukaszewski, Ph.D; Ying He, M.Sc.; Anik Cloutier, M.Sc.; Rong Wu, M.D.; Jean-Luc Bigras, M.D.; Bernard Thebaud, M.D.; Thuy Mai Luu, M.D.; and Anne Monique Nuyt, M.D.
This study was funded by an investigator-initiated research award from Merck Sharpe Dohme/University of Montreal.
Note: Actual presentation is 4:30 p.m. ET Thursday, September 15, 2016.
- Researcher photo, blood pressure and pregnancy images are located in the right column of this release link http://newsroom.heart.org/news/link-discovered-between-preterm-birth-and-risk-of-heart-disease?preview=d55810527d13be5e81275c79ff83d94e
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