DALLAS, August 3 -- The ability of some individuals to develop new coronary arteries that help to re-route blood flow around artery blockages might be the result of their ability to produce a growth factor, a protein that helps to generate new blood vessels, according to a paper in Circulation: Journal of the American Heart Association.
Heart specialists have long been puzzled by the fact that some patients are able to form networks of new blood vessels, called coronary artery collateral beds, whereas other patients are not. A strong collateral blood supply can help reduce the severity of heart attacks, or even prevent them, experts say.
A team of Israeli researchers has identified a possible explanation for this phenomenon. They found that the ability to grow the new vessels in the heart strongly correlates with how much vascular endothelial growth factor (VEGF) a person produces when the heart muscle receives insufficient oxygen -- a condition called hypoxia.
The Israeli team studied 51 patients, all of whom had a blockage of 70 percent or greater in at least one coronary artery. The patients underwent diagnostic angiography -- an X-ray that shows where a narrowing has occurred in an artery. These angiograms also showed researchers the extent of collateral blood supply in each patient. The patients were then divided into three groups depending on the extent of their collateral beds. The levels of VEGF were also tested.
The researchers found no significant difference in the patients' ability to produce VEGF when cells received normal levels of oxygen. However, the patients differed markedly in VEGF production when the cells got insufficient oxygen. Those patients who produced the most VEGF during hypoxia also had the most extensive collateral blood supply.
This correlation of VEGF production with the number of collateral blood vessels
remained even after researchers considered factors that might adversely affect
the extent of coll
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Contact: Carole Bullock
caroleb@heart.org
214-706-1279
American Heart Association
2-Aug-1999