NEW ORLEANS, Nov. 12 In one of the largest follow-up studies to date, researchers have shown that gene therapy for heart disease may relieve chest pain and does not increase the risk for cancer, according to a study reported today at the American Heart Associations Scientific Sessions 2000. Since gene therapy is used to stimulate the growth of new blood vessels, there has been concern that therapy may lead to overgrowth of other cells in the body, increasing the risk for cancer or other problems.
Among 102 patients in the study, there were no significant differences in deaths, heart attacks or cancer over the course of one year, whether they received placebo or a high or low dose of the protein used in the gene therapy.
The long-term safety looks excellent, says lead author Timothy D. Henry, M.D., director of interventional cardiology at Hennepin County Medical Center and associate professor of medicine at the University of Minnesota in Minneapolis. There was no increase in adverse events, which some scientists have suggested might occur. If anything, it looks as if there is a lower rate of adverse events in patients getting the higher dose.
A new concept in heart research is that prodding new vessel growth will increase the blood flow to the heart in people whose arteries are narrowed by fatty deposits. Such deposits reduce the flow of blood and oxygen to the heart, which can cause chest pain known as angina. The deposits can also trigger heart attacks.
The protein, called vascular endothelial growth factor (VEGF), is produced by the body and initiates the growth of new blood vessels, a process called angiogenesis. VEGF is one of a number of proteins involved in vessel growth.
Researchers are exploring two ways to use it: One is gene therapy, in which the gene that commands cells to produce VEGF is introduced into heart cells, that will then produce the protein. The other approach, which Henry and his colleagues used, is to treat pa
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Contact: Maggie Francis or Carole Bullock
504-670-4000
American Heart Association
11-Nov-2000