The researchers will present their findings from this and other studies at the American Heart Association Scientific Sessions 2005 Nov. 13 through 16 in Dallas. They are pursuing a variety of approaches to interrupt the complex processes leading to plaque formation and rupture, seeking new ways to treat and even prevent atherosclerosis.
Apolipoprotein A-I (apo A-I) is a protein that becomes part of HDL, or "good" cholesterol. About 25 years ago, a family in northern Italy was found by Italian researchers to have a mutation in the gene responsible for making the protein. The mutant form (apo A-I Milano) appeared to protect its carriers from cardiovascular disease. In 1994, Cedars-Sinai researchers led by Prediman K. Shah, M.D., director of the Division of Cardiology and the Atherosclerosis Research Center, showed for the first time that intravenous injection of a genetically engineered form of the protein markedly reduced arterial plaque buildup in animals fed a high cholesterol diet. A series of subsequent studies in genetically engineered mice conducted in Shah's laboratory confirmed the potent effects of apo A-I Milano protein on prevention and reversal of plaque build-up.
Based on the results of Shah's studies, a clinical trial was conducted in humans with similar results. After five weeks of once-a-week injections, apo A-I Milano significantly shrank plaque in coronary arteries. The protein appeared to actually remove bad cholesterol, e
Contact: Sandy Van
Cedars-Sinai Medical Center