A Non-Surgical Alternative for Those with Peripheral Arterial Disease?

Clinical Trials of rFGF-2 Will Show If New Protein Stimulates Growth of Collateral Arteries

Robert J. Lederman

For millions of Americans, simple walking can become an unpleasant experience because their legs don’t receive enough blood. This is often due to peripheral arterial disease — a chronic condition in which arteries supplying blood to the legs become blocked by a build-up of plaque. The restricted blood flow causes a painful, debilitating condition called claudication, which is similar to angina experienced by people with certain types of heart disease. Claudication is also a marker for serious atherosclerotic disease elsewhere, including the brain and the heart.

Peripheral arterial disease affects more than six million Americans. Although not fatal in itself, individuals with it may die of complications of coronary artery diseases and, less often, of complications of cerebrovascular disease. Now, researchers at the Medical School are studying a new growth protein that shows promise in stimulating the body to grow new blood vessels. They hope to determine if the protein, called recombinant fibroblast growth factor-2 (rFGF-2), can help increase blood flow to the legs by encouraging the growth of collateral arteries around the blockage — in essence, stimulating the growth of natural by-passes.

Investigators in the Therapeutic Angiogenesis Program hope to determine if rFGF-2 and similar proteins that promote new blood vessel growth can provide a non-surgical alternative for those with peripheral artery disease. The study is called TRAFFIC (Therapeutic Angiogenesis of rFGF-2 for Intermittent Claudication), and the Medical School is one of two institutions coordinating the trial, which will be conducted at 20 U.S. medical centers.

RFGF-2 is a genetically engineered form of a protein produced naturally in humans that stimulates the growth of new blood vessels. The protein has shown promise in recent studies at the U-M as a potential treatment for angina in patients with coronary artery disease. Previous investigations of rFGF-2 showed that it stimulated the growth of new blood vessels in animals, and earlier clinical studies showed that it was well tolerated by humans across a wide range of doses.

“This study is the largest one to date examining therapeutic angiogenesis as a therapy for peripheral artery disease,” says Robert J. Lederman, M.D., an interventional cardiologist and assistant professor of internal medicine. Lederman serves as the national co-principal investigator on the study. “Therapeutic angiogenesis is very exciting because there is great potential to improve severe and debilitating symptoms in patients who are not eligible for conventional surgical or catheter-based treatments.”

More information about the Michigan Therapeutic Angiogenesis Program is available on the Web at: http://www.med.umich.edu/tap/.

Lederman can be contacted at rlederma@umich.edu.