Quick treatment with a new "microparticle" therapy might significantly reduce the damage caused by a heart attack, according to a new study conducted in mice.
After a heart attack, much of the damage to the heart muscle is caused by inflammatory cells called macrophages that hurry to the site of the oxygen-starved tissue, the researchers said.
However, the researchers found that injecting biodegradable microparticles into the bloodstream of mice within 24 hours after a heart attack reduced inflammation-related damage by 50 percent, enabling the heart to pump much more blood.
The researchers said the microparticles bind to the inflammatory cells and divert them to the spleen, where they die away. The particles are made of poly (lactic-co-glycolic) acid, a biodegradable substance already approved by the U.S. Food and Drug Administration for use in re-absorbable sutures.
The study was published Jan. 15 in the journal Science Translational Medicine.
"This is the first therapy that specifically targets a key driver of the damage that occurs after a heart attack," study author Daniel Getts, a visiting scholar in microbiology and immunology at Northwestern University's Feinberg School of Medicine, said in a university news release.
"There is no other therapy on the horizon that can do this," Getts said. "It has the potential to transform the way heart attacks and cardiovascular disease are treated."
Two heart experts said the approach does hold promise.
Dr. Barbara Sherry, head of the Center for Immunology & Inflammation at the Feinstein Institute for Medical Research, in Manhasset, N.Y., called the work "very exciting."
"The power of this approach lies in the fact that it targets the inflammatory macrophage itself, redirecting this major source of inflammatory mediators away from the inflamed tissues," she said. Sherry cautioned, however, that trials in humans will be key to seeing if the therapy truly works.
"It will be important to consider the impact of this approach on immune function," she said. "Will patients receiving this therapy have [weakened immune systems] and therefore be susceptible to other infections?"
Dr. Roger Hajjar, director of the Cardiovascular Research Center at Icahn School of Medicine at Mount Sinai, in New York City, echoed that concern. "The therapeutic potential of these immune modifying particles is great," Hajjar said.
He added, however, that "with immune modulation, one has to be careful, especially in the setting of heart muscle damage."
Getts and his colleagues also said the microparticles reduced damage and repaired damaged tissue linked to many other inflammatory diseases, including West Nile virus infection, colitis, inflammatory bowel disease and multiple sclerosis.
"The potential for treating many different diseases is tremendous," Stephen Miller, a research professor at Northwestern, said in the news release. "In all these disease models, the microparticles stop the flood of inflammatory cells at the site of the tissue damage, so the damage is greatly limited and tissues can regenerate."
Getts, Miller and their colleagues have teamed with a startup company to produce a refined version of the microparticles and hope to begin a clinical trial with heart attack patients within two years.