Heart attack damage slashed with micro particle therapy

First therapy to target damage after heart attack could transform field.  After a heart attack, much of the damage to the heart muscle is caused by inflammatory cells that rush to the scene of the oxygen-starved tissue. But that inflammatory damage is slashed in half when microparticles are injected into the blood stream within 24 hours of the attack, according to new preclinical research from Northwestern Medicine® and the University of  Sydney in Australia.

When biodegradable microparticles were injected after a heart attack, the size of the heart lesion was reduced by 50 percent and the heart could pump significantly more blood.

“This is the first therapy that specifically targets a key driver of the damage that occurs after a heart attack,” said investigator Daniel Getts, a visiting scholar in microbiology-immunology at Northwestern University Feinberg School of Medicine. “There is no other therapy on the horizon that can do this. It has the potential to transform the way heart attacks and cardiovascular disease are treated.”

The micoparticles work by binding to the damaging cells — inflammatory monocytes — and diverting them to a fatal detour. Instead of racing to the heart, the cells head to the spleen and die.

The particles are made of poly (lactic-co-glycolic) acid, a biocompatible and biodegradable substance already approved by the Food and Drug Administration for use in re-absorbable sutures. A microparticle is 500 nanometers, which is 1/200th size of a hair.

The scientists’ study showed the microparticles reduced damage and repaired tissue in many other inflammatory diseases. These include models of West Nile virus, colitis, inflammatory bowel disease, multiple sclerosis, peritonitis and a model that mimics blood flow after a kidney transplant.

“The potential for treating many different diseases is tremendous,” said investigator Stephen Miller, the Judy Gugenheim Research Professor at Feinberg. “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 Nicholas King, professor of viral immunopathology at the University of Sydney School of Medical Sciences, are corresponding authors on the paper, which will be published January 15 in Science Translational Medicine.

Contact: Marla Paul
marla-paul@northwestern.edu