A heart attack — it starts with a blockage. A clot limits blood flow to the heart muscle, and soon, that muscle starts to die.
“Those cells start to die because of lack of oxygen, and they put off signals that attract white blood cells into the heart tissue,” said Dr. Stephen Miller, a Northwestern medicine researcher, microbiology and immunology,
Their job is to clean up and cart away the dead cardiac cells. But, initially, the white blood cells make matters worse. They produce a chemical that boosts inflammation in the already damaged area.
In their lab, Northwestern medicine researchers Stephen Miller and Rachael Terry created a diversion. They used microparticles so tiny you can’t see the thousands contained in these vials.
“They have to be a certain size and characteristic in order to work. The most important characteristic is they have to have a negative charge,” Miller said.
Attracted to the negative charge, the white blood cells gobbled up the microparticles, then changed direction.
“If we inject microparticles within 24 hours of inducing a heart attack in an animal model, the microparticles are uptaken by the inflammatory cells in the blood and they are then detoured so they don’t go to the heart and increase damage but instead they detour themselves to the spleen, where they end up dying,” Miller said.
The results in their animal study were promising.
“We reduced the tissue damage by 40 to 50 percent by administering these particles for four consecutive days starting 24 hours after the induced heart attack. We also measured the pumping action of the heart and showed the pumping action was maintained at a much higher level in animals treated with the particles versus those that were not,” Miller said.