Medical doctors’ practices for fighting the plaque buildup in arteries that can cause strokes and heart attacks are based on at least a partially incorrect understanding of the fundamental nature of those plaques, according to new research from the University of Virginia’s School of Medicine published in the online journal Nature Medicine in May 2015. The findings may lead to revised treatments for atherosclerosis, also known as hardening of the arteries.
“The leading cause of death worldwide is complications of atherosclerosis,” said Gary Owens, PhD, director of UVA’s Robert M. Berne Cardiovascular Research Center, in a press release. “The most common end-stage disease is when an atherosclerotic plaque ruptures. If this occurs in one of your large coronary arteries, it’s a catastrophic event.
“Once a plaque ruptures, it can induce formation of a large clot that can block blood flow to the downstream regions. This is what causes most heart attacks. The clot can also dislodge and cause a stroke if it lodges in a blood vessel in the brain. As such, understanding what controls the stability of plaques is extremely important.”
Doctors believed that smooth muscle cells within the arteries helped deter the plaque buildup from dislodging. Those smooth muscle cells were thought to block the plaque as part of the body’s defense mechanism.
The researchers found that the plaque actually contains many of the smooth muscle cells — and they may make the plaque worse.
The researchers made the discovery by genetically tagging newly formed smooth muscle cells in mice and following them as atherosclerosis developed.