Abnormal cells may signal hidden heart risk
Damage to blood vessel lining shows up in blood tests
Many people who go to a hospital with chest pain don’t end up having a heart attack. A new study that identifies certain abnormal cells in patients’ blood might lead to screening tests to spot those who remain at risk, despite passing standard diagnostic tests.
In people experiencing the opening throes of a heart attack, cells from the inner lining of blood vessels — called endothelial cells — get set adrift in the bloodstream, researchers report in the March 21 Science Translational Medicine. Heart attack patients have higher numbers of these endothelial cells in their blood than healthy people, and the patients’ cells take abnormal shapes, says Eric Topol, a cardiologist at Scripps Research Institute in La Jolla, Calif.
“These are sick cells that have been subjected to profound inflammation,” he says.
Topol and his colleagues found the abnormal cells using a new technology that sorts blood cells so well that it can detect a single endothelial cell among millions of blood cells. The researchers obtained blood samples from 50 people with a median age of 58.5, as they arrived at a hospital with chest pains that turned out to be heart attacks. The scientists also tested blood from 44 younger healthy volunteers and from 10 healthy people age-matched to the heart attack patients.
The blood test found four times as many circulating endothelial cells in the heart attack group as in the healthy volunteers. The unusual cells also clustered together and often contained multiple nuclei.
“This is a fascinating insight,” says cardiologist Christopher Boos at Poole Hospital in Dorset, England. “But this is very much in the exploratory phase,” he adds, since the researchers have yet to prove that the abnormal cells come from the coronary arteries. Heart attacks occur when plaque in the coronary arteries tears loose, forming a blood clot that can clog the arteries and disrupt blood flow to the heart muscle.
But sometimes, Topol says, a person gets chest pain but shows no other evidence of a heart attack. The patient’s heart rhythm is good, blood flow to the heart muscle is adequate and blood analysis shows no telltale signs of dying heart cells. In these people, the body has often dissolved a clot before any of that damage could occur, Topol says.
In future studies, he hopes to study whether these people have abnormal endothelial cells in circulation. Evidence of that would suggest an unstable coronary plaque — a heart attack still waiting to happen.
“Discovering unstable plaques,” Boos says, “is one of the key unmet needs of cardiology.”
The new study looked for the misshapen endothelial cells themselves. But a test for use in the clinic, Topol says, would more likely search for a gene or protein signature of these abnormal cells to spot at-risk patients who could then be prescribed aspirin or other anti-clotting drugs.