MONDAY, April 26, 2004 (HealthDayNews) -- High blood levels of a protein called ST2 point to serious trouble in the weeks after a heart attack, Harvard researchers have found.
Now they're trying to figure out just what that means.
"We think ST2 levels are a barometer of how heart cells are doing," said study author Dr. Richard T. Lee, an associate professor of medicine at Brigham and Women's Hospital and Harvard Medical School. "We're trying very hard to figure out the biology behind this, to see why the heart is doing this -- whether it is trying to protect heart cells or making things worse."
The research appears in the April 27 issue of Circulation.
The journal report uses data on about 810 heart attack patients in two separate studies. It shows initial levels of ST2 were significantly higher in patients who died or who developed new or worsening congestive heart failure in the 30 days after the heart attack.
The risk was directly proportional to ST2 blood levels, the study found. The 25 percent of patients with the highest blood levels were seven times more likely to die within 30 days of a heart attack than the 25 percent with the lowest levels. The risk of either death or heart failure was four times greater for those with the highest levels.
ST2 and the cell receptors with which it interacts were identified only a few years ago, with much of the original work done in Japan.
"There has been an idea that it might be a receptor that would be targeted for diseases of the immune system," Lee said. "It is a close relative of other receptors in the immune system. But a lot of these things seem to overlap, so a finding in one part of the body starts to show itself in the heart."
The researchers believe heart muscle cells secrete one form of ST2 under stress -- during a heart attack, for example, when healthy heart muscle must work harder to make up for dying tissue.
It also appears the inflammation found in damaged heart tissue stimulates production of ST2 in neighboring cells, Lee said.
But the predictions based on ST2 levels are independent of those made by measurements of C-reactive protein, a marker of inflammation, and that is a good thing, he said.
"A blood test of one marker that shows the same thing as a test of another marker would not be very useful," Lee explained.
Eventually, measuring ST2 levels could help pick out heart attack patients at high risk of heart failure and other problems, but studies of the protein could provide more basic information about the heart and its reaction to trouble, he said.
"For us, the important thing is not only that lead to a blood test to improve patient care, but that it reveals a totally new pathway of how the heart is trying to protect itself," Lee said.