Richard T Lee

Updated:Mar 21,2011

Richard T. Lee, M.D.

Richard T LeeA study has determined that heart attack patients with the highest levels of a “stress” protein called ST2 found in cardiac cells were seven times more likely to die within 30 days after heart attack than patients with the lowest levels.  When death and heart failure rates were combined, those with the highest levels of ST2 had a four-fold increased risk of death or congestive heart failure compared to those with lower levels.

ST2 levels increase in patients after heart attack, peaking about 12 hours after the event.  Researchers had found that ST2 is associated with worse outcomes in non-ischemic heart failure, but until now, its predictive value in acute myocardial infarction (heart attack) had not been studied.

“The significance of the data is two-fold,” said Richard T. Lee, M.D., senior author of the study and associate professor of medicine at Brigham and Women’s Hospital and Harvard Medical School in Boston.  “First, the data suggest that this pathway of inflammation may occur in the early events of heart attack.  Second, ST2 levels provide a novel biomarker that can offer prognostic information on heart attack victims, independent of the usual clinical predictors.”

When other risk factors were controlled for such as age, blood pressure, heart rate and location of heart attack – the researchers found that increased levels of ST2 remained an independent predictor of death after heart attack.

“The big picture is that despite all the things we do for heart attack patients, some will go on to die or develop heart failure,” Lee said.  “We need more tools in our toolbox to not only pick out those patients who may do worse, but also to stop the development of heart failure.”

ST2 is associated with such heart cell stress as increased heart rate and higher systolic blood pressure.  Researchers also believe it is secreted under conditions of myocardial overload such as heart attack, when the remaining living heart muscle must work harder to make up for the dying tissue.  The inflammatory response of damaged tissues may further stimulate the production of the protein in neighboring cells.

“Heart muscle cells rapidly secrete one form of this protein when they become mechanically overloaded,” Lee said.  “When some heart muscle dies during the heart attack and the living heart muscle is stretched, the heart cells put out more ST2.”

A similar overload occurs during the progression of heart failure, where ST2 levels are associated with the patient’s prognosis.

While a blood test for ST2 may help predict the prognosis of patients after a heart attack, measuring ST2 will not help in diagnosing heart attacks, according to the researchers.  This is because not just heart muscle cells can secrete ST2.  For example, patients with asthma can also have increased levels of ST2 in their blood.

“We have a lot to learn, but we are excited about any new tool that could help in the prognosis of patients after a heart attack,” Lee said.

Lee received AHA Grant-in-Aid support from the Northeast Affiliate in 1992 and the National Center in 1996.  The AHA has also supported fellows training under Lee’s direction.