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ShareJune 11, 2003 — DALLAS, June 10 – Italian researchers have found another link between inflammation and heart disease, they report in today’s rapid access issue of Circulation: Journal of the American Heart Association.
A protein that promotes inflammation and immune responses known as Chlamydia pneumonia heat shock protein 60 (Cp-HSP60) appears to be a strong indicator of heart disease and may lead to new ways to identify people at risk for it, says lead author Luigi Marzio Biasucci, M.D., assistant professor of cardiology, Catholic University of Rome.
“Ninety-nine percent of patients with acute coronary syndrome tested positive for Cp-HSP60 in their blood,” he says.
Acute coronary syndrome (ACS) characterizes patients with angina (chest pain) typically caused by atherosclerotic plaque disease or heart attack. ACS represents the more severe forms of coronary atherosclerosis.
Researchers studied 219 patients admitted to a coronary care unit with acute coronary syndrome, 40 patients with stable angina who were free of chest pain for two weeks or more and 100 healthy volunteers (controls) matched for age, sex and risk factors. Blood samples were analyzed from all subjects at baseline and samples were taken again from 41 ACS patients an average of 350 days later.
Ninety-nine percent (217) of ACS patients were positive for Cp-HSP60, while only 20 percent of the stable angina patients were positive and no controls were positive for the protein, Biasucci says.
Researchers also tested for high sensitivity C-reactive protein (CRP) – a marker of inflammation recently linked with heart disease – and discovered that elevated CRP was “found in 60 percent of acute coronary syndrome patients, in 25 percent of the stable angina patients and in 8 percent of the healthy controls,” he says.
The test was 99 percent effective in finding Cp-HSP60 and 94 percent accurate in ruling out the presence of Cp-HSP60. Biasucci adds that the antibody test cannot differentiate between unstable angina and heart attack because there was no difference in the Cp-HSP60 antibody levels between the two heart problems. When researchers rechecked the 41 patients about a year later, the Cp-HSP60 levels had dropped substantially, suggesting that Cp-HSP60 spikes during acute episodes and drops when the heart is stabilized.
Biasucci notes that many researchers have been searching for a link between heart disease and infection. “Heat shock proteins might supply that linkage,” he says. But there are still several unanswered questions, including why elevations in Cp-HSP60 don’t appear to correspond to active Chlamydia pneumonia infection, he says.
Cp-HSP60 is very similar to another group of heat shock proteins called human (hu) HSP60 and this may explain the contradiction, he says.
“It is possible that the antibodies to Cp-HSP60 that we are detecting are actually an immune response against hu-HSP60,” he says.
He concludes that while it appears that Cp-HSP60 could be a useful marker for acute coronary syndrome, its effectiveness must be confirmed in larger studies.
Co-authors are Giovanna Liuzzo, M.D., Ph.D.; Alessandra Ciervo, Ph.D.; Andrea Petrucca, M.D.; Maddalena Piro, M.D.; Dominick J. Angiolillo, M.D.; Filippo Crea, M.D.; Antonio Cassone, M.D. and Attilio Maseri M.D.
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The above story is reprinted from materials provided by American Heart Association.
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