DALLAS, Nov. 9 -- Individuals with unstable angina who have higher levels of a protein associated with inflammation are more likely to have a heart attack than individuals with lower levels, according to a study in today's Circulation: Journal of the American Heart Association.
The substance called C-reactive protein -- CRP -- circulates in the blood. Levels of the protein rise when the body is fending off an infection. Previous studies indicate that men with high levels of CRP have triple the risk of heart attack and double the risk of stroke compared to men with lower CRP levels. In women, studies have shown that elevated levels of CRP may increase the risk of a heart attack by as much as seven times.
Oscar O. Bazzino, M.D., chief of cardiology at the Italian Hospital of Buenos Aires in Argentina and lead author of the study, says the research is the first to demonstrate the independent value of CRP in individuals who are medically stabilized after an episode of severe chest pain caused by blockages in a blood vessel of the heart. Individuals with the condition, called unstable angina, are at high risk for developing a heart attack or stroke.
The study included 105 unstable angina patients admitted to the Italian Hospital.
Individuals with unstable angina and high levels of CRP -- greater than 1.5 milligrams per deciliter -- had nearly double the risk of heart attacks within 90 days of hospital discharge compared to patients with lower CRP levels. The findings provide new insight into CRP, a substance that in recent years has been recognized as a possible risk factor for heart disease and stroke. Researchers have suggested that the blockages in blood vessels, called plaque, are collections of cellular components, including CRP. Thus the amount of CRP in the blood may be a sign of severe atherosclerosis, the disease process that leads to heart attacks and strokes.
The patients in the study were hospitalized for an average of eight
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Contact: Carole Bullock
caroleb@heart.org
214-706-1279
American Heart Association
7-Nov-1999