In a report that went online in the "rapid track" portion of the website of Circulation, the journal of the American Heart Association, today, Dr. Lawrence Chan, chief of the BCM division of diabetes, endocrinology and metabolism, and members of his laboratory said that when mice genetically prone to develop atherosclerosis also produced a human form of C-reactive protein, they developed larger lesions associated with the buildup of fatty plaque in the arteries than did those who did not produce the protein.
"Our study supports the use of C-reactive protein as a marker of risk for heart disease," said Chan. "Not only that, but it identifies at least one mechanism by which the protein contributes to the development of atherosclerosis." He said this is the first time these facts have been demonstrated in living animals.
Atherosclerosis is associated with deposits of fatty plaque in the walls of arteries. When this significantly narrows the heart's arteries, patients face an increased risk of heart attack.
C-reactive protein is an indication that there is inflammation in the body. When its levels are high, physicians suspect that an individual's risk of developing heart disease is equally elevated. Chan and his colleagues, including Dr. Antoni Paul, a postdoctoral fellow at BCM who did most of the laboratory analysis, identified high levels of an arterial wall cell surface protein called angiotensin type 1 receptor in the atherosclerotic deposits in the mice that expressed C-reactive protein. Mice that lacked C-reactive protein had lower levels of the receptor.
High levels of the receptor make cells more susceptible to inflammatory attack, said Chan. Some medications now used to treat heart disease block a form of angiotensin receptor and could be more effective in individuals with high levels of C-reactive protein, he said.
Further research will be needed to confirm that, he said.