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| Vol. 22, No. 21 |
| November 15, 2000 |
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Missing Link Connects Inflammation to Heart Attack By TANYA DEASON-SHARP The University of Texas M. D. Anderson Cancer Center
Research published in the Oct. 31 issue of the American Heart Association journal Circulation provides a crucial missing link connecting inflammation to heart attack. Researchers have determined that the C-reactive protein, or CRP, can directly activate human coronary endothelial cells, which line the blood vessels. This finding suggests that CRP is not merely a marker of inflammation, but also plays a direct role in some heart attacks. Researchers say healthy men and women who go on to have heart attacks are likely to have high levels of CRP in their blood, which signals silent inflammation. However, it remains a mystery why a marker of inflammation can be such a strong predictor of risk. "We knew that people who have elevated levels of CRP in their blood frequently have an increased risk of coronary events," said Dr. Edward T. H. Yeh, newly appointed chairman of the Department of Cardiology at The University of Texas M. D. Anderson Cancer Center. "Now we know the relationship between CRP and endothelial cells in bringing about heart attacks." In the study, conducted by a team of researchers at The University of Texas Health Science Center at Houston and led by Dr. Yeh, endothelial cells from human coronary arteries were cultured and exposed to CRP at levels frequently observed in patients with unstable angina. The endothelial cells were examined with a fluorescence-activated cell sorter 24 hours later. Dr. Yeh said the cells showed a marked increase in three cell adhesion molecules, which are Velcro-like proteins that recruit circulating immune cells from the blood to enter the wall of the arteries. These immune cells can then damage the artery wall, which ultimately precipitates a heart attack. "This discovery produces the smoking gun linking CRP to heart attack," said Dr. Yeh. "These findings are of special interest because blocking CRP's influence on the endothelial cells may become a new way of preventing and treating heart attacks in the future." Dr. Yeh said further studies are needed to determine the basic mechanism whereby CRP activates endothelial cells. This study was conducted by Dr. Yeh and UT-Houston co-authors Dr. James T. Willerson, interim president, and Dr. Vincenzo Pasceri, research fellow, who also are affiliated with the Texas Heart Institute. Dr. Yeh recently joined M. D. Anderson's faculty as chairman of the new cardiology department. The new department, formerly a section of the internal medical specialties department, will significantly expand the scope of cardiology services offered at M. D. Anderson. While cancerous tumors in the heart are fairly rare and make up a small fraction of the cardiology department's patient load, a large number of cancer patients who come to M. D. Anderson need cardiology expertise. They may have co-existing heart problems that must be treated before they can embark on rigorous courses of radiation therapy or chemotherapy, invasive surgery or bone marrow transplantation. Cancer patients also may experience heart problems after certain procedures, such as an operation to remove a lung or treatments involving certain drugs. Dr. Yeh said his department will not only care for those patients, but also will conduct clinical research to determine which patients are most susceptible to such complications and develop protocols to minimize such risks for future patients. ©2006 Texas Medical Center E-Mail: tmcinfo@texmedctr.tmc.edu URL: http://www.tmc.edu/tmcnews/11_01_00/page_06.html |