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New Clue to Sudden Coronary Death WEDNESDAY, December 10, 2003 (HealthDayNews) — An exquisitely detailed study of tissue from people who died suddenly of coronary disease reveals an unexpected mechanism of death — one that could be manipulated to reduce the risk of those deaths, pathologists say. Sudden death can occur when one of the fatty deposits called plaques that build up in artery walls ruptures, spewing debris that blocks the blood vessel and stops blood flow to the heart or brain. Analysis of plaque from 24 people who died suddenly of coronary causes shows fatal ruptures can occur when tiny blood vessels that have grown into the plaque burst, researchers at the Armed Forces Institute of Pathology report in the Dec. 11 issue of the New England Journal of Medicine. Several mechanisms that can cause plaque rupture have been known, says study author Frank D. Kolodgie, a research scientist at the institute. They include inflammation, the sudden breakdown of cells, or an excess buildup of fats in the plaque. The new study shows that hemorrhages of the blood vessels that invade plaques can cause them to rupture, Kolodgie says. That finding makes angiogenesis, the process of blood vessel growth, a possible target of treatment. "If you can prevent angiogenesis, you may be able to stabilize those plaques so they are less prone to rupture," Kolodgie says. When he and his colleagues tested plaques from the coronary patients, they looked for a molecule called glycophorin A and for excess amounts of iron, both of which are signals of a hemorrhage. Both were found in plaques that were the most unstable and most likely to rupture. To verify the finding, the researchers force-fed rabbits with fat-rich foods to stimulate formation of plaques in their arteries. Analysis of the rabbit plaques gave results similar to those found in the human samples, the researchers say. The new study links the buildup of fats inside a plaque to the tiny blood vessels that invade the plaque, says Dr. Donald D. Heistad, professor of cardiology at the University of Iowa, who wrote an accompanying editorial. "When these blood vessels burst, they release red blood cells into the plaque," Heistad explains. "Red blood cells themselves have lots of fat in their membranes. So, a lot of the fat in the core of a plaque before it ruptures may come from these blood cells." Until now, harmful angiogenesis has been of interest primarily in cancer. Dr. Judah Folkman of Harvard Medical School has proposed that cancers can be treated by stopping angiogenesis, so tumors are starved of the blood they need to grow. The idea of stopping angiogenesis in heart patients collides with one current aim of gene therapy for heart disease, to stimulate the growth of new blood vessels to keep blood flowing to the heart and brain when arteries become clogged, Heistad says. "You can worry that these studies can be harmful," he says. "The good part is that you might stimulate the growth of blood vessels where they are needed. The bad part is that you may stimulate growth of blood vessels in plaque, where they may be harmful." SOURCES: Frank D. Kolodgie, Ph.D., research scientist, Armed Forces Institute of Pathology, Washington, D.C.; Donald D. Heistad, M.D., professor, cardiology, University of Iowa, Iowa City; Dec. 11, 2003, New England Journal of Medicine; American Academy of Family Physicians; American Heart Association.

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