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Fatty plaque more likely to cause a heart attack than calcified plaque

DALLAS, Feb. 27 – In the first study of its kind, researchers found that lipid deposits within artery plaques have more structural stress – and are more likely to rupture – than plaques containing calcium, according to a report in today’s Circulation: Journal of the American Heart Association.

“Calcification does not seem to reduce the structural stability of coronary artery plaques, while higher lipid reservoirs carry a significantly higher risk of rupture,” says senior author Richard T. Lee, M.D., a researcher in the Cardiovascular Division of Brigham and Women’s Hospital, Harvard Medical School.

“Identifying factors that contribute to or break down the structural stability of arterial plaque will help cardiologists tag which patients are most at risk, and which is the optimal treatment to reduce this risk,” he says.

The researchers’ findings underscore the value of lipid-lowering therapies in preventing heart attacks. “Decreasing the extent of lipid build-up can dramatically lower internal stresses and prevent tearing of the plaque,” he says.

When arterial plaque deposits rupture and tear away the top of the plaque, the body reacts by forming blood clots on the ruptured area. If a clot blocks a coronary artery, it can result in a heart attack. If a carotid artery leading to the brain is blocked, it can cause a stroke. “Our study suggests that calcification may indicate more extensive or a more aggressive form of coronary artery disease, but the individual calcified plaque does not necessarily lead to a heart attack,” says Lee. “These results have potential implications for the evaluation of and intervention for coronary artery disease. Treatment to reduce cholesterol build-up in the arteries may be more useful than therapies that target the calcification of specific plaques.”

In an autopsy study, Lee and his colleagues compared the composition and structural integrity of plaques in 20 human coronary artery lesions, half of which were ruptured at the time of death. The arteries were obtained from 19 men and one woman, ages 35 to 86 years old. The team measured the amount of structural stress on calcified plaque versus fatty, or lipid-rich plaque. They made these measurements using a computerized structural analysis technique called finite element analysis – a standard engineering technique used to build planes and cars, etc. This technique is not often used in cardiology research, however researchers chose this method of analysis due to the complex nature of arterial plaque composition, says Lee.

According to the examinations, lipid material caused more stress on the artery lesions, making them more likely to rupture and cause a heart attack. The researchers found that fatty plaques were up to 25 percent less stable than calcified plaques. Cholesterol-lowering statin drugs can reduce the amount of lipids deposited on arterial walls and, thus, the risk of plaque rupture. In large trials, statins have been associated with 30-35 percent reductions in heart attacks and strokes. While the underlying preventive mechanism is unclear, researchers believe that the drugs reduce the fat content of plaques, making them more stable. “We need to understand how other factors like inflammation or infection weaken the plaque, since many patients will have heart attacks even though they are taking lipid-lowering medications,” says Lee.

Like the initial signs of atherosclerosis – fatty build-up in the artery walls – some plaque calcification begins at an early age, often in the teens. While the sequence of events leading to such calcification is not well understood, it has, until recently, been perceived as a passive process wherein calcium is absorbed from the blood into the plaque area. Recent studies have shown, however, that it is a regulated, organized process similar to bone formation, and animal studies suggest there might be a genetic component to the process. Co-authors include Hayden Huang, M.D.; Renu Virmani, M.D.; Hesham Younis, M.D.; Allen P. Burke, M.D.; and Roger D. Kamm, M.D.

American Heart Association. February 2001.

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