Inflamed arteries linked to heart attacks
September 1, 1997 2 minutes read
Inflamed arteries linked to heart attacks
Doctors can predict with some degree of accuracy about half the people who’ll eventually have heart attacks. They’re fairly certain high cholesterol levels contribute. But that other half who get heart attacks or strokes have normal cholesterol levels.
There may soon be a way to predict heart attack risk more accurately. And in addition, there may be a way to prevent heart attacks and stroke with antibiotics, vaccines, and anti-inflammatory drugs.
A recent study shows that chronic low-grade inflammation of the coronary arteries caused by a bacterial or viral infection may play an important role in causing heart attacks and stroke. An infection attracts disease-fighting white blood cells or monocytes to the blood vessel walls. These, in turn, release a host of chemicals that stimulate the growth of smooth muscle cells and contribute to the development of clogging deposits. Further studies are needed, but if the initial findings are borne out, someday there may be a test for the presence of infection that would serve as a long-range predictor.
A study reported in the April issue of New England Journal of Medicine drew upon the Physicians’ Health Study which has tracked 22,000 male doctors since 1982.1 An early outcome of the study demonstrated the dramatic effect of aspirin in reducing heart attacks. Data from this recent study, drawing on an evaluation of only a thousand men, provides insight into why aspirin is so effective its anti-inflammatory effects may exert a powerful preventive benefit.
Suspected culprits are the bacteria Chlamydia pneumoniae and Helicobacter pylori and the viruses cytomegalovirus and herpes simplex. Another theory is that the trigger for inflammation may not be an agent, but rather the atherosclerotic process itself.
Reference
1. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997; 336:973-979.
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