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Antibiotics Don't Fight Heart Disease

Two studies find no effect from drugs meant to fight chronic infection

WEDNESDAY, April 20, 2005 (HealthDay News) -- A theory that looked good in the laboratory -- that giving antibiotics to people with cardiac problems would reduce the risk of heart attack or stroke -- has failed in real-life trials.

Heart patients who also had long-term infections with Chlamydia pneumoniae, a bacterium that causes respiratory illness, did no better when given regular doses of antibiotics than patients who did not get the drugs, according to two studies in the April 21 issue of the New England Journal of Medicine.

Chlamydia pneumoniae is different from the better-known Chlamydia that is one of the most common sexually transmitted infectious agents. Infection with C.pneumoniae, as it is formally called, is much more common, with more than 80 percent of Americans carrying antibodies to the bug, explained Dr. Christopher P. Cannon, a cardiologist at Brigham and Women's Hospital who helped conduct one of the studies.

C.pneumoniae infection usually causes transient symptoms, similar to those of the common cold, but then the bacterium takes up permanent residence in the body, where it can harm arteries.

"This is a foreign substance that the body reacts to," Cannon said. "It gets into the arteries and creates inflammation that can help plaque rupture."

Arterial plaque is comprised of cholesterol-rich fatty deposits that can clog arteries. A heart attack, stroke or other major cardiovascular event can occur when a plaque ruptures, blocking an artery.

Experts have long theorized that medications that cut chronic infection might cut heart disease risks, too.

The Brigham and Women's trial included nearly 4,200 people who had been hospitalized for such an event. Half of then were given regular doses of the antibiotic gatifloxacin for two years, and the other half got a placebo. There was a slight reduction in deaths and severe cardiovascular events for those who got the antibiotic, but it was not even close to being statistically significant -- 23.7 percent for the antibiotic group, 25.1 percent for the placebo group.

Maybe antibiotic treatment is just too little and too late for these people, Cannon said. People hospitalized for heart conditions usually have a variety of risk factors, such as high cholesterol levels or high blood pressure, and perhaps "trying to treat one part of the problem doesn't have a big impact," he speculated.

Another explanation is that a Chlamydia infection might help start the process of artery blockage, "but then 20 or 30 or 40 years later, it is too late to treat the problem," Cannon said.

The second study, led by researchers at the University of Washington, used a different antibiotic, azithromycin, and had a different patient population, 4,012 people with stable coronary artery disease. Again, a four-year follow-up found no difference in the occurrence of coronary events such as heart attacks between those who got the drug and those who got a placebo.

Dr. J. Thomas Grayston, an emeritus professor of epidemiology who led the study, was philosophical about the outcome.

"The trails were not really designed to study whether Chlamydia pneumoniae was involved in heart disease," he said. "Instead, we jumped over to see if antibiotics worked. If they did, there would be a tremendous upside. If not, it was a trial that did no-one harm."

In explaining the results, "there are two possibilities," said Dr. Jeffrey L. Anderson, a professor of medicine at the University of Utah who wrote an accompanying editorial and has done laboratory studies of Chlamydia and heart disease. "One is that this whole idea of infection increasing the risk of heart disease and stroke is wrong. More likely, we've taken the wrong approach. Giving antibiotics to everyone isn't going to work."

Studies in real life and the laboratory support the infection-heart disease link, Anderson said. Several papers have found an increased incidence of heart attack and stroke in the weeks after people have an infection. And animal studies done in Anderson's lab found that the process of artery blockage was accelerated in rabbits infected with Chlamydia who were fed a high-fat diet.

"But maybe we just used the wrong antibiotics or the disease was so advanced that it was just too late" in the human trials, Anderson said. Or maybe Chlamydia hides so well in arterial plaque that the antibiotic can't get to it, he said.

In any case, it's back to the drawing board, Anderson said: "We have got to figure out how the risk occurs and how to reduce it."

Maybe intervention has got to begin much earlier, Cannon said. "One intriguing idea is that if we had a vaccine that prevented infection in the first place, it might reduce the damage," he said. "But that is something that is not easily created or tested."

More information

A fact sheet on Chlamydia pneumoniae is offered by the U.S. Centers for Disease Control and Prevention.

SOURCES: Christopher P. Cannon, M.D., cardiologist, Brigham and Women's Hospital, Boston; J. Thomas Grayston, M.D., emeritus professor, epidemiology, University of Washington, Seattle; Jeffrey L. Anderson, professor, medicine, University of Utah, Salt Lake City; April 21, 2005, New England Journal of Medicine
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