Does tetracycline limit heart attacks?
A century ago, infections were suspected to lead to heart disease. With the advent of antibiotics, interest in this theory waned. In the past 2 decades, however, researchers have again begun searching for a tie between infections and atherosclerosis, the formation of fatty plaques in blood vessels.
In the late 1980s, Finnish scientists found that compared with healthy people, cardiac patients carried higher concentrations of antibodies signaling the presence of a bacterium called Chlamydia pneumoniae, which causes respiratory infections. That finding launched a flurry of research. Recently, preliminary studies in people who have had heart attacks show that those given antibiotics in addition to typical post-heart attack medicine fare better than those who don't get antibiotics.
Researchers now report in the Feb. 3 JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION another hint that certain antibiotics may prevent some heart attacks.
Heart attack patients are less likely than other patients to have taken a common antibiotic, tetracycline, within the past 3 years, says study coauthor Christoph R. Meier, an epidemiologist at Boston University Medical Center in Lexington. Tetracycline is the drug of choice against C pneumoniae and a variety of other pathogens.
Meier and his colleagues analyzed data from 3,315 heart attack patients and 13,139 patients without heart problems. All lived in the United Kingdom. Each heart patient was matched by age, sex, and date of antibiotic treatment with four noncardiac patients. In both groups, people were excluded if they were over 75 years old, were diabetic, had high blood pressure, or had a previous history of cardiovascular disease.
The comparison showed that heart attack patients were only two-thirds as likely to have used tetracycline as were the noncardiac patients. Use of most other antibiotics, including penicillin, was similar in both groups.
Although the study doesn't prove that tetracycline prevented heart attacks, it "provides another piece of evidence that implicates infection as a causative agent in cardiovascular disease," says Paul W. Ewald, an evolutionary biologist at Amherst (Mass.) College.
Moreover, Ewald says, people in this study were taking tetracycline, often at low doses, for a variety of diseases. Cardiac benefits might be greater if doctors were to prescribe doses specifically targeted to C. pneumoniae, he says.
The study is limited, however, by its 3-year time frame, says F. Javier Nieto, an epidemiologist at Johns Hopkins Medical Institutions in Baltimore. "Atherosclerosis develops over decades."
Attributing a protective effect to recent antibiotic use "is not very consistent with what we know about the disease, unless the effect ... is on the acute events that precede a heart attack," Nieto says.
One such event could be inflammation that causes plaque to break off a blood-vessel wall, lodge in an artery, and induce a heart attack. Other research has shown that C. pneumoniae can stimulate inflammation in blood vessel walls, says Bill Fong, director of infectious diseases at St. Michael's Hospital in Toronto.
Although the new study supports other recent research linking infections with heart attacks, "it should not be construed [to mean] the general public should start taking antibiotics to prevent heart disease," Fong says.
Even if infections are definitively tied to heart disease, treating them won't exclude high cholesterol and other risk factors from posing dangers, Meier says. Indeed, infections may work with such conditions to cause heart disease, he suggests.
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|Title Annotation:||cardiac arrest|
|Article Type:||Brief Article|
|Date:||Feb 6, 1999|
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