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    Study Investigates Role of Bacterial Infection after Angioplasty

    What really causes coronary artery disease and the ensuing complications that result? According to Franz-Josef Neumann, M.D. from Deutsches Herzzentrum in Munich, Germany, it isn't likely to be the recent suspect, a microorganism called Chlamydia pneumonaie. Even if it does contribute to coronary artery disease, Dr. Neumann warns that taking antibiotics to eradicate the pathogen does not seem to provide any real benefit. He presented his research of C. pneumonaie and heart disease at the 49th Annual Scientific Session of the American College of Cardiology being held in Anaheim, California.

    High cholesterol, smoking, high blood pressure, diabetes, age and obesity are well-known risk factors for coronary heart disease, but together account for only one third to one half of all cases. Furthermore, for approximately one third of those who undergo a procedure to open up those clogged blood vessels, the arteries will narrow again, in a process called restenosis. Conventional risk factors, however, do not predict which patients will develop restenosis.

    While infection and inflammation may well be the culprits behind both of these problems, researchers are struggling to identify the microorganism(s) involved and to find ways to prevent and treat the damage they may cause.

    Hopes were that C. pneumonaie would provide answers to questions about the source of arterial inflammation and coronary artery disease, much the same way that Helicobacter pylori answered questions about ulcers.

    Dr. Neumann presented the results of his research exploring the possibility that antibiotic treatment to wipe out C. pneumonaie could retard the progression of coronary artery disease and reduce the risk of thrombosis (clotting) and restenosis.

    Research focused on 1000 participants who had a successful stent placement and were able to take the test antibiotic, roxithromycin, chosen due to its effectiveness against C. pneumonaie. Divided into two demographically similar groups, one took 300 mg of the antibiotic once a day for 28 days; the other group took a placebo in the same manner.

    Results indicated that there was no association between the presence of C. pneumonaie and the occurrence of restenosis. Additionally, participants who took the effective antibiotic had no improved outcomes as a result of the treatment.

    Dr. Neumann added that there was one significant finding in his study: He found a substantially higher level of an inflammation marker called C-reactive protein in participants who were experiencing restenosis.

    Editorial comment: Restenosis after angioplasty affects about 33 percent of those undergoing the procedure. It is unclear who will develop this problem. There have been several reports describing an increased incidence of infections (bacterial and viral) in those blood vessels in which plaques developed and restenosis occurred. Chlamydia is one of the suspected culprits. In addition, a substantial amount of evidence points to the role of inflammation caused by infection in the atherosclerotic process. The study here suggests that treating patients for Chlamydia does not prevent restenosis. It is unclear if the bacteria plays a role in plaque formation leading to atherosclerosis (a different process from restenosis), or whether infection with Chlamydia would cause a plaque to rupture and lead to a heart attack.



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