Antibiotic Slows Atherosclerosis in People with Chlamydia Pneumonia Antibodies

Cite: American Heart Association - October 15, 2002
Co-authors include
Kerstin Winbeck, M.D.
Jürgen Klingelhöfer, M.D.
Thorleif Etgen, M.D.
Bastian Conrad, M.D.

DALLAS, Oct. 15 – Long-term antibiotic treatment may slow the progress of early atherosclerosis in stroke patients who have antibodies to a pneumonia-causing bacteria in their bloodstream, scientists report in today’s rapid access issue of Circulation: Journal of the American Heart Association.

“Our data imply for the first time to our knowledge that antibiotic treatment in patients over age 55 with Chlamydia pneumoniae (Cp) antibodies and prevalent cerebrovascular disease is associated with a reduced progression of early stages of carotid atherosclerosis,” says study author Dirk Sander, M.D., a researcher with the neurology department at Technical University of Munich.

Chlamydia pneumoniae – the bacteria that causes pneumonia – has been associated with atherosclerosis. Studies have also associated the Cp antibody with heart attack and stroke. Other research has corroborated the association of Cp with atherosclerosis based on the organism’s presence in atherosclerotic lesions and its absence in healthy artery tissue.

Other researchers have also described the benefits of antibiotics on vessel disease.

Sander’s team evaluated the effect of the antibiotic roxithromycin on progressive thickening of the carotid (neck) artery in 272 stroke patients (average age 64) for two years. Of the 125 that tested positive for the Cp antibody, 62 received a twice-daily, 150-milligrams dose of roxithromycin, while 63 got twice-daily placebo for 30 days. Of the 147 Cp-negative patients, 74 were assigned to the drug and 73 to placebo.

Researchers measured intima to media thickness (IMT) of the common carotid artery with ultrasound. Increased IMT indicates atherosclerosis. Each patient had undergone both IMT and blood tests for Cp antibodies at least three years before the start of the study’s antibiotic regimen. Patients infected with Cp in the past have antibodies that react when their blood is exposed to the microorganism in the laboratory.

C-reactive protein (CRP) levels were also established for each patient. CRP is a marker of general systemic inflammation, including irritation of vascular walls.

In the baseline period, IMT progressed in Cp patients at a rate of 0.12 millimeters a year (mm/year) compared to 0.07 mm/year in patients without the antibody, regardless of other cardiovascular risk factors. After two years of antibiotic treatment, progression was significantly reduced Cp positive patients compared to Cp-positive patients who did not receive roxithromycin. The progression was 0.07 mm/year in patients taking antibiotics versus 0.11 mm/year in untreated patients.

Treatment significantly decreased CRP levels in treated Cp-positive patients but not in the placebo Cp-positive group, an effect that remained unchanged even after adjusting for smoking, age, diabetes, blood pressure or cholesterol levels.

However, researchers observed no significant difference between the groups in subsequent cardiovascular events at follow-up, and saw no change in IMT in Cp-negative patients who received antibiotic therapy.

Roxithromycin therapy was associated with an average reduction of IMT progression of 0.04 mm a year, which equals about a 1.5 percent to 2 percent reduction in heart risk, Sander says. This small risk reduction requires clinical trials with long-term follow-up to demonstrate the probable benefits of antibiotic therapy in patients testing positive for Cp antibodies, he says.