Infection May Raise Atherosclerosis Risk
Cytomegalovirus carries highest hazard ratio for cardiovascular events.
Patients with infections, particularly recurring infections, may be at increased risk of developing atherosclerosis, according to Stephen Epstein, MD, from the Cardiovascular Research Institute at the Washington Hospital Center.
“Despite the recent negative results of antibiotic trials, there is increasing evidence suggesting that infection does influence atherogenesis and the clinical events relating to atherosclerosis,” Epstein said. “Most interestingly, it appears that the genetic makeup of an individual modulates the proatherosclerotic
effects of infectious agents.”
Epstein said that several early studies indicated that there may not be a link between infection and atherosclerotic cardiovascular events, and many doctors have dismissed theories that the two could be related.
Longer antibiotic therapy
Recent studies that have linked infection to atherosclerosis-related cardiovascular events have some limitations, particularly regarding antibiotic therapy. “Relatively brief periods of antibiotic therapy, with relatively long follow-up, are characteristic of these randomized antibiotic trials,” he said.
“It is, therefore, not unreasonable to think that truly definitive trials ruling out an effect of antibiotic treatment would require more prolonged treatment.”
Study of pathogens
To further examine this issue, Epstein and colleagues studied six pathogens and their relationship to cardiovascular events: cytomegalovirus, herpes simplex virus type 1, herpes simplex virus type 2, hepatitis A, Chlamydia pneumoniae and Helicobacter pylori.
“These pathogens were selected because they produce either a persistent infection or a persistent antibody response in the host,” Epstein said.
During a three-year follow-up, researchers determined the relative hazards of developing a cardiovascular event associated with each of these infections (Figure). The hazard ratio was highest for cytomegalovirus.
“These studies provide reasonable evidence that infection and particularly pathogen burden play an important role in coronary artery disease,” Epstein said. “Antibiotic therapy specifically targeting Chlamydia or other bacteria is unlikely to have a major impact on coronary artery disease events, even if infection does play a role in atherogenesis and in atherosclerotic cardiovascular events.”
Epstein said there could be a direct cause and effect between infection and atherosclerosis. Infection leads to both inflammation and immune responses. These immune responses can, in time, lead to atherosclerosis; the pathogen burden exacerbates this process.