Abstract
Atherosclerosis is a multifactorial disease with an important inflammatory component. Inflammatory cells such as T-lymphocytes, macrophages and monocytes play a key role not only in its origin but also during plaque rupture. In addition, it has been suggested that infection could be the cause of atherosclerosis. Serologic studies involving polymerase chain reaction, immunocytochemistry and electron microscopy support the hypothesis of an association between Chlamydia pneumoniae and atherosclerosis. This intracellular pathogen is able to replicate in macrophages, vascular cells and smooth muscle cells. C. pneumoniae can then release inflammatory cytokines which contribute to instability of the plaque. C. pneumoniae may be recovered through cell culture from coronary atherosclerotic plaques and has a strong association with one allele, of the major histocompatibility system among patients with acute coronary syndromes. Other intracellular pathogens that have been implicated in atherosclerosis include cytomegalovirus, Mycoplasma pneumoniae and Helicobacter pylori. To test the hypothesis that C. pneumoniae plays a role in the instability of plaque, we conducted a prospective clinical trial, using the macrolide antibiotic roxithromycin in 202 patients. The preliminary results show a statistically significant reduction in the incidence of acute coronary events at 30 days.
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Gurfinkel, E. (1998). Link between intracellular pathogens and cardiovascular diseases. In Clinical Microbiology and Infection (Vol. 4, pp. 4S33-4S36). Decker Europe. https://doi.org/10.1111/j.1469-0691.1998.tb00701.x
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