<EMPH TYPE="ITAL">Chlamydia pneumoniae</EMPH> as an Emerging Risk Factor in Cardiovascular Disease

Abstract

Recent appreciation of atherosclerosis as a chronic, inflammatory disease has rekindled efforts to examine the role that infectious agents may play in atherogenesis. In particular, much interest has focused on infection with Chlamydia pneumoniae. The possibility that a prokaryote contributes to atherogenesis has high clinical interest, as C pneumoniae infection may be a treatable risk factor. To review the evidence implicating C pneumoniae in the pathogenesis of atherosclerosis, we searched MEDLINE for articles published between January 1966 and October 2002 on the association of C pneumoniae and atherosclerosis. We also used online resources, texts, meeting abstracts, and expert opinion. We included 5 types of studies (epidemiological, pathology based, animal model, cell biology, and human antibiotic treatment trials) and extracted diagnostic, pathophysiologic, and therapeutic information from the selected literature; consensus was reached on interpretation discrepancies. Chlamydia pneumoniae is associated with atherosclerosis by epidemiological and pathology-based studies. Animal model and cell biology studies suggest that the pathogen can modulate atheroma biology, including lipid- and inflammatory-related processes. Although some preliminary antibiotic treatment trials in patients with coronary artery disease indicated a reduction in recurrent coronary events, larger studies have not shown benefits in individuals with stable coronary artery disease. It is unlikely that C pneumoniae infection is necessary to initiate atherosclerosis. Furthermore, conventional antibiotic therapy may not eradicate the organism or reduce mortality in individuals with atherosclerotic vascular disease. Nevertheless, the current body of evidence establishes this pathogen as a plausible, potentially modifiable risk factor in cardiovascular disease.

Hepatitis C virus RNA localization in human carotid plaques

“…(Panel B) HCV RNA detection in serum and plaque tissue by nested RT-PCR. Lanes 1 and 11: 100 bp DNA molecular weight marker; lanes 2-10: PCR results from serum and plaque samples from two representative patients (from Table 1): patient #7 (lanes [2][3][4][5] showing HCV RNA sequences in both serum and plaque; patient #3 (lanes 7-10) in plaque tissue only. Lanes 12 and 13 (positive controls): serum sample from an HCV-positive patient and synthetic HCV RNA, respectively.…”

“…Localization of the infective agent inside the plaque has been shown for most pathogens for whom a deeper evidence of such an association exists, suggesting the importance of local pathogenetic mechanism/s. [4][5][6][7] Available data suggest that the infection burden for atherosclerosis development and progression is mainly sustained by those infectious agents which possess particular tropism for cells of the vascular wall. 8 Chlamydia pneumoniae is capable of infecting vascular endothelial cells and smooth muscle cells, whereas cytomegalovirus and herpes virus foster the recruit-ment of monocyte/macrophages and T cells for atherosclerotic lesions.…”

Atherosclerotic Vascular Disease Conference

“…45 Pathological analysis has shown evidence of Chlamydia pneumoniae within the plaque. 54 Patients with atherosclerosis have increased titers of antibodies against chlamydia, Helicobacter pylori, herpes simplex virus, and cytomegalovirus. Several ongoing clinical trials are evaluating the role of antibiotics in prevention of atherosclerosis.…”

Pathogenesis of Chlamydia pneumonia Persistent Illnesses in Autoimmune Diseases

“…More recently, C. pneumonia seropositivity was associated with enhanced intima-media thickness of arteries. While these studies clearly associate TWAR organisms with atheromatous plaques, the role of TWAR infection in the pathogenesis of atherosclerosis is unknown [10,36].…”