Potential association of Helicobacter cinaedi with atrial arrhythmias and atherosclerosis

Abstract

Helicobacter cinaedi has been increasingly recognized as an emerging pathogen. Reports of recurrent bacteremia and isolation of H. cinaedi organisms from a patient with myopericarditis led us to postulate that H. cinaedi is associated with chronic inflammatory cardiovascular diseases such as atrial arrhythmias and atherosclerosis. To assess any association of H. cinaedi with atrial arrhythmias, a retrospective case-control study of patients attending Kumamoto University Hospital from 2005 to 2009 was performed. The arrhythmia status of these patients was determined from their electrocardiography and electrophysiological studies. Multiple logistic regression analysis was used to identify independent risk factors. In a comparison of case patients (n = 132) with control subjects (n = 137), H. cinaedi seropositivity was identified as an independent risk factor for atrial arrhythmia (odds ratio, 5.13; 95% confidence interval, 3.0-8.7; P < 0.001). There were no significant differences, however, between these two groups with respect to anti-H. pylori IgG concentrations, anti-Chlamydophila pneumoniae IgG concentrations, and other studied variables. IgG concentrations against H. cinaedi and H. pylori were inversely correlated, which suggests cross-immunity between these two bacteria. Also, to explore any association of H. cinaedi with atherosclerosis, immunohistochemical analysis of atherosclerotic aortic tissues collected post mortem from nine patients was performed. Immunohistochemistry of atherosclerotic aortic tissues from all nine patients detected H. cinaedi antigens inside CD68 + macrophages. These findings provide the first evidence, to our knowledge, of a possible association of H. cinaedi with atrial arrhythmias and atherosclerosis.

Pericoronary Pseudotumor Caused by Helicobacter Cinaedi

“…Although Helicobacter species are recognized as major pathogens associated with gastrointestinal tract infection, H. cinaedi is commonly isolated from compromised patients. [6][7][8]10) However, there have been increasing reports of infection in immunocompetent patients in whom H. cinaedi has been isolated from blood and caused recurrent bacteremia and latent or chronic infections. [6][7][8]10) Recently Lewis, et al 9) reported isolation of H. cinaedi from an immunocompetent patient with myopericarditis.…”

“…[6][7][8]10) Recently Lewis, et al 9) reported isolation of H. cinaedi from an immunocompetent patient with myopericarditis. Khan, et al 10) also reported that H. cinaedi is possibly associated with atrial arrhythmias and atherosclerosis. Because these reports suggested that H. cinaedi is a causative factor in cardiovascular disease, it is plausible that this organism induced formation of a tumor-like lesion around the coronary artery.…”

“…[6][7][8] H. cinaedi infection is reportedly associated with cardiovascular disease. 9,10) We here report a case of a pericoronary pseudotumor caused by H. cinaedi.…”

Helicobacter spp. Other than H. pylori

“…Alternately, H. cinaedi infection could induce production of auto-antibodies (molecular mimicry), as occurs in other infections, which could be responsible for the observed inflammation. Using immunohistochemistry, the authors also found H. cinaedi antigens inside CD68 + macrophages, suggesting that H. cinaedi could be associated with atherosclerosis as well [8]. In another study [9], 31 of 105 (29.5%) specimens from the coronary plaques of Iranian patients who underwent coronary artery bypass graft were Helicobacter spp.…”

“…A Japanese retrospective case-control study assessed the association of Helicobacter cinaedi seropositivity and atrial arrhythmia in 135 patients. Using multiple logistic regression analysis, the authors found that seropositivity to H. cinaedi, but not to H. pylori or Chlamydia pneumoniae, was an independent risk factor for atrial arrhythmia [8]. The authors suggest that latent H. cinaedi infection or the ongoing presence of bacterial antigens could trigger local, weak, persistent, and long-term inflammatory responses in cardiac tissues, which would lead to tissue remodeling and fibrosis.…”