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Recent Advances in Inflammation & Allergy Drug Discovery

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ISSN (Print): 2772-2708
ISSN (Online): 2772-2716

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Research Article

Association between Cardiac Atrioventricular Conduction and Antibodies to Chlamydia Pneumoniae in Fibromyalgia Patients

Author(s): Basant K. Puri*, Georgia Tuckey, Lucy Cowans, Gary S. Lee and Armin Schwarzbach

Volume 17, Issue 2, 2023

Published on: 10 August, 2023

Page: [127 - 132] Pages: 6

DOI: 10.2174/2772270817666230705140935

Price: $65

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Abstract

Background: Fibromyalgia patients may complain of cardiovascular symptoms, including chest pain and palpitations. It has been proposed that infection by Chlamydia pneumoniae might be common in fibromyalgia. Chlamydia pneumoniae infection has also been hypothesized to be a causative factor in cardiac disease.

Objective: This study aims to test the hypothesis that there is an association between atrioventricular conduction and antibodies to Chlamydia pneumoniae in fibromyalgia.

Methods: Thirteen female fibromyalgia patients underwent serum Chlamydia pneumoniae IgG assays and 12-lead electrocardiography in a cross-sectional study. None of the patients was taking medication which might affect atrioventricular conduction, and none suffered from hypothyroidism, renal disease, hepatic disease, or carotid hypersensitivity.

Results: There was a significant positive correlation between the PR interval duration and the serum Chlamydia pneumoniae IgG level (r = 0.650; p = 0.016).

Conclusion: This study supports the hypothesis of an association between atrioventricular conduction and antibodies to Chlamydia pneumoniae in fibromyalgia patients. It suggests that the higher the level of such antibodies, the greater the electrocardiographic PR interval, and therefore the slower the atrioventricular conduction. Potential pathophysiological mechanisms include a chronic inflammatory response to Chlamydia pneumoniae and the action of the bacterial lipopolysaccharide. The latter may involve stimulators of interferon genes, activation of the cardiac NOD-like receptor protein 3 inflammasomes, and downregulation of fibroblast growth factor 5 in the heart.

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