纤维肌痛患者心脏房室传导与肺炎衣原体抗体的关系

Basant K Puri, Georgia Tuckey, Lucy Cowans, Gary S Lee, Armin Schwarzbach
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引用次数: 0

摘要

背景:纤维肌痛患者可能主诉心血管症状,包括胸痛和心悸。有人提出,肺炎衣原体感染可能是常见的纤维肌痛。肺炎衣原体感染也被假设为心脏病的一个致病因素。目的:本研究旨在验证纤维肌痛患者房室传导与肺炎衣原体抗体相关的假说。方法:对13例女性纤维肌痛患者进行了血清肺炎衣原体IgG检测和12导联心电图横断面研究。所有患者均未服用影响房室传导的药物,无甲状腺功能减退、肾脏疾病、肝脏疾病或颈动脉过敏。结果:PR间隔时间与血清肺炎衣原体IgG水平呈显著正相关(r = 0.650;P = 0.016)。结论:本研究支持纤维肌痛患者房室传导与肺炎衣原体抗体相关的假设。提示此类抗体水平越高,心电图PR间期越长,因此房室传导越慢。潜在的病理生理机制包括对肺炎衣原体的慢性炎症反应和细菌脂多糖的作用。后者可能涉及干扰素基因的刺激、心脏nod样受体蛋白3炎症小体的激活和心脏成纤维细胞生长因子5的下调。
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Association between Cardiac Atrioventricular Conduction and Antibodies to Chlamydia Pneumoniae in Fibromyalgia Patients.

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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