Effect of periodontitis on susceptibility to atrial fibrillation in an animal model☆

Abstract 

Background

Inflammation is implicated in the pathophysiology of atrial fibrillation (AF). Periodontitis causes a general inflammatory response. Whether periodontitis is related to AF is unknown.

Objective

The aim of the study was to test the hypothesis that inflammation facilitates AF.

Methods

Twenty-two adult mongrel canines of either sex were used for this study. Periodontitis was induced in 12 dogs (periodontitis group) by tying 2-0 silk ligatures at the second premolar of mandibula. Ten healthy dogs were used as controls. Before the ligation procedure and on the day 30, 60, and 90 after ligation, an electrophysiologic evaluation was performed to measure atrial refractoriness and AF inducibility by delivering a single atrial extrastimuli in the high right atrium, atrial septum (AS), and coronary sinus (CS), respectively. Before each electrophysiologic study, blood samples were taken for determining the levels of C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α). Animals were killed after 90 days. The hearts and mandibulae were harvested for morphological study, and the periodontal disease severity was quantified.

Results

Atrial effective refractory period (AERP) shortened, and AF inducibility increased progressively in the periodontitis group. At a drive length of 300 milliseconds, AERP in the CS was 126.7 ± 13.0 milliseconds and 107.5 ± 9.7 milliseconds after 60 and 90 days of ligation, respectively (vs 165.8 ± 10.8 milliseconds at baseline; P < .001). By CS pacing, AF was induced in 5 and 10 of 12 dogs on day 60 and 90 after ligation, respectively (vs 1/12 at baseline; P < .05 and P < .01, respectively). Elevation of CRP and TNF-α occurred after 60 days of ligation (CRP, 13.42 ± 2.21 mg/L vs control, 1.92 ± 0.38 mg/L; P < .001; TNF-α, 9.85 ± 1.72 mg/L vs control, 3.36 ± 0.75 mg/L; P < .001) and reached the peak at the end of the study (CRP, 31.38 ± 2.69 mg/L vs control, 1.99 ± 0.40 mg/L; P < .001; TNF-α, 12.32 ± 1.07 mg/L vs control, 3.24 ± 0.53 mg/L; P < .001). There was a negative correlation between the levels of serum inflammatory factors and AERP values (P < .05). Alveolar bone level decreased in the periodontitis group (P < .001). The long axis (P < .001) of atrial cardiomyocytes including the right atrial appendage (25.50 ± 3.58 μm vs 18.14 ± 3.32 μm), AS (24.78 ± 3.45 μm vs 17.47 ± 2.57 μm), and left atrial appendage (31.90 ± 4.80 μm vs 18.78 ± 2.42 μm) from the periodontitis group was larger than the control group. The short axis of atrial cardiomyocytes was larger than the control group, too (P < .001). Inflammatory cells were more generally found in the atria of the periodontitis group (P < .001). Myolysis affected some atrial cardiomyocytes of the dogs with periodontitis.

Conclusion

Periodontitis led to inflammatory responses in the atrial myocardium, which disturbed the structural and electrophysiologic properties of the atrium and facilitated AF.

Keywords: Atrial fibrillation, Periodontitis, Canine, Inflammation