BACKGROUND: Recent studies have indicated an association between periodontitis and atrial fibrillation (AF), although the underlying mechanisms remain unclear. Porphyromonas gingivalis (P ginigivalis ) is a causative agent of periodontal disease and is highly pathogenic. This study focused on P gingivalis and aimed to investigate the relationship among periodontitis, atrial translocation of P gingivalis , and atrial fibrosis and AF. METHODS: An experiment was conducted using P gingivalis –infected C57BL/6J mice, in which P gingivalis was inoculated into the pulp of the molars. Immunohistochemistry was used to visualize the localization of P gingivalis , and loop-mediated isothermal amplification was employed to detect P gingivalis DNA in the left atrium. AF inducibility was examined by intracardiac stimulation. Moreover, left atrial appendage specimens were obtained from 68 patients with AF. A periodontal examination was conducted before the surgery, and the periodontal epithelial surface area and periodontal inflamed surface area, which are quantitative indices used to determine the clinical severity of periodontitis, were measured. The bacterial number of P gingivalis in human atrial tissue was analyzed via quantitative polymerase chain reaction. Atrial fibrosis was assessed using Azan-Mallory staining. RESULTS: The translocation path of P gingivalis from the dental granuloma to the left atrium via the circulatory system was demonstrated by immunohistochemistry and loop-mediated isothermal amplification in P gingivalis –infected mice, which showed a higher degree of atrial fibrosis (21.9% versus 16.3%; P =0.0003) and a higher AF inducibility (30.0% versus 5.0%; P =0.04) than the control mice. Upregulation of galectin-3 and transforming growth factor-beta 1 in the left atrium was observed in P gingivalis –infected mice. Moreover, immunohistochemistry revealed that P gingivalis was also present in human atrial tissue. The number of P gingivalis in the human atrial tissue was positively correlated with periodontal epithelial surface area (ρ=0.35; P =0.004), periodontal inflamed surface area (ρ=0.52, P <0.0001), and the degree of atrial fibrosis (ρ=0.38; P =0.002). CONCLUSIONS: P gingivalis translocation to the left atrium correlates with the clinical severity of periodontitis, which may exacerbate atrial fibrosis and AF. Atrial translocation of P gingivalis is a potential pathway explaining the causal relationship between periodontitis and AF.

Earlier studies have shown that visit-to-visit blood pressure (BP) variability (VVV) served as a significant independent risk factor of stroke, specifically, in the high-risk elderly of cardiovascular disease (CVD). Although the mechanism is not clearly understood, arterial remodeling such as carotid artery, coronary artery and large aortic artery would be a strong moderator in the relationship between VVV and CVD incidence. Recent studies have provided evidence that VVV predicted the progression of arterial stiffness. While the class of antihypertensive agents is suggested to be an important determinant of VVV, long-acting calcium channel blockers use (CCBs) is associated with the reduction of VVV, and thus, is suggested to decrease the arterial stiffness. Specifically, the relationship between VVV and coronary arterial remodeling has never been reviewed until now. This article summarizes the recent literature on these topics. In the elderly hypertensives, strict BP control using CCBs could play a pivotal role in suppressing arterial stiffening via VVV reduction.

Background: Periodontitis has not been recognized as a modifiable risk factor for atrial fibrillation (AF). This prospective nonrandomized study investigated whether periodontal treatment improves the AF ablation outcome. Methods and Results: We prospectively enrolled 288 AF patients scheduled to undergo initial radiofrequency catheter ablation. Each patient underwent periodontal inflamed surface area (PISA; a quantitative index of periodontal inflammation) measurement. All eligible patients were recommended to receive periodontal treatment within the blanking period, and 97 consented. During the mean follow‐up period of 507±256 days, 70 (24%) AF recurrences were documented. Patients who exhibited AF recurrences had a higher PISA than those who did not (456.8±403.5 versus 277.7±259.0 mm ² , P =0.001). These patients were categorized into high‐PISA (>615 mm ² ) and low‐PISA (<615 mm ² ) groups according to the receiver operating characteristic analysis for AF recurrence (area under the curve, 0.611; sensitivity, 39%; specificity, 89%). A high PISA, as well as female sex, AF duration, and left atrial volume, were the statistically significant predicter for AF recurrence (hazard ratio [HR], 2.308 [95% CI, 1.234–4.315]; P =0.009). In patients with a high PISA, those who underwent periodontal treatment showed significantly fewer AF recurrences ( P =0.01, log‐rank test). The adjusted HR of periodontal treatment for AF recurrence was 0.393 (95% CI, 0.215–0.719; P =0.002). Conclusions: Periodontitis may serve as a modifiable risk factor for AF. PISA is a hallmark of AF recurrence, and periodontal treatment improves the AF ablation outcome, especially for those with poor periodontal condition.