Periodontal Treatment During the Blanking Period Improves the Outcome of Atrial Fibrillation Ablation.

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 mm2, P=0.001). These patients were categorized into high-PISA (>615 mm2) and low-PISA (<615 mm2) 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.

Clinical Features of Tachycardia-induced Cardiomyopathy in Patients with Atrial Fibrillation.

Objective Atrial fibrillation (AF) is the most common cause of tachycardia-induced cardiomyopathy (TIC). However, which patients with AF are prone to developing TIC remains unclear. In this study, we investigated the clinical features of AF patients with TIC. Methods This single-center study included 722 patients with AF (average age, 63.1±10.2 years old; 191 women) who underwent radiofrequency catheter ablation. We defined TIC as an initial left ventricular ejection fraction (LVEF) of <40% and a >20% recovery of the LVEF after successful AF ablation and compared the clinical characteristics between the TIC and control groups. Results The proportions of type 2 diabetes (30.5% vs. 14.7%), renal dysfunction (34.2% vs. 23.8%), hypertension (67.1% vs. 54.8%), and persistent AF (62.2% vs. 32.2%) were significantly higher in the TIC group (n=82) than in the control group (n=640). The atrioventricular nodal effective refractory period (AVNERP) (303±72 ms vs. 332±86 ms; p=0.017) was significantly shorter in the TIC group than in the control group. A multivariable analysis found that persistent AF [odds ratio (OR), 3.19; 95% confidence interval (CI), 1.94-5.24], renal dysfunction (OR, 1.87; 95% CI, 1.06-3.32), and type 2 diabetes (OR, 2.30; 95% CI, 1.31-4.05) were significantly associated with TIC. Conclusion Comorbid renal dysfunction and type 2 diabetes were clinical features of AF patients with TIC. Persistent AF, and short AVNERP may be involved in the development of TIC.

Conduction velocity mapping in atrial fibrillation using omnipolar technology.

BACKGROUND: Recent studies have shown that atrial slow conduction velocity (CV) is associated with the perpetuation of atrial fibrillation (AF). However, the criteria of CV measurement have not been standardized. The aim of this study was to evaluate the relationship between the slow CV area (SCVA) measured by novel omnipolar technology (OT) and AF recurrence. METHODS: This study included 90 patients with AF who underwent initial pulmonary vein isolation (PVI). The segmented surface area of the SCVA was measured by left atrial (LA) electrophysiological mapping using OT before the PVI. The proportion of the SCVA at each cutoff value of CV (from < 0.6 to < 0.9 m/s) was compared between the patients with and without AF recurrence. RESULTS: During a mean follow-up period of 516 ± 197 days, the recurrence of AF after the initial PVI was observed in 23 (25.5%) patients. In patients with AF recurrence, the proportion of the SCVA in the LA posterior, LA appendage (LAA), and LA anterior were significantly higher than those without AF recurrence. The multivariate analysis indicated that the proportion of the low voltage area and the SCVA in the LA anterior (local CV < 0.7 m/s) were independent predictors of AF recurrence (hazard ratio [HR], 1.07; 95% confidence interval [CI], 1.01-1.14; p = 0.03; HR, 1.40; 95% CI, 1.07-1.83; p = 0.01, respectively). CONCLUSION: By evaluating the local CV using OT, it was indicated that SCVA with CV < 0.7 m/s in the LA anterior is strongly associated with AF recurrence after PVI.

Relationship Between Fibrosis, Endocardial Endothelial Damage, and Thrombosis of Left Atrial Appendage in Atrial Fibrillation.

BACKGROUND: Left atrial appendage (LAA) thrombus (LAAT) and ischemic stroke are considered important in atrial cardiomyopathy with progressive atrial fibrosis and endocardial endothelial damage. OBJECTIVES: This study aimed to obtain histological evidence to clarify the association between LAA fibrosis and endocardial endothelial damage with LAAT, ischemic stroke, and clinical risk factors. METHODS: Ninety-six patients with atrial fibrillation (AF) scheduled to undergo LAA excision during surgery were enrolled. They underwent transesophageal echocardiography before the surgery to validate the LAA function/morphology and LAAT presence or absence. The resected LAAs were subjected to Azan-Mallory staining and CD31 immunohistochemistry to quantify the degree of fibrosis and endocardial endothelial damage staged as F1-F4 and E1-E4 per the quantiles. RESULTS: Patients with an LAAT and/or ischemic stroke history had higher fibrosis degrees (18.4% ± 9.9% vs 10.4% ± 7.0%, P < 0.0001) and lower CD31 expressions (0.27 [IQR: 0.05-0.57] vs 1.02 [IQR: 0.49-1.65]; P < 0.0001). Also, higher CHADS2 was associated with a higher degree of fibrosis and lower CD31 expression. Multivariate logistic regression analysis revealed that endothelial damage (E4) was associated with an LAAT and/or ischemic stroke history independent of AF type (paroxysmal or nonparoxysmal) with an OR of 3.47. Among patients with nonparoxysmal AF, fibrosis (F4, OR: 3.66), endothelial damage (E4, OR: 4.62), and LAA morphology (non-chicken-wing, OR: 3.79) were independently associated with LAAT and/or stroke. The degree of fibrosis correlated significantly with endothelial damage (R = -0.38, P = 0.0001). CONCLUSIONS: These histological findings may be essential in considering the pathophysiology of LAAT and stroke within the atrial cardiomyopathy context.

Progression from paroxysmal to persistent atrial fibrillation in pacemaker patients with tachycardia-bradycardia syndrome: a multicenter study.

Progression from paroxysmal to persistent atrial fibrillation (AF) is occasionally encountered in patients with previous pacemaker implantation (PMI) for the treatment of tachycardia-bradycardia syndrome (TBS). We aimed to determine the rate of its incidence occurring within the early years after PMI and the predictors. We studied TBS patients who received PMI at 5 core cardiovascular centers. The end point was a conversion from paroxysmal to persistent AF. We extracted 342 TBS patients out of 2579 undergoing PMI. During 5 ± 3.1 years of follow-up, 114 (33.3%) reached the end point. The time to the end point was 2.9 ± 2.7 years. The event rates within a year and 3 years after the PMI were 8.8% and 19.6%, respectively. In the multivariate hazard analyses, hypertension (hazard ratio [HR] 3.2, P = 0.03) and congestive heart failure (HR 2.1, P = 0.04) were found to be independent predictors of the end point occurring within a year after the PMI. Congestive heart failure (HR 1.82, P = 0.04), left atrial diameter of ≥ 40 mm (HR 4.55, P < 0.001), and the use of antiarrhythmic agents (HR 0.58, P = 0.04) were independently associated with the 3-year end point. Prediction models including combinations of those 4 parameters for the 1- and 3-year incidence both exhibited a modest risk discrimination (both c-statistics 0.71). In conclusion, early progression from paroxysmal to persistent AF was less frequent than expected in the TBS patients with PMI. Factors related to atrial remodeling and no use of antiarrhythmic drugs may facilitate the progression.

Relationship Between Periodontitis and Atrial Fibrosis in Atrial Fibrillation: Histological Evaluation of Left Atrial Appendages.

BACKGROUND: Atrial fibrosis contributes to the onset and persistence of atrial fibrillation (AF) and AF-related stroke. Periodontitis, a common infectious and inflammatory disease, aggravates some systemic diseases. However, the association of periodontitis with AF and with atrial fibrosis has remained unclarified. OBJECTIVES: The authors aimed to elucidate the relationship between periodontitis and atrial fibrosis by studying resected left atrial appendages (LAAs). METHODS: Seventy-six patients with AF (55 with nonparoxysmal AF, 25 with mitral valve regurgitation, 18 with LAA thrombus) who were scheduled to undergo LAA excision during cardiac surgery were prospectively enrolled. All patients underwent an oral examination, and the remaining number of teeth, bleeding on probing, periodontal probing depth, and periodontal inflamed surface area (PISA) were evaluated as parameters of periodontitis. The degree of fibrosis in each LAA was quantified by Azan-Mallory staining. RESULTS: Bleeding on probing (R = 0.48; P < 0.0001), periodontal probing depth of ≥4 mm (R = 0.26; P = 0.02), and PISA (R = 0.46; P < 0.0001) were positively correlated with atrial fibrosis. Among patients with >10 remaining teeth, PISA was positively and strongly correlated with atrial fibrosis (R = 0.57; P < 0.0001). After adjustments for age, AF duration, BMI, mitral valve regurgitation, and CHADS2 (congestive heart failure, hypertension, age, diabetes, previous stroke/transient ischemic attack) score, PISA was significantly associated with atrial fibrosis (ß = 0.016; P = 0.0002). CONCLUSIONS: The authors histologically revealed the association of periodontitis with atrial fibrosis. This indicates that periodontitis, which is modifiable, is likely a risk factor for AF.

Initial experience of novel over the wire type decapolar catheter for ventricular arrhythmias originating from left ventricular summit.

BACKGROUND: Previously, direct monitoring of local activation at the communicating vein (CV) has been reported to be useful for the ablation of ventricular arrhythmias (VAs) originating from the left ventricular (LV) summit. In this study, we evaluated the performance of the novel over-the-wire (OTW)-type decapolar catheter for VAs originating from the LV summit. METHODS: Overall, 17 patients who underwent catheter ablation for idiopathic VAs originating from the LV summit were included in this study. Of these, seven patients underwent mapping of the epicardial LV outflow tract with the novel 2.7 Fr OTW-type decapolar catheter (EPstar FIX AIV), and ten underwent mapping with the standard 2.0 Fr octopolar catheter (EPstar FIX 2F) procedure (AIV group = EPstar FIX AIV and control group = EPstar FIX 2F). RESULTS: No significant differences in the baseline characteristics were observed between the two groups. In the AIV group, all patients achieved successful catheter positioning in the target CV, whereas in the control group, two patients failed to achieve the same. The novel catheter not only advanced to the target vessels using a 0.014-in guidewire but it was also used for contrast injection from the catheter lumen, which enabled accurate and safe positioning. As a result, the earliest activation time preceding QRS onset during the VA, recorded at the CV, was significantly earlier when compared with the control group (44.66 ± 11.23 ms vs. 32.16 ± 4.26 ms, P = 0.007). CONCLUSIONS: Compared with the conventional electrode catheter, this novel multipolar electrode catheter is more effective for mapping local activation at the CV.

GJA1 gene polymorphism is a genetic predictor of recurrence after pulmonary vein isolation in patients with paroxysmal atrial fibrillation.

BACKGROUND: Atrial fibrillation (AF) and recurrence of AF after pulmonary vein isolation (PVI) have been linked to sinus node dysfunction. OBJECTIVE: The purpose of this study was to investigate the association between the heart rate-associated single nucleotide polymorphisms (SNPs) identified in genome-wide association studies and recurrence of AF after PVI. METHODS: In this study, patients with paroxysmal AF who underwent initial PVI, including 522 patients for screening and 172 patients for replication, were recruited and 21 heart rate-associated SNPs identified in genome-wide association studies were genotyped. The association between these SNPs and the recurrence of AF was investigated. RESULTS: Throughout the follow-up period of 21 ± 12 months, 119 patients with paroxysmal AF (22.8%) exhibited AF recurrences in the screening set. The rate of AF recurrence was significantly associated with the minor allele C of the gap junction alpha-1 protein (GJA1) rs1015451 (additive model: odds ratio 2.07; P = 9.32 × 10-7), but not with other SNPs. This association was confirmed in the replication set (allelic model: odds ratio 1.81; P = 2.70 × 10-2). Multivariate analysis revealed that the recurrence of AF after AF ablation was independently related to the GJA1 SNP rs1015451 additive model, duration of AF >1 year, AF from non-pulmonary vein foci, and thicker interventricular septum. CONCLUSION: The GJA1 SNP rs1015451, coding for a gap junction protein (connexin-43), may be considered a novel genetic marker for AF recurrence after PVI.

A mimic of tachycardia-bradycardia syndrome in a patient with long-standing persistent atrial fibrillation.

Pause following incessant tachycardia is often encountered in clinical practice. We encountered a rare arrhythmic condition mimicking tachycardia-bradycardia syndrome. We hereby describe the step-by-step diagnostic process.