Heart Rate Variability and Atria Function in Children at Late Follow-Up Evaluation After Atrioventricular Node Slow-Pathway Radiofrequency Ablation

This study was designed to assess the changes in the conductive system, autonomic dysfunction, and global and regional function of the atria and ventricles in children late after slow-pathway radiofrequency ablation (RFA). The study enrolled 22 children, who has successfully undergone RFA 2 to 5 years previously (RFA group) and 20 healthy children (control group). Electrophysiologic study was performed for the RFA group. Holter monitoring and echocardiography were performed for all the children. At a late follow-up assessment, the RFA children were free of paroxysms, whereas 8 of the 22 children (36%) reported transient palpitations. Both mean and maximal heart rates (HR) were significantly increased, whereas indices of HR variability (% of succesive normal sinus RR intervals exceeding 50 ms [pNN50], root mean square of the succesive normal sinus RR interval difference [rMSSD], high-frequency component [HFC]) were significantly decreased in the RFA group compared with preablation and control data. Left atrial (LA) and right atrial (RA) volumes were significantly higher, and atria deformation indices were significantly lower in the RFA group. Correlations were found between the mean HR and the volumes of LA (r = 0.477; p < 0.001) and RA (r = 0.512; p < 0.001). A negative correlation between the maximal LA volume and the longitudinal strain rate (SR) during relaxation (r = –0.476; p = 0.03) and a positive correlation between the minimal LA volume and both longitudinal SR (r = 0.361; p = 0.03) and strain (ε) (r = 0.375; p = 0.024) during contraction were shown. These data suggest a possible link between atrial dysfunction and the hyperadrenergic state after RFA

Association between atrial fibrillation and <i>Helicobacter pylori</i>

The connection between atrial fibrillation (AF) and H. pylori (HP) infection is still matter of debate. We performed a systematic review and metanalysis of studies reporting the association between AF and HF. A systematic review of all available reports in literature of the incidence of HP infection in AF and comparing this incidence with subjects without AF were analysed. Risk ratio and 95% confidence interval (CI) and risk difference with standard error (SE) were the main statistics indexes. Six retrospective studies including a total of 2921 were included at the end of the selection process. Nine hundred-fifty-six patients (32.7%) were in AF, whereas 1965 (67.3%) were in normal sinus rhythm (NSR). Overall, 335 of 956 patients with AF were HP positive (35%), whereas 621 were HP negative (65%). In addition, 643 of 1965 NSR patients (32.7%) were HP positive while 1,322 were negative (67.3%; Chi-square 2.15, p = 0.21). The Cumulative Risk Ratio for AF patients for developing an HP infection was 1.19 (95% CI 1.08–1.41). In addition, a small difference risk towards AF was found (0.11 [SE = 0.04]). Moreover, neither RR nor risk difference were influenced by the geographic area at meta-regression analysis. Finally, there was a weak correlation between AF and HP (coefficient = 0.04 [95% CI −0.01–0.08]). We failed to find any significant correlation between H. pylori infection and AF and, based on our data, it seems unlikely than HP can be considered a risk factor for AF. Further larger research is warranted

Induction of Atrial Fibrillation by Neutrophils Critically Depends on CD11b/CD18 Integrins

Background: Recent observational clinical and ex-vivo studies suggest that inflammation and in particular leukocyte activation predisposes to atrial fibrillation (AF). However, whether local binding and extravasation of leukocytes into atrial myocardium is an essential prerequisite for the initiation and propagation of AF remains elusive. Here we investigated the role of atrial CD11b/CD18 mediated infiltration of polymorphonuclear neutrophils (PMN) for the susceptibility to AF. Methods and Results: C57bl/6J wildtype (WT) and CD11b/CD18 knock-out (CD11b(-/-)) mice were treated for 14 days with subcutaneous infusion of angiotensin II (Ang II), a known stimulus for PMN activation. Atria of Ang II-treated WT mice were characterized by increased PMN infiltration assessed in immunohistochemically stained sections. In contrast, atrial sections of CD11b(-/-) mice lacked a significant increase in PMN infiltration upon Ang II infusion. PMN infiltration was accompanied by profoundly enhanced atrial fibrosis in Ang II treated WT as compared to CD11b(-/-) mice. Upon in-vivo electrophysiological investigation, Ang II treatment significantly elevated the susceptibility for AF in WT mice if compared to vehicle treated animals given an increased number and increased duration of AF episodes. In contrast, animals deficient of CD11b/CD18 were entirely protected from AF induction. Likewise, epicardial activation mapping revealed decreased electrical conduction velocity in atria of Ang II treated WT mice, which was preserved in CD11b(-/-) mice. In addition, atrial PMN infiltration was enhanced in atrial appendage sections of patients with persistent AF as compared to patients without AF. Conclusions: The current data critically link CD11b-integrin mediated atrial PMN infiltration to the formation of fibrosis, which promotes the initiation and propagation of AF. These findings not only reveal a mechanistic role of leukocytes in AF but also point towards a potential novel avenue of treatment in AF