Efficacy and safety of the application of extensive ablation in patients with atrioventricular re-entrant tachycardia (a retrospective study).

Radiofrequency catheter ablation (RFCA) has become the standard effective therapy for supraventricular tachycardia, but the reported success rates of ablation have differed across a large number of single-center studies. The main reason for tachycardia recurrence is accessory pathway (Ap)-mediated tachycardia, and the use of the RFCA strategy may be related to recurrence. This study compared the efficacy and safety of two different RFCA strategies for Ap-mediated tachycardia. We compared patients (group M) who underwent RFCA at multiple sites to patients (group S) who underwent RFCA at a single site during the index procedure for Ap-mediated tachycardia. The efficacy and safety were assessed in the two groups. Follow-up was conducted, and the main complications and the incidence of recurrence after RFCA procedures were recorded. Eight hundred eighty-two patients with 898 Aps were enrolled in group S, and 830 patients with 843 Aps were enrolled in group M. The cumulative number of recurrences (rates) in group M and group S at the 1st, 3rd, 6th, 12th, and 24th months after ablation were 4 (0.5%) and 17 (1.9%), p < 0.05; 5 (0.6%) and 27 (3.0%), p < 0.05; 6 (0.7%) and 34 (3.8%), p < 0.05; 6 (0.7%) and 43 (4.8%), p < 0.05; and 7 (0.8%) and 45 (5.0%), p < 0.05, respectively. Complications of chest pain, overactive vasovagal reaction, steam pop, and angina pectoris were rare in both groups. One patient in group M suffered from myocardial infarction before extensive ablation. No valve damage, cardiac tamponade, or other serious adverse events occurred in either group. The extensive ablation strategy reduced the recurrence rate and the need for subsequent ablation of the Ap without increasing the risk of complications.

High mobility group box 1 induces calcification of aortic valve interstitial cells via toll-like receptor 4.

Chronic inflammation and the calcification of aortic valve interstitial cells (AVICs) are the primary etiologies of calcific aortic valve disease (CAVD). However, the underlying mechanism remains to be elucidated. The present study investigated the importance of high mobility group box 1 (HMGB1) via toll­like receptor 4 (TLR4) for the regulation of inflammation and calcification in AVICs. It was determined that the expression levels of HMGB1 and TLR4 were increased in the calcific region of aortic valves with CAVD. In cultured primary AVICs from wild­type mice, HMGB1 treatment demonstrated a dose-dependent increase in mineralization levels and osteogenic gene expression. These effects were significantly reduced in AVICs obtained from TLR4 knockout mice (TLR4­/­). In addition, calcification was inhibited by TLR4-specific antibodies in primary AVICs. HMGB1 induced the activation of p38 and nuclear factor-κB (NF-κB) in TLR4­/­ primary AVICs, and inhibited p38 and NF­κB in wild­type AVICs treated with TLR4­specific antibodies. The present study demonstrated that TLR4 may function as an essential mediator of HMGB1­induced calcification and in the activation of p38 and NF-κB.