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BackgroundElevated levels of N-terminal pro-B natriuretic peptide (NT-proBNP) and left ventricular hypertrophy (LVH) are independent risk factors for heart failure (HF). In addition, right ventricular pacing (RVP) is an effective treatment strategy for bradyarrhythmia, but long-term RVP is associated with HF. However, there is limited evidence on the independent and combined association of NT-proBNP and left ventricular mass index (LVMI) with HF risk in elderly diabetic patients with long-term RVP.MethodsBetween January 2017 and January 2018, a total of 224 elderly diabetic patients with RVP at Fuwai Hospital were consecutively included in the study, with a 5-year follow-up period. The study endpoint was the first HF readmission during follow-up. This study aimed to explore the independent and joint relationship of NT-proBNP and LVMI with HF readmission in elderly diabetic patients with long-term RVP, using a multivariate Cox proportional hazards regression model.ResultsA total of 224 (11.56%) elderly diabetic patients with RVP were included in the study. During the 5-year follow-up period, a total of 46 (20.54%) patients suffered HF readmission events. Multivariate Cox proportional hazards regression analysis showed that higher levels of NT-proBNP and LVMI were independent risk factors for HF readmission [NT-proBNP: hazard risk (HR) = 1.05, 95% confidence interval (CI): 1.01–1.10; LVMI: HR = 1.14, 95% CI: 1.02–1.27]. The optimal cut-off point of NT-proBNP was determined to be 330 pg/ml by receiver operating characteristic (ROC) curve analysis. Patients with NT-proBNP > 330 pg/ml and LVH had a higher risk of HF readmission compared to those with NT-proBNP ≤ 330 pg/ml and non-LVH (39.02% vs. 6.17%; HR = 7.72, 95% CI: 1.34–9.31, P < 0.001).ConclusionIn elderly diabetic patients with long-term RVP, NT-proBNP and LVMI were associated with the risk of HF readmission. Elevated NT-proBNP combined with LVH resulted in a significantly higher risk of HF readmission.

BackgroundVentricular arrhythmias in patients with hypertrophic cardiomyopathy (HCM) may lead to sudden cardiac death (SCD). We aimed to investigate the relationship between electrocardiogram (ECG) indicators and the risk of appropriate implantable cardioverter-defibrillator (ICD) therapy in HCM.MethodsThe HCM patients receiving ICD implantation were enrolled consecutively. QT interval correction (QTc) was calculated using Bazett's formula. Long or deep S wave in V4 lead was defined as duration time >50 ms and/or voltage amplitude >0.6 mV. The endpoint in our study was at least one ICD appropriate therapy triggered by ventricular tachyarrhythmia (VT) or ventricular fibrillation (VF), including anti-tachyarrhythmia pacing (ATP) and electrical shock.ResultsA total of 149 patients with HCM (mean age 53 ± 14 years, male 69.8%) were studied. Appropriate ICD therapies occurred in 47 patients (31.5%) during a median follow-up of 2.9 years. Cox regression analysis showed that long or deep S wave in V4 lead [hazard ratio (HR) 1.955, 95% confidence interval (CI) 1.017–3.759, P = 0.045] and QTc interval (HR 1.014, 95% CI 1.008–1.021, P < 0.001) were independent risk factors for appropriate ICD therapy. The ROC showed that the optimal cut-off point value for the QTc interval to predict the appropriate ICD therapy was 464 ms, and the AUC was 0.658 (95% CI 0.544–0.762, P = 0.002). The AUC for S wave anomalies in V4 lead was 0.608 (95% CI 0.511–0.706, P = 0.034). We developed a new model that combined the QTc interval and S wave anomalies in V4 lead based on four patient groups. Patients with QTc ≥464 ms and long or deep V4-S wave had the highest risk of developing appropriate ICD therapy (log-rank P < 0.0001). After adding QTc interval and V4-S wave anomalies into the HCM-risk-SCD model, the prediction effect of the new model was significantly improved, and the NRI was 0.302.ConclusionsIn this HCM cohort, QTc and S wave anomalies in V4 lead were found to be significant and strong predictors of the risk of appropriate ICD therapy. Patients with QTc ≥464 ms and long or deep S wave had the highest risk. After QTc interval and V4-S wave anomalies adding to the HCM-risk-SCD model, the prediction effect is significantly improved.

Low-density lipoprotein receptor-related protein 6 (LRP6) plays a critical role in cardiovascular homeostasis. The deficiency of LRP6 is associated with a high risk of arrhythmias. However, the association between genetic variations of LRP6 and sudden cardiac death (SCD) remains unknown. This study aims to explore the association between common variants of LRP6 and the prognosis of chronic heart failure (CHF) patients. From July 2005 to December 2009, patients with CHF were enrolled from 10 hospitals in China. The single-nucleotide polymorphism (SNP) rs2302684 was selected for the evaluation of the effect of LRP6 polymorphisms on the survival in patients with CHF. A total of 1,437 patients with CHF were finally included for the analysis. During a median follow-up of 61 months (range 0.4–129 months), a total of 546 (38.0%) patients died, including 201 (36.8%) cases with SCD and 345 (63.2%) cases with non-SCD. Patients carrying A allele of rs2302684 had an increased risk of all-cause death (adjusted HR 1.452, 95% CI 1.189–1.706; P < 0.001) and SCD (adjusted HR 1.783, 95% CI 1.337–2.378; P < 0.001). Therefore, the SNP rs2302684 T>A in LRP6 indicated higher risks of all-cause death and SCD in patients with CHF. LRP6 could be added as a novel predictor of SCD and might be a potential therapeutic target in the prevention of SCD in the CHF population.

Introduction: For patients who develop atrioventricular block (AVB) following transcatheter aortic valve replacement (TAVR), right ventricular pacing (RVP) may be associated with adverse outcomes. We assessed the feasibility of conduction system pacing (CSP) in patients who developed AVB following TAVR and compared the procedural and clinical outcomes with RVP.Methods: Consecutive patients who developed AVB following TAVR were prospectively enrolled, and were implanted with RVP or CSP. Procedural and clinical outcomes were compared among different pacing modalities.Results: A total of 60 patients were enrolled, including 10 who were implanted with His bundle pacing (HBP), 20 with left bundle branch pacing (LBBP), and 30 with RVP. The HBP group had significantly lower implant success rate, higher capture threshold, and lower R-wave amplitude than the LBBP and RVP groups (p < 0.01, respectively). The RVP group had a significantly longer paced QRS duration (153.5 ± 6.8 ms, p < 0.01) than the other two groups (HBP: 121.8 ± 8.6 ms; LBBP: 120.2 ± 10.6 ms). During a mean follow-up of 15.0 ± 9.1 months, the LBBP group had significantly higher left ventricular ejection fraction (LVEF) (54.9 ± 6.7% vs. 48.9 ± 9.1%, p < 0.05) and shorter left ventricular end-diastolic diameter (LVEDD) (49.7 ± 5.6 mm vs. 55.0 ± 7.7 mm, p < 0.05) than the RVP group. While the HBP group showed trends of higher LVEF (p = 0.016) and shorter LVEDD (p = 0.017) than the RVP group. Four patients in the RVP group died—three deaths were due to progressive heart failure and one was due to non-cardiac reasons. One death in the LBBP group was due to the non-cardiac reasons.Conclusions: CSP achieved shorter paced QRS duration and better cardiac structure and function in post-TAVR patients than RVP. LBBP had a higher implant success rate and better pacing parameters than HBP.

Introduction: His bundle pacing (HBP) is the most widely used physiological pacing modality, but difficulties in locating the His bundle lead to high fluoroscopic exposure. An electroanatomical mapping (EAM) system can be an efficient tool to achieve HBP implantation with near-zero fluoroscopic visualization.Methods: In the study, 20 patients who had indications for pacemaker implantation were prospectively enrolled and underwent HBP implantation either with the conventional fluoroscopy approach (the standard group) or guided by a novel KODEX-EPD mapping system (the EAM-guided group). The success rate, procedural details, pacing parameters, and procedure-related complications were compared between the two groups.Results: In the study, 20 consecutive patients were randomized with 10 patients in each group. HBP was successfully achieved in nine patients in the standard group and nine patients in the EAM-guided group. The procedural time was similar between the EAM-guided group vs. the standard group (85.40 ± 22.34 vs. 86.50 ± 15.05 min, p = 0.90). In comparison with the standard group, the EAM-guided group had a significant shorter total fluoroscopic time (FT) (1.45 ± 0.58 vs. 12.36 ± 5.46 min, p < 0.01) and His lead fluoroscopic time (HL-FT) (0.84 ± 0.56 vs. 9.27 ± 5.44 min, p < 0.01), while lower total fluoroscopic dose (3.13 ± 1.24 vs. 25.38 ± 11.15 mGy, p < 0.01) and His lead fluoroscopic dose (1.85 ± 1.17 vs. 19.06 ± 11.03 mGy, p < 0.01). No significant differences were observed in paced QRS duration and pacing parameters between the two groups. During a 3-month follow-up, one patient had a capture threshold increased >1 V/1.0 ms in the standard group, while no other complications were recorded in either group.Conclusion: The KODEX-EPD system could facilitate HBP implantation with significantly reduced FT and dose without compromising the procedural time.

Extraintestinal pathogenic Escherichia coli (ExPEC) is one of the top pathogens responsible for bloodstream infection and severe, often fatal, sepsis. Although the virulence factors and host immune responses to ExPEC infection have been investigated, the responses to a particular ExPEC strain could be very different. In this study, we investigated the mechanisms of Cyclooxygenase-2 (COX-2) up-regulation in influencing the host defenses against infection of ExPEC XM O2:K1:H7. Our results demonstrated that ExPEC XM O2:K1:H7 infection in mouse and RAW264.7 macrophages leads to COX-2 up-regulation, and COX-2 inhibition significantly enhances ExPEC infection. The up-regulation of COX-2 in macrophages was mediated by Toll-like receptor 4 (TLR4) through the activation of p38 and extracellular signal-regulated kinase/Mitogen-activated protein kinase (ERK/MAPK) pathways. Further studies showed that COX-2 inhibition significantly decreased autophagy in macrophages during ExPEC XM O2:K1:H7 infection. Autophagy inhibition significantly enhanced, while induction reduced ExPEC XM O2:K1:H7 survival in macrophages. In addition, COX-2 inhibition significantly increased macrophage cell death during ExPEC XM O2:K1:H7 infection and increased the expression of anti-inflammatory cytokine interleukin-10 (IL-10). Our results indicate that COX-2 up-regulation benefits host defense against ExPEC XM O2:K1:H7 infection by increasing autophagy in macrophages and by reducing IL-10 expression and macrophage cell death during ExPEC infection.