Background: Left bundle branch area pacing (LBBAP) is a recently proposed method for conduction system pacing. We performed a meta-analysis of controlled studies to compare the clinical outcome in patients who received LBBAP vs. biventricular pacing (BVP) for cardiac resynchronization therapy (CRT).Methods: PubMed, Embase, and Cochrane's Library databases were searched for relevant controlled studies. A random-effect model incorporating the potential heterogeneity was used to synthesize the results.Results: Four non-randomized controlled studies including 249 patients with heart failure (HF) for CRT were included, and the patients were followed for 6–12 months. Compared with BVP, LBBAP was associated with significantly shortened QRS duration [mean difference (MD): −29.18 ms, 95% confidence interval (CI): −33.55–24.80, I2 = 0%, P < 0.001], improved left ventricular ejection fraction (MD: 6.93%, 95% CI: 4.69–9.17, I2 = 0%, P < 0.001), reduced left ventricular end-diastolic dimension (MD: −2.96 mm, 95% CI: −5.48 to −0.44, I2 = 0%, P = 0.02), and improved New York Heart Association class (MD: −0.54, 95% CI: −0.84 to −0.24, I2 = 65%, P < 0.001). Moreover, patients who received LBBAP were more likely to achieve echocardiographic [odds ratio (OR): 5.04, 95% CI: 2.17–11.69, I2 = 0%, P < 0.001] and clinical (OR: 7.33, 95% CI: 1.62–33.16, I2 = 0%, P = 0.01) CRT responses.Conclusion: Current evidence from non-randomized studies suggests that LBBAP appears to be a promising method for CRT, which is associated with more remarkable improvements of symptoms and cardiac function in HF patients with indication for CRT.

Nesfatin-1 is a neuropeptide produced in the hypothalamus. It is known that Nesfatin-1 is involved in food uptake, fat storage, and other metabolic regulation. We hypothesized that Nesfatin-1 may play a role in cardiovascular tissue. Free fatty acids (FFAs) are known to be the risk factor for cardiovascular diseases. FFAs mediated endothelial dysfunction is the critical mechanism of many cardiovascular disorders. The present study explores the protective effects of Nesfatin-1 on FFAs-induced endothelial inflammation and the underlying mechanism. We found that significantly increased lactate dehydrogenase (LDH) release and production of inflammatory factors were observed in FFAs treated human aortic endothelial cells (HAECs), accompanied by the enhanced attachment of U937 monocytes to HAECs and upregulated cell adhesion molecule vascular cell adhesion molecule-1 (VCAM-1), which were dramatically reversed by the treatment with Nesfatin-1. In addition, the promoted level of nuclear regulator NF-κB p65 and transcriptional function of NF-κB in FFAs treated HAECs were greatly suppressed by HAECs. Growth Factor Independent 1 Transcriptional Repressor 1 (Gfi1), an important negative regulator of NF-κB activity, was significantly downregulated in HAECs by FFAs and was upregulated by Nesfatin-1. Lastly, the inhibitory effects of Nesfatin-1 against FFAs-induced NF-κB activation and adhesion of U937 monocytes to HAECs were abolished by the knockdown of Gfi1. In conclusion, our data reveal that Nesfatin-1 inhibited FFAs-induced endothelial inflammation mediated by the Gfi1/NF-κB signaling pathway.

Insufficient invasion of trophoblast cells is one of the important causes of preeclampsia (PE). Circular RNA (circRNA) has been proven to regulate the biological functions of trophoblast cells and mediate the progression of PE. The expression of circ_0085296, microRNA (miR)-942-5p, and thrombospondin 2 (THBS2) was detected by quantitative real-time PCR. In addition, the interaction between miR-942-5p and circ_0085296 or THBS2 was confirmed by dual-luciferase reporter assay and RIP assay. Our data showed that circ_0085296 was upregulated in the placental tissues of PE patients. Silenced circ_0085296 could enhance the proliferation, migration, invasion, and angiogenesis of HTR-8/SVneo cells. Besides, circ_0085296 was found to act as miR-942-5p sponge. Function analysis results suggested that miR-942-5p inhibitor reversed the positive regulation of circ_0085296 knockdown on the biological functions of HTR-8/SVneo cells. Moreover, THBS2 was a target of miR-942-5p, and its overexpression also reversed the promotion effect of miR-942-5p on the proliferation, migration, invasion, and angiogenesis of HTR-8/SVneo cells. Also, circ_0085296 was discovered to positively regulate THBS2 by sponging miR-942-5p. To sum up, our results revealed that circ_0085296 could inhibit trophoblast cells proliferation, migration, invasion, and angiogenesis by regulating miR-942-5p/THBS2, confirming that circ_0085296 might be a potential therapeutic target for PE.

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