Artificial intelligence (AI) has significantly improved the screening and diagnostic efficiency of ventricular arrhythmia (VA) through electrocardiogram (ECG) interpretation and wearable device monitoring. In the treatment field, AI has made significant progress in assisting the localization of premature ventricular contraction origins and optimizing strategies for implantable cardioverter defibrillator therapies. AI models excel in predicting the risk of fatal VA, providing robust support for individualized prevention and treatment. This review further discusses challenges such as data quality, model interpretability, and clinical translation, as well as the role of multimodal data integration and interdisciplinary collaboration in advancing the precision medicine for VA. In the future, AI is expected to play a more pivotal role in remote healthcare, and individualized diagnosis and treatment, comprehensively enhancing diagnostic accuracy, treatment efficiency, and quality of life for VA patients.

This article focuses on the application of artificial intelligence (AI) technology in the diagnosis and treatment of arrhythmias, and briefly introduces the latest relevant research findings from both domestic and international sources. It not only outlines the capability of AI in significantly improving the detection efficiency and accuracy of arrhythmia screening and diagnosis, but also emphasizes its value in the prediction of arrhythmia and the risk of its related complications, and guidance of its clinical treatment. Furthermore, this article summarizes the challenges faced by AI in arrhythmia management, including data quantity and quality issues, the “black box” effect in AI learning process, model generalization issues, ethical issues in technology, and the clinical acceptance of AI models. Finally, it looks forward to the prospect of AI technology deeply integrating with medicine, and comprehensive application in all aspects of arrhythmia diagnosis and treatment, so as to optimize medical resource allocation and medical service workflows, increase medical efficiency and quality, and improve patients’ prognoses.

Objective  To investigate the regulatory role and underlying mechanism of circular RNA circHECTD1, a potential diagnostic biomarker for coronary heart disease (CHD), in macrophage polarization. Methods  A lipopolysaccharide-induced M1 macrophage polarization model was used to simulate a low-grade inflammatory response process. Quantitative real-time PCR (qRT-PCR) was employed to detect the expression levels of circHECTD1 and N6-methyladenosine (m6A) regulatory factors. Western blotting was performed to measure the expression of M1 phenotype marker proteins and autophagyrelated proteins. Intracellular reactive oxygen species (ROS) levels were assessed by flow cytometry. Results  Silencing circHECTD1 significantly reduced the expression of M1 phenotype-related proteins and inflammatory cytokines, decreased ROS levels, and enhanced cellular autophagy. Disordered expression of multiple m6A regulatory factors was observed in both the cellular model and peripheral blood mononuclear cells (PBMCs) from CHD patients. Significant differences in the expression levels of multiple m6A methylation regulators were identified between CHD and control groups, suggesting their potential value in CHD diagnosis. Univariate and multivariate Logistic regression analysis revealed that the m6A regulators of METTL3, METTL14, ALKBH5, and YTHDC2 were significantly associated with CHD risk. Further analysis showed that the expression of METTL14 and ALKBH5 were significantly upregulated in advanced stages of atherosclerosis. The expression level of circHECTD1 significantly correlated with FTO, YTHDF3, ALKBH5, METTL3, METTL14, and YTHDF2. In vitro experiment results demonstrated that silencing METTL14 and ALKBH5 markedly downregulated circHECTD1 expression, indicating that METTL14 and ALKBH5 positively regulated circHECTD1 expression. Conclusion  Dysregulation of m6A regulatory factors may be closely associated with the occurrence and development of CHD, potentially mediated through the regulation of circHECTD1 expression and function.

Objective  To investigate the impact of long non-coding RNA ZFAS1 (lncZFAS1) on the initiation and progression of cardiomyocyte fibrosis. Methods  HL-1 mouse cardiac myocytes were induced by transforming growth factor-β (TGF-β) to establish a cardiomyocyte fibrosis model. LncZFAS1 overexpression vectors or small interfering RNA (siRNA) were transfected into the model. Protein levels of α-smooth muscle actin (α-SMA) and collagen Ⅰ were detected by western blotting; lncZFAS1 overexpression and interference fragments were transfected into the cardiomyocyte fibrotic model. The transcriptional level of lncZFAS1 was measured via real-time quantitative PCR. Cell proliferation viability was assessed using the CCK-8 assay, apoptosis rate was analyzed by flow cytometry, and LC3 autophagy puncta formation was examined using cellular immunofluorescence. Results  Compared with the control group, the TGF-β induction group showed significantly increased protein expression of α-SMA, collagen Ⅰ and LC3 B, significantly decreased p62 protein expression, elevated lncZFAS1 expression, enhanced cell viability and autophagy puncta formation, and reduced apoptosis rate (all P<0.05). After interfering with lncZFAS1 in the model, it showed a decrease in the expression level of lncZFAS1, a decrease in cell viability and the number of autophagy puncta, an increase of apoptosis rate and expression of p62 protein, and a decrease in the expression of LC3 B protein, all with statistically significant differences (all P<0.05). However, after overexpression of lncZFAS1, the opposite results were presented. Conclusion  LncZFAS1 promotes the initiation and progression of cardiomyocyte fibrosis by regulating cellular autophagy. Targeted inhibition of lncZFAS1 may provide a novel therapeutic strategy for delaying the progression of cardiovascular diseases.

Objective  To explore the relationship between epicardial fat thickness (EFT), serum secreted frizzled-related protein 5 (SFRP5), wingless-type MMTV integration site family member 5a (Wnt5a), and in-stent restenosis (ISR) in patients with acute ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). MethodsA total of 128 STEMI patients who had undergone emergency PCI were enrolled. After a 12-month follow-up, they were divided into a non-ISR group (80 cases) and an ISR group (48 cases) based on coronary angiography results. The general data between the two groups were compared, as well as the EFT before discharge and 1 month after surgery, and the serum levels of SFRP5 and Wnt5a measured before surgery and 1 month postoperatively. The differences in the levels of these indicators among patients with varying degrees of coronary artery lesions were also examined. Pearson correlation analysis was used to evaluate the association between EFT and serum levels of SFRP5 and Wnt5a 1 month after surgery. Multivariate Logistic regression analysis was applied to identify the risk factors of ISR in STEMI patients after PCI. ROC curve analysis was used to assess the predictive value of EFT, and serum SFRP5 and Wnt5a levels for ISR. ResultsThe EFT values of the ISR group before discharge and 1 month after surgery were both greater than those of the non-ISR group (all P<0.01). The serum SFRP5 level of the ISR group was lower than that of the non-ISR group 1 month after surgery, while the serum Wnt5a level was higher (all P<0.01). Compared to pre-operative levels, serum SFRP5 levels increased 1 month after surgery in the non-ISR group but decreased in the ISR group (both P<005). Serum Wnt5a levels showed a mild increase 1 month after surgery compared to pre-operative levels in the non-ISR group, but increased significantly in the ISR group (both P<0.05). The serum SFRP5 level 1 month after surgery was significantly lower in the three-vessel disease group than that in the single- or two-vessel disease groups (P<0.05). EFT 1 month after surgery showed a negative correlation with SFRP5 and a positive correlation with Wnt5a. Both univariate Logistic regression analysis and Logistic regression analysis adjusted for factors such as age and BMI demonstrated that EFT, and serum SFRP5 and Wnt5a levels 1 month after surgery were independent influencing factors for ISR. ROC curve analysis revealed that the combination of these three markers yielded an AUC value of 0.906, which was higher than that of detection with any single indicator. Conclusion  Increased EFT, decreased serum SFRP5, and elevated serum Wnt5a 1 month after surgery are closely related to ISR in STEMI patients after PCI. Early detection of these markers facilitates the prediction of ISR, and the combined detection offers superior predictive value.

Objective  To investigate the application of dexmedetomidine via programmed intermittent epidural bolus (PIEB) for labor analgesia in hypertensive disorder of pregnancy (HDP) parturients, and its effect on umbilical artery flow and maternal-fetal outcomes. Methods  This study was a prospective, and double-blind clinical study. A hundred HDP parturients who had undergone labor analgesia were selected, and randomly divided into group A and B, each with 50 cases by random number table method. Group A received continuous epidural infusion, while group B received PIEB. Based on the visual analogue scale (VAS), the degree of pain before analgesia (T0), 1 h after analgesia (T1), 2 h after analgesia (T2), and at the time of complete cervical dilation (T3) were compared between the two groups of parturients. We simultaneously recorded the changes of umbilical artery flow at T0-T2 ［umbilical artery resistance index (RI), pulsation index (PI) and the ratio of maximum systolic blood velocity to diastolic blood velocity (S/D)］, maternal vital signs at T0 and T1 ［heart rate (HR) and mean arterial pressure (MAP)］, and the occurrence of adverse maternalfetal outcomes and adverse reactions in the two groups. ResultsComparison of VAS scores at different time points within each group showed statistically significant differences (all P<0.01). VAS scores at T1, T2 and T3 were all lower than that at T0(all P<0.05). VAS score of the group B at T2 was lower than that at T1(P<0.05). VAS score of the group B at T3 was lower than that at T2(P<0.05), while the VAS score of the group B at T2 or T3 were both lower than that of the group A (both P<0.01). There was no statistically significant difference in VAS score between the two groups at T0 and T1(P>0.05). Statistically significant differences were observed in RI, PI, and S/D values across different time points within both groups (all P<0.01). At T1 and T2, the RI, PI, and S/D ratio of fetuses in both groups all decreased compared to T0(all P<0.05). At T2, the RI, PI and S/D ratio of fetuses in both groups were all lower than those at T1(all P<0.05). There were no statistically significant differences in fetal RI, PI, and S/D ratio between the two groups at T0, T1 or T2(all P>0.05). At T1, HR and MAP in the two groups were both lower than those at T0(both P<0.05), while HR and MAP of the group B were both lower than those of the group A (both P<0.05). There were no statistically significant differences in the total incidences of adverse maternal-fetal outcomes or drug adverse reactions between the two groups (all P>0.05). Conclusion  Dexmedetomidine via PIEB could improve the effect of labor analgesia in HDP parturients, and maintain stability of fetal umbilical hemodynamics and maternal vital signs, with a high safety.