Background: Ventricular arrhythmias are associated with sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM). Previous studies have found the late gadolinium enhancement (LGE) on cardiac magnetic resonance (CMR) was independently associated with ventricular arrhythmia (VA) in HCM. The risk stratification of VA remains complex and LGE is present in the majority of HCM patients. This study was conducted to determine whether the scar heterogeneity from LGE-derived entropy is associated with the VAs in HCM patients.Materials and Methods: Sixty-eight HCM patients with scarring were retrospectively enrolled and divided into VA (31 patients) and non-VA (37 patients) groups. The left ventricular ejection fraction (LVEF) and percentage of the LGE (% LGE) were evaluated. The scar heterogeneity was quantified by the entropy within the scar and left ventricular (LV) myocardium.Results: Multivariate analyses showed that a higher scar [hazard ratio (HR) 2.682; 95% CI: 1.022–7.037; p = 0.039] was independently associated with VA, after the adjustment for the LVEF, %LGE, LV maximal wall thickness (MWT), and left atrium (LA) diameter.Conclusion: Scar entropy and %LGE are both independent risk indicators of VA. A high scar entropy may indicate an arrhythmogenic scar, an identification of which may have value for the clinical status assessment of VAs in HCM patients.

Ischemic cardiomyopathy (ICM) caused by coronary artery disease always leads to myocardial infarction and heart failure. Identification of novel transcriptional regulators in ICM is an effective method to establish new diagnostic and therapeutic strategies. In this study, we used two RNA-seq datasets and one microarray dataset from different studies, including 25 ICM and 21 non-failing control (NF) samples of human left ventricle tissues for further analysis. In total, 208 differentially expressed genes (DEGs) were found by combining two RNA-seq datasets with batch effects removed. GO and KEGG analyses of DEGs indicated that the response to wounding, positive regulation of smooth muscle contraction, chromatin, PI3K-Akt signaling pathway, and transporters pathways are involved in ICM. Simple Enrichment Analysis found that NFIC-binding motifs are enriched in promoter regions of downregulated genes. The Gene Importance Calculator further proved that NFIC is vital. NFIC and its downstream genes were verified in the validating microarray dataset. Meanwhile, in rat cardiomyocyte cell line H9C2 cells, two genes (Tspan1 and Hopx) were confirmed, which decreased significantly along with knocking down Nfic expression. In conclusion, NFIC participates in the ICM process by regulating TSPAN1 and HOPX. NFIC and its downstream genes may be marker genes and potential diagnostic and therapeutic targets for ICM.

P acing-induced cardiomyopathy (PICM) results from the detrimental effect of frequent right ventricular pacing. [1] The diagnosis relies on a combination of pacing-associated ventricular dyschrony manifested with ECG wide LBBB-pattern QRS duration and clinical assessment, imaging studies. Conduction system pacing (CSP), such as His bundle pacing (HBP) and left bundle branch pacing (LBBP), may help to prevent PICM, [2] but the criteria for optimal patient selection remain inadequately defined. Recent study demonstrated that left bundle branch pacing (LBBP) improves left ventricular (LV) function in patients with PICM by restoring physiological activation propagation in the left ventricle. [3] However, it is important to note that some patients may not well respond to LBBP. The etiology of varied responses to LBBP in patients with PICM remains poorly understood, and reliable predictive models for these differential outcomes are currently lacking. FDG imaging serves as a valuable tool for estimating the energetic metabolism of myocardial cells that is relevant to cardiac mechanical work, while may yield the value in understanding the mechanism of cardiac response to pacing therapy. Herein，we present two PICM patients underwent LBBP upgrades with significant postoperative electrocardiographic improvement, yet exhibited different 18 F-FDG imaging characteristics and follow-up outcomes.