Circulating N-terminal pro-B-type natriuretic peptide (NT pro-BNP), high- sensitivity C-reactive protein (hs-CRP) and big endothelin (big-ET) have been shown to be increased in heart failure and to contribute to both hemodynamic deterioration and cardiovascular remodeling. Here, we examined the prognostic value of the three neurohormones at admission in a population of hospitalized patients with dilated cardiomyopathy (DCM).

Recent studies have demonstrated that myocardial calpain triggers caspase-3 activation and myocardial apoptosis in models of sepsis, whereas the inhibition of calpain activity down-regulates myocardial caspase-3 activation and apoptosis. However, the mechanism underlying this pathological process is unclear. Therefore, in this study, our aim was to explore whether the Hsp90/Akt signaling pathway plays a role in the induction of myocardial calpain activity, caspase-3 activation and apoptosis in the septic mice.

Purpose of review: Hypertrophic cardiomyopathy (HCM) is one of the leading causes of sudden cardiac death (SCD) in younger people and athletes. It is crucial to identify the risk factors for SCD in individuals with HCM. This review, based on recent systematic literature studies, will focus on the risk factors for SCD in patients with HCM. Recent findings: An increasing number of studies have further explored the risk factors for SCD in patients with HCM, and new risk markers have emerged accordingly. In addition, more accurate SCD risk estimation and stratification methods have been proposed and continuously improved. Summary: The identification of independent risk factors for HCM-related SCD would likely contribute to risk stratification. However, it is difficult to predict SCD with absolute certainty, as the annual incidence of SCD in adult patients with HCM is approximately 1%. The review discusses the established risk factors, such as a family history of SCD, unexplained syncope and some new risk factors. Taken together, the findings of this review demonstrate that there is a need for further research on individual risk factors and that SCD risk stratification in HCM patients remains a clinical challenge.

Alcoholic cardiomyopathy (ACM) is considered one of the main causes of left ventricular dysfunction and is the leading cause of nonischemic dilated cardiomyopathy (DCM) in developed countries. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM. This study aimed to identify risk factors related to a poor outcome in ACM patients. Retrospective cohort study. This study included 321 patients with ACM admitted to our hospital between 2003 and 2013. This study aimed to investigate the clinical characteristics and outcomes of the patients with ACM, and the primary endpoint of the study was all-cause mortality, which was assessed through patient medical records (review of patient hospital records and periodic examination of patients in the outpatient clinic) and medical follow-up calls with trained personnel. All-cause mortality was assessed using Kaplan–Meier survival curves, and the risk factors were assessed using Cox regression. A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups. After a median follow-up period of 3.78 years (interquartile range: 2.08–6.52 years), 83 (27.7%) patients were dead. The independent predictors of all-cause mortality due to ACM were the QRS duration (HR: 1.014; 95% CI: 1.004–1.019; P = .003), systolic blood pressure (HR: 0.980; 95% CI: 0.963– 0.997; P = .020), and New York Heart Association classification (HR: 1.595; 95% CI: 1.110–2.290; P = .011) at admission. Our study indicated that the QRS duration, systolic blood pressure, and New York Heart Association classification at admission provided independent prognostic information in patients with ACM.

Current research on the stellate ganglion (SG) has shifted from merely understanding its role as a collection of neurons to recognizing its importance in immune regulation. As part of the autonomic nervous system (ANS), the SG plays a crucial role in regulating cardiovascular function, particularly cardiac sympathetic nerve activity. Abnormal SG function can lead to disordered cardiac electrical activity, which in turn affects heart rhythm stability. Studies have shown that excessive activity of the SG is closely related to the occurrence of arrhythmias, especially in the context of inflammation. Abnormal activity of the SG may trigger excessive excitation of the sympathetic nervous system (SNS) through neuroimmune mechanisms, thereby increasing the risk of arrhythmias. Simultaneously, the inflammatory response of the SG further aggravates this process, forming a vicious cycle. However, the causal relationship between SG, inflammation, and arrhythmias has not yet been fully clarified. Therefore, this article deeply explores the key role of the SG in arrhythmias and its complex relationship with inflammation, providing relevant clinical evidence. It indicates that interventions targeting SG function and inflammatory responses have potential in preventing and treating inflammation-related arrhythmias, offering a new perspective for cardiovascular disease treatment strategies.