The World Health Organization announced that COVID-19, with SARS-CoV-2 as its pathogen, had become a pandemic on 11 March 2020. Today, the global epidemic situation is still serious. With the development of research, cardiovascular injury in patients with COVID-19, such as arrhythmia, myocardial injury, and heart failure, is the second major symptom in addition to respiratory symptoms, and cardiovascular injury is related to the prognosis and mortality of patients. The incidence of arrhythmia in COVID-19 patients ranges from 10% to 20%. The potential mechanisms include viral infection-induced angiotensin-converting enzyme 2 expression change, myocarditis, cytokine storm, cardiac injury, electrophysiological effects, hypoxemia, myocardial strain, electrolyte abnormalities, intravascular volume imbalance, drug toxicities and interactions, and stress response caused by virus infection. COVID-19 complicated with arrhythmia needs to be accounted for and integrated in management. This article reviews the incidence, potential mechanisms, and related management measures of arrhythmia in COVID-19 patients.

Introduction: The aim of this study was to investigate the relationship between ferroptosis and myocardial fibrosis in atrial fibrillation (AF).Material and methods: The patient’s left atrial appendage tissue was obtained in cardiac surgery. Sirius red staining, Prussian blue and Western blot were used to detect staining to assess histological fibrosis and ferroptosis changes.Results: There is a certain correlation between the degree of tissue fibrosis and ferroptosis in AF (r = 0.7763, p = 0.0004). The key proteins related to the regulation of ferroptosis were significantly abnormal in the AF group.Conclusions: Ferroptosis is involved in myocardial fibrosis of AF and is a potential target for the diagnosis, prevention and treatment of AF.

Aortic dissection (AD) is a life-threatening acute aortic syndrome. There are limitations and challenges in the discovery and application of biomarkers and drug targets for AD. Mendelian randomization (MR) analysis is a reliable analytical method to identify effective therapeutic targets. We aimed to identify novel therapeutic targets for AD and investigate their potential side-effects based on MR analysis. Data from protein quantitative trait loci (pQTLs) were used for MR analyses to identify potential therapeutic targets. We probed druggable proteins involved in the pathogenesis of aortic dissection from deCODE. In this study, a two-sample MR analysis was conducted, with druggable proteins as the exposure factor and data on genome-wide association studies (GWAS) of AD as the outcome. After conducting a two-sample MR, summary data-based Mendelian randomization (SMR) analysis and colocalization analysis were performed. A protein–protein interaction (PPI) network was also constructed to delve into the interactions between identified proteins. After MR analysis and the Steiger test, we identified five proteins as potential therapeutic targets for AD. SMR analysis and colocalization analysis also confirmed our findings. Finally, we identified ASPN (OR = 1.36, 95% CI: 1.20, 1.54, p = 4.22 × 10⁻⁵) and SPOCK2 (OR = 0.57, 95% CI: 0.41, 0.78, p = 4.52 × 10⁻⁴) as the core therapeutic targets. Through PPI network analysis, we identified six druggable targets, enabling the subsequent identification of six promising drugs from DrugBank for treating AD. This discovery of specific proteins as novel therapeutic targets represents a significant advancement in AD treatment. These findings provide more effective treatment options for AD.

(1) Background: Concomitant mild aortic valve disease is frequently found in patients undergoing rheumatic mitral valve surgery. To date, only a limited number of single-center studies have specifically addressed the untreated baseline aortic valve disease long-term progression and reoperation rate. Thus, we conducted a meta and landmark analysis to systematically review the issue. (2) Methods: This study investigated the long-term prognostic of baseline mild aortic valve disease in patients undergoing rheumatic mitral valve surgery, based on evidence from PubMed, Embase, Cochrane Library, and Web of Science databases. (3) Results: Meta analysis revealed that patients with mild aortic valve disease had a higher risk of disease progression, with a 3.3-fold risk in the 0–5-year follow-up, which jumped to a hazard ratio of 6.42 in longer-term follow-up (5–25 years). Patients with aortic stenosis had an 8.37-fold risk of progression compared with aortic regurgitation and appeared to be poorly related to the time cut-off. Similarly, higher reoperation rates at long-term follow-up were seen in aortic stenosis patients. (4) Conclusions: This study suggests that patients with mild aortic valve disease at baseline have poorer long-term aortic valve-related progression and reoperation rates, especially aortic stenosis. For those with concomitant aortic stenosis, further investigation of the impact of lesion progression is warranted.