Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia globally, linked to significant cardiovascular morbidity and mortality. Catheter ablation has emerged as a primary therapeutic approach, yet substantial recurrence rates limit its long-term efficacy. This review critically examines the molecular mechanisms underlying AF recurrence post-ablation, synthesizing recent findings from current literature. Key molecular pathways identified include structural remodeling mediated by fibrosis involving transforming growth factor-beta 1 (TGF-β1) and matrix metalloproteinases (MMPs), ion-channel dysregulation, inflammatory pathways, autonomic nervous system imbalance, and genetic and epigenetic alterations. Despite considerable advances, critical gaps persist due to small, heterogeneous studies and insufficient long-term follow-up. Comprehensive mechanistic research integrating genomics, proteomics, and advanced imaging is urgently needed to better characterize these pathways. Future studies must validate biomarkers such as TGF-β1, MMPs, connexins, and novel markers like GDF-15 and relaxin. Clinical translation of these molecular insights through precision diagnostics and personalized interventions holds great promise to enhance patient selection, optimize ablation strategies, reduce recurrence, and ultimately improve clinical outcomes in AF management.
Background Esophageal varices (EVs) develop as a complication of chronic liver disease and, when left unaddressed, can lead to variceal hemorrhage manifesting as severe hematemesis and occasionally, melena. Due to its frequent negative associations, early diagnosis and the implementation of non-selective beta blocker primary prophylaxis are imperative. Although upper gastrointestinal endoscopy has historically been used to image and identify EVs, patients frequently find this intrusive treatment to be uncomfortable and burdensome. It can also be expensive and challenging for patients who live in remote places and healthcare deserts, where access to healthcare is limited. Therefore, it is crucial to identify non-invasive markers for the prediction of variceal bleeding and EVs in individuals with chronic liver disease. Methodology A cross-sectional observational study was done at Osmania General Hospital, a tertiary healthcare center in Hyderabad, India. The study sample consisted of patients with chronic liver disease who underwent upper gastrointestinal endoscopy during the study period in keeping with the inclusion and exclusion criteria. In a sample of 103 patients, the mean age was 10.72±45.55 years, with 22 females (21.4%) and 81 males (78.6%). The majority (85, 82.5%) had alcoholic chronic liver disease, while 14 (13.6%) had other etiologies, and four (3.9%) had infectious causes. Data were collected to calculate the Child-Pugh score, AST to platelet ratio index (APRI), model for end-stage liver disease (MELD) score, and fibrosis-4 (FIB-4) index. The patients were observed and followed up for a duration of three months. The data were evaluated using chi-squared tests and independent t-tests, chosen according to their relevance, to assess the utility of these scores as non-endoscopic predictors of EVs and esophageal variceal bleeding (EVB). Results The results indicated that only the FIB-4 index was found to be a significant predictor of Grade 2 or higher grades of EV according to the Pacquet classification. The FIB-4 index was significantly higher in the Grade 2 or higher EV group (p = 0.029) with t(101) = 1.98. Conclusion Thus, the study demonstrates that ≥ Grade 2 EV on upper gastrointestinal endoscopy can be predicted using the FIB-4 index. Even though our study shows that the FIB-4 index is a useful noninvasive predictor of EV, large-scale studies with bigger sample sizes and longer follow-up times are necessary to ensure accurate clinical application.
Background: Despite the significant research and development of COVID-19 diagnostic and therapeutic approaches, the virus still poses a concern, particularly to groups that are already vulnerable. Several individuals experienced cardiac problems like myocardial infarction, arrhythmia, heart failure, cardiomyopathy, myocarditis, and pericarditis after they had recovered from the infection. Early diagnosis and timely management of sequelae are part of the therapy. However, there are gaps in the knowledge of the diagnostic and definitive treatment options for COVID-19 myocarditis. This review focuses on myocarditis associated with COVID-19. Objective: This systemic review provides the most recent overview of myocarditis caused by COVID-19, including clinical manifestations, diagnostic techniques, available treatments, and outcomes. Methods: The PubMed, Google Scholar, and ScienceDirect servers were used to conduct a systematic search in compliance with the PRISMA guidelines. Boolean search terms included “(COVID-19)” OR “(COVID19)” OR “(COVID-19 VIRUS INFECTION)” AND “(MYOCARDITIS)”. The results were tabulated and analyzed. Results: A total of 32 studies, including 26 case reports and 6 case series, were included in the final analysis, and 38 cases of COVID-19-associated myocarditis were analyzed. Middle-aged men constituted the most affected population (60.52%). Dyspnoea (63.15%), chest pain or discomfort (44.73%), and fever (42.10%) were the prevalent presentations. ST-segment abnormalities were reported in 48.38% of cases on electrocardiography testing. Leucocytic infiltration (60%) was the frequent finding obtained on endomyocardial biopsy. Cardiac magnetic resonance imaging yielded myocardial oedema (63.63%), and late gadolinium enhancement (54.54%) as the most common findings. Reduced ejection fraction (75%) was the frequent result obtained on echocardiography. Corticosteroids (76.31%) and immunomodulators (42.10%) were the well-established in-hospital medications. Veno-arterial extracorporeal membrane oxygenation (35%) was the most common intervention used to support the treatment. The frequent in-hospital complications were cardiogenic shock (30.76%), followed by pneumonia (23.07%). The mortality rate was 7.9%. Conclusion: Early detection and timely management of myocarditis are essential to reduce the risk of developing further complications. It is crucial to emphasize the need to evaluate COVID-19 as a possible cause of myocarditis in populations that are young and healthy to avoid fatal consequences.