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As HF and diabetes are recognised inflammatory conditions, with reports of enhanced activation of the NLRP3 inflammasome, we will also consider evidence linking microtubule organisation, inflammation and the association to mitochondrial motility. Diabetes is a global pandemic but with limited treatment options for diabetic cardiomyopathy, therefore we also discuss potential therapeutic approaches to target the mitochondrial-microtubule-inflammatory axis.Atrial fibrillation (AF) is the most prevalent cardiac arrhythmia worldwide and results in a significantly increased ischemic stroke (IS) risk. IS risk stratification tools are widely being applied to guide anticoagulation treatment decisions and duration in patients with non-valvular AF (NVAF). The CHA2DS2-VASc score is largely validated and currently recommended by renowned guidelines. However, this score is heavily dependent on age, sex, and comorbidities, and exhibits only moderate predictive power. Finding effective and validated clinical biomarkers to assist in personalized IS risk evaluation has become one of the promising directions in the prevention and treatment of NVAF. A number of studies in recent years have explored differentially expressed biomarkers in NVAF patients with and without IS, and the potential role of various biomarkers for prediction or early diagnosis of IS in patients with NVAF. In this review, we describe the clinical application and utility of AF characteristics, cardiac imaging and electrocardiogram markers, arterial stiffness and atherosclerosis-related markers, circulating biomarkers, and novel genetic markers in IS diagnosis and management of patients with NVAF. We conclude that at present, there is no consensus understanding of a desirable biomarker for IS risk stratification in NVAF, and enrolling these biomarkers into extant models also remains challenging. Further prospective cohorts and trials are needed to integrate various clinical risk factors and biomarkers to optimize IS prediction in patients with NVAF. However, we believe that the growing insight into molecular mechanisms and in-depth understanding of existing and emerging biomarkers may further improve the IS risk identification and guide anticoagulation therapy in patients with NVAF.Obesity has a strong impact on the pathogenesis of cardiovascular disease, which raises enthusiasm to understand how excess adiposity causes vascular injury. Adipose tissue is an essential regulator of cardiovascular system through its endocrine and paracrine bioactive products. Obesity induces endothelial dysfunction, which often precedes and leads to the development of cardiovascular diseases. Connecting adipose tissue-endothelial cell interplay to endothelial dysfunction may help us to better understand obesity-induced cardiovascular disease. This Mini Review discussed (1) the general interactions and obesity-induced endothelial dysfunction, (2) potential targets, and (3) the outstanding questions for future research.Background Stanford type A aortic dissection (AAD) is a catastrophic disease. An immune infiltrate has been found within the aortic wall of dissected aortic specimens. The recall and activation of macrophages are key events in the early phases of AAD. Herein, the immune filtration profile of AAD was uncovered. Methods Gene expression data from the GSE52093, GSE98770 and GSE153434 datasets were downloaded from the Gene Expression Omnibus (GEO). The differentially expressed genes (DEGs) of each dataset were calculated and then integrated. A protein-protein interaction (PPI) network was established with the Search Tool for the Retrieval of Interacting Genes/Proteins (STRING), and the hub genes were identified in Cytoscape. Furthermore, gene ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis of hub genes were performed. Finally, we set GSE52093 and GSE98770 as the training set and GSE153434 as the validation set to assess immune infiltration in AAD using CIBERSial cell apoptosis, hypoxia and the interaction of cytokines and chemokines. Conclusion The monocyte-macrophage system plays a major role in immune-inflammatory responses in the development of AAD. Several hub genes are involved in this process via diverse mechanisms.An increasing number of cardiovascular adverse effects, emergency room visits, and deaths have been linked to energy drinks. In this review, we summarized available published literature assessing electrophysiological and ischemic adverse effects associated with energy drink consumption. Overall, 32 case reports and 19 clinical trials are included in this review. Ventricular arrhythmia, supraventricular arrhythmia, and myocardial ischemia were amongst the most commonly reported in case reports with 3 having a fatal outcome. Although serious ischemic changes, arrhythmias, or death were not observed in clinical trials, significant electrophysiological changes, such as PR/PQ interval shortening/prolongation, QT/QTc shortening/prolongation, and ST-T changes, were noted. QT/QTc interval prolongation appears to be the most significant finding in clinical trials, and there appears to be a dose-response relationship between energy drink consumption and QTc prolongation. The exact mechanisms and the particular combination of ingredients behind energy drink-induced cardiac abnormalities require further evaluation. Until more information is available, energy drink use should be considered as part of the differential diagnosis in appropriate patients presenting with electrocardiographic changes. Further, certain patient populations should exercise caution and limit their energy drink consumption.Background The relationship between fasting hyperglycemia (FHG) and new-onset atrial fibrillation (AF) in patients with acute myocardial infarction (AMI) is unclear, and whether their co-occurrence is associated with a worse in-hospital and long-term prognosis than FHG or AF alone is unknown. Objective To explore the correlation between FHG and new-onset AF in patients with AMI, and their impact on in-hospital and long-term all-cause mortality. Methods We performed a retrospective cohort study comprising 563 AMI patients. The patients were divided into the FHG group and the NFHG group. The incidence of new-onset AF during hospitalization was compared between the two groups and sub-groups under different Killip grades. [https://www.selleckchem.com/products/turi.html TRULI molecular weight] Logistic regression was used to assess the association between FHG and new-onset AF. In-hospital mortality and long-term all-cause mortality were compared among patients with FHG, AF, and with both FHG and AF according to 10 years of follow-up information. Results New-onset AF occurred more frequently in the FHG group than in the NFHG group (21.