Dyslipidemia is a metabolic disorder characterized by quantitative and/or qualitative abnormalities in serum lipid levels. Elevated serum cholesterol levels can modify the turnover and recruitment of ionic channels in myocytes and cellular homeostasis, including those of inflammatory cells. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling, which is the substrate of atrial fibrillation (AF). Data about the association between increased lipid serum levels and AF are few and contrasting. Lipoprotein (a), adiposity, and inflammation seem to be the main drivers of AF; in contrast, low-density lipoproteins, high-density lipoproteins and triglycerides are not directly involved in AF onset. The present review aimed to describe the pathophysiological link between dyslipidemia and AF, the efficacy of lipid-lowering therapies in atherosclerotic cardiovascular disease (ASCVD) patients with and without AF, and the impact of lipid-lowering therapies on AF incidence.

Despite great progress in treating atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques for AF ablation, many unanswered questions remain regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional alterations in the cardiomyocyte resulting from altered ionic fluxes and cardiomyocyte electrophysiology. Electric instability and electrical remodeling underlying the arrhythmia may result from oxidative stress, also caused by possible mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet fully elucidated; however, the reduction in AF burden after therapeutic interventions that improve mitochondrial fitness tends to support this concept. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and the current pharmacological treatment options that target mitochondria to prevent or improve the outcome of AF.

Interest in advanced echocardiographic imaging methods is growing. Left atrial strain (LAS) is among recently developed echocardiographic parameters. LAS represents an index of tissue deformation of the left atrium (LA). This parameter is an expression of LA function. Several arrhythmias are caused by impaired LA function. LAS can be assessed with a resting echocardiogram. The evaluation of LAS during stress echocardiography represents another model for assessing LA function. The development of altered LAS during physical or pharmacological stress is a predictor of early LA disease. Our review aims to evaluate the relationship between alterations in LAS and the development of atrial fibrillation (AF), and the diagnostic and prognostic roles of the stress echocardiogram in clinical practice.

Background: Cardiac arrest (CA) is a life-critical condition. Patients who survive after CA go into a defined post-cardiac arrest syndrome (PCAS). In this clinical context, the role of the echocardiogram in recent years has become increasingly important to assess the causes of arrest, the prognosis, and any direct and indirect complications dependent on cardiopulmonary resuscitation (CPR) maneu-vers. Methods: We have conduct a narrative revision of literature. Results: The aim of our review is to evaluate the increasingly important role of the transthoracic and transesophageal echocardiogram in the CA phase and especially post-arrest, analyzing the data already present in the literature. Conclusion: Transthoracic and transesophageal echocardiogram in the CA phase take on important diagnostic and prognostic role.

Background: Immune checkpoint inhibitors (ICIs), such as anti-programmed death (PD)-1 and anti-cytotoxic T-lymphocyte-associated protein (CTLA)-4 agents, have revolutionized oncology but are associated with immune-related adverse events (irAEs). Among these, ICI-associated myocarditis (ICI-M) is a rare but life-threatening complication, with mortality rates ranging from 27% to 50%. Objective: This narrative review summarizes the pathogenesis, epidemiology, clinical presentation, diagnostic methods, and management strategies for ICI-induced myocarditis, specifically highlighting emerging biomarkers and immunosuppressive therapeutic approaches. Results and Discussion: ICI-M typically presents within the first 65 days of treatment and is significantly more frequent with combination therapies. Pathologically, it is characterized by myocyte necrosis and massive infiltration of cluster of differentiation (CD)4+ and CD8+ T-cells, often overlapping with myositis (irM/M). Diagnosis relies on a multimodal approach. Management requires immediate ICI cessation and initiation of high-dose corticosteroids as first-line therapy. For steroid-refractory cases, second-line options include mycophenolate mofetil (MMF), intravenous immunoglobulin (IVIG), and emerging therapies like abatacept and ruxolitinib. Rechallenge with ICIs after high-grade ICI-M must be approached with extreme caution by the multidisciplinary team (MDT). Emerging biomarkers and omics techniques hold promise for earlier diagnosis and risk stratification. Conclusions: ICI-M is a rare yet highly lethal cardiac complication demanding high clinical vigilance and timely diagnosis. Management hinges on an aggressive multidisciplinary approach, aiming to minimize toxicity while balancing oncological efficacy.

Despite great progress in the treatment of atrial fibrillation (AF), especially with the development of increasingly effective invasive techniques, many questions remain unanswered regarding the pathogenic mechanism of the arrhythmia and its prevention methods. The development of AF is based on anatomical and functional changes in the myocardium that result from disturbed ion flows and altered electrophysiology of the cardiomyocyte. Electrical instability and electrical remodeling underlying arrhythmia may result from oxidative stress, caused by mitochondrial dysfunction. The role of mitochondrial dysfunction in the pathogenesis of AF is not yet completely clarified; however, it is emphasized by the reduction of AF burden after therapeutic interventions that improve mitochondrial well-being. This selected review aims to summarize the mechanisms of mitochondrial dysfunction related to AF and current pharmacological treatment options tar-geting mitochondria to prevent or improve the outcome of AF.