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.

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.

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.

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.

Takotsubo syndrome (TTS) is an acute coronary syndrome of unknown prevalence with a physiopathological mechanism that is not yet fully understood. The course is generally benign. Current therapeutic management is based on limited evidence. Oxidative stress seems to play a role in the pathogenesis of cardiovascular diseases, especially regarding the endothelial dysfunction underlying TTS. The present review aims to describe the pathophysiological mechanisms linking oxidative stress and TTS, explore the impact of oxidative stress on TTS, and evaluate the efficacy of anti-oxidative stress therapies on TTS.

Interest in advanced echocardiographic imaging methods is growing. The left atrial strain (LAS) is among the recently developed echocardiographic parameters. LAS represents an index of tissue deformation of the left atrium (LA). This parameter is an expression of the LA function. Several arrhythmias depend on the 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 the alterations of the LAS and the development of atrial fibrillation (AF), and the diagnostic and prognostic role of the stress echocardiogram in clinical practice.