Long QT syndrome is characterized by prolongation of the corrected QT (QTc) interval on the surface electrocardiogram and is associated with precipitation of torsade de pointes (TdP), a polymorphic ventricular tachycardia that may cause sudden death. Acquired long QT syndrome describes pathologic excessive prolongation of the QT interval, upon exposure to an environmental stressor, with reversion back to normal following removal of the stressor. The most common environmental stressor in acquired long QT syndrome is drug therapy. Acquired long QT syndrome is an important issue for clinicians and a significant public health problem concerning the large number of drugs with this adverse effect with a potentially fatal outcome, the large number of patients exposed to these drugs, and our inability to predict the risk for a given individual. In this paper, we focus on mechanisms underlying QT prolongation, risk factors for torsades de pointes and describe the short- and long-term treatment of acquired long QT syndrome.

Atrial fibrillation (AF) has different underlying substrates. Atrial remodeling involves electrophysiological and structural abnormalities that promote the development and perpetuation of AF. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling. The mechanistic links between atrial remodeling and inflammation are complex while diverse underlying diseases and conditions may affect these pathways. Inflammatory markers have also been associated with AF development, recurrence, perpetuation, total AF burden as well as with thromboembolic complications. The development of specific anti‐inflammatory interventions in this setting seems to be challenging and complicated. Several agents with pleiotropic properties, including anti‐inflammatory, have been tested in experimental and clinical settings with variable results. This updated review provides a concise overview of all available data regarding the role of inflammation in AF including the predictive role of inflammatory markers. Also, current knowledge and future directions on anti‐inflammatory strategies are critically discussed.

Obesity is a worldwide health problem with epidemic proportions that has been associated with atrial fibrillation (AF). Even though the underlying pathophysiological mechanisms have not been completely elucidated, several experimental and clinical studies implicate obesity in the initiation and perpetuation of AF. Of note, hypertension, diabetes mellitus, metabolic syndrome, coronary artery disease, and obstructive sleep apnea, represent clinical correlates between obesity and AF. In addition, ventricular adaptation, diastolic dysfunction, and epicardial adipose tissue appear to be implicated in atrial electrical and structural remodeling, thereby promoting the arrhythmia in obese subjects. The present article provides a concise overview of the association between obesity and AF, and highlights the underlying pathophysiological mechanisms.

Chronic obstructive pulmonary disease (COPD) is independently associated with atrial fibrillation (AF). Decreased oxygenation, hypercapnia, pulmonary hypertension, diastolic dysfunction, oxidative stress, inflammation, changes in atrial size by altered respiratory physiology, increased arrhythmogenicity from nonpulmonary vein foci commonly located in the right atrium, and respiratory drugs have been implicated in the pathogenesis of AF in COPD. The understanding of the relationship between COPD and AF is of particular importance, as the presence of the arrhythmia has significant impact on mortality, especially in COPD exacerbations. On the other hand, COPD in AF is associated with AF progression, success of cardioversion, recurrence of AF after catheter ablation, and increased cardiovascular and allcause mortality. Treatment of the underlying pulmonary disease and correction of hypoxia and acid-base imbalance represents first-line therapy for COPD patients who develop AF. Cardioselective b-blockers are safe and can be routinely used in COPD. In addition, AF ablation was proved to be efficient and safe, and improves quality of life in these patients. This review presents the association between COPD and AF, describes the pathophysiological mechanisms implicated in AF development in COPD, underlines the prognostic significance of AF in COPD patients and vice versa, and highlights emerging therapeutic approaches in this setting.

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