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In a multicenter, randomized trial of patients with atrial fibrillation and a low risk of thromboembolic events, treatment with the anticoagulant rivaroxaban showed no benefit in reducing cognitive decline, stroke or transient ischemic attack when compared to placebo.

Numerous factors can contribute to sudden cardiac death, from underlying disease after myocardial infarction to genetic variants that can claim young lives. In 'Bedside to Bench', Stanley Nattel examines recent clinical studies suggesting that a particular type of readout on an electrocardiogram (ECG) may increase the risk of the condition. This ECG 'variant' is relatively common and was previously thought to be benign. In 'Bench to Bedside', Gordon Tomaselli and Andreas Barth take a look at studies at the bench examining how oxidative stress may promote sudden cardiac death.

Spiral-wave generators, or 'rotors', have been identified by advanced mapping methods in experimental and clinical atrial fibrillation (AF). In this Review, Nattel and colleagues describe the concepts of phase mapping and spiral-wave rotors, and summarize the ways in which rotor sources might be involved in AF maintenance. They also consider the relevance of spiral-wave rotors to the management of patients with AF.

Omega-3 fatty acids have anti-inflammatory, antioxidant and membrane-stabilizing properties that indicate they could be useful in suppressing cardiac rhythm disorders. These natural dietary constituents are of particular interest for the treatment of atrial fibrillation, a common and problematic cardiac arrhythmia. However, a new, well-designed clinical study has raised major questions about their value for this indication.

In this Review, Nattel and colleagues discuss the evidence suggesting a pathophysiological role of cardiomyocyte inflammatory signalling in atrial fibrillation, consider the therapeutic potential associated with these signalling pathways, including strategies promoting the resolution of inflammation, and highlight crucial questions to be addressed in future research.

Atrial fibrillation (AF) usually begins in a self-terminating paroxysmal form. In this Review, Nattel and Dobrev extensively summarize the electrophysiological basis for paroxysmal AF occurrence and maintenance, as well as the molecular mechanisms forming the underlying substrate, drawing on data from both patients with AF and animal models of spontaneous AF. The authors also consider potential factors governing progression from paroxysmal to persistent AF.

Recent developments in the understanding of the mechanisms of cardiac arrhythmias have opened up unprecedented opportunities for drug development. Here, Nattel and Carlsson review emerging findings in the development of new types of anti-arrhythmic compounds targeting two particularly important cardiac arrhythmias: atrial fibrillation and ventricular fibrillation.

Cardiac arrhythmias produce considerable morbidity and mortality, and are challenging to treat. Advances reported in 2015 will help to guide physicians in the use of therapeutic approaches ranging from established pharmaceutical agents through ablation of arrhythmic sources to novel uses of implanted devices for life-threatening bradyarrhythmias and tachyarrhythmias.

Cardiac rhythm disorders, or 'arrhythmias', are major sources of morbidity and mortality, and have been challenging to treat because classic pharmacological therapies are often ineffective and sometimes dangerous. In the past decade, groundbreaking developments have revolutionized the management of arrhythmias and prepared the groundwork for new advances in the future.

Strategies to improve the function of damaged hearts with progenitor cells have stalled. Here, the authors show that gene transfer of a calcium-dependent potassium channel enhances the functional properties and ability of explant-derived cells to improve heart function after a heart attack.

A mutation in Shugoshin-1 causes the Chronic Atrial and Intestinal Dysrhythmia (CAID) Syndrome, but the underlying mechanisms are unknown. Here, the authors show that Shugoshin-1 controls cardiac pacemaker activity by interacting with HCN4 to enhance its cell-surface expression, and that the CAID-Syndrome mutation disrupts cardiac pacemaking by interfering with this important non-canonical interaction.

Heart atria produce a large pool of calcitonin (previously well-recognized as a thyroid-secreted hormone with roles in calcium and bone metabolism) that in the heart acts as a paracrine signal controlling atrial fibrosis and fibrillation.

In this Review, Nattel and colleagues discuss the role of cellular senescence in cardiac disease, summarize the therapeutic strategies that are being developed for targeting senescence and consider the potential implications for improving the management of patients with heart disease.

By analyzing bulk and single-cell RNA-sequencing datasets generated from left atrial appendages of individuals with atrial fibrillation and non-affected controls, Leblanc and Yiu identify cell-type-specific genes and transcriptomic programs implicated in atrial fibrillation, a cardiomyocyte-specific androgen receptor signaling signature and an anti-fibrotic effect of NR4A1 inhibition in atrial cardiofibroblasts.

New insights into the mechanisms underlying atrial fibrillation have identified promising new approaches to prevent the fundamental processes that lead to the generation of arrhythmia. Dobrev and colleagues discuss the rationale for developing new anti-atrial fibrillation drugs, the molecular and structural motifs that they target, and the results obtained in experimental and clinical studies.

Mutations in ion-transport proteins can destabilize the electrical activity of the heart, causing sudden death. It now seems that mutations in a protein that anchors ion transporters to cell membranes can have the same effect.

Available treatments for atrial fibrillation (AF) often lack sufficient efficacy or have considerable complications, but novel therapies based on the underlying molecular mechanisms of AF can provide useful alternatives. MicroRNAs (miRNAs) regulate gene transcription, and constitute a promising therapeutic approach for the treatment of AF. In this Review article, Luo et al. provide a comprehensive overview of the mechanisms of miRNA action, and explore the available experimental evidence supporting a role for miRNAs as novel therapeutic targets for AF.

Postoperative atrial fibrillation complicates 20–40% of cardiac surgical procedures. In this Review, the authors summarize the epidemiological and clinical features of postoperative atrial fibrillation, the available pathophysiological evidence and the recommended prophylactic and therapeutic approaches.

Atrial fibrillation occurs when cardiac electrical impulses become disordered, leading to a rapid and irregular heartbeat. Lip and colleagues discuss the mechanisms that underlie this common arrhythmia and outline current strategies and potential future developments for its diagnosis and management.

The association between exercise and increased risk of atrial fibrillation among athletes is well established. In this Review, Guasch and Mont discuss the evidence supporting the existence of exercise-induced arrhythmias and describe the special considerations for management of these patients.