Atrial cardiomyopathy: Diagnosis, clinical implications and unresolved issues in anticoagulation therapy

Atrial cardiomyopathy (AC) is an evolving pathophysiological entity that has expanded our understanding regarding the atrium and its role in arrhythmogenesis and cardiac thromboembolism. The pathological myocardium in AC promotes arrhythmogenesis through mechanical dysfunction (hypocontractility, fibrosis), adverse alterations of the endothelium and secretion of prothrombotic factors (IL-6, IL-8, TNF-a). ‘Red flags’, indicative of AC, can be recognized either non-invasively by electrocardiography, echocardiography and cardiac magnetic resonance imaging or invasively by high-density electroanatomical mapping as low bipolar voltage areas of the affected myocardium. Signs of AC have been strongly associated with an increased risk of ischemic stroke, even embolic strokes of undetermined source, regardless of the coexistence of atrial fibrillation (AF). The underlying existence of AC has been negatively correlated with the success rate of catheter ablation of AF. The clinical value of AC is the provision of a novel pathway regarding the potential mechanisms of cerebrovascular events of cardiac thromboembolic origin. In addition, AC may serve as a risk stratification tool to predict the long-term responders of AF catheter ablation.