Atrial fibrillation (AF) is the most common arrhythmia in the world. Despite the large number of studies focused on the causes and mechanisms of AF, it remains a clinical challenge. Atrial electrical and structural remodelling caused by AF is responsible for the perpetuation of the arrhythmia. However, a validated noninvasive method for assessment of atrial fibrosis in clinical practice is lacking. In this review, we aim to present an update about the origins and mechanisms of atrial remodelling, particularly focusing on atrial fibrosis, and compare imaging techniques that can detect atrial changes and greatly contribute to the clinical management of patients with AF.

Cardiac amyloidosis is a rare, infiltrative cardiomyopathy that presents with thickened ventricular walls and progressive heart failure. The morphological findings and clinical features are shared with many other diseases (i.e. hypertrophic cardiomyopathy, ‘athlete's heart,’ Fabry disease, and hypertensive cardiomyopathy), and misdiagnosis occurs frequently. Cardiologists have many instruments that can help reach a correct diagnosis in a relatively short time. As tiles of a mosaic are placed to create an image, thoughtful and smart use of the different diagnostic tools available allows the opportunity to identify amyloid infiltration of the myocardium. When the myocardium is involved, prognosis is poor, so identification of its involvement is crucial for disease management. The diagnostic process begins with an accurate evaluation of clinical elements and includes cardiovascular imaging (echocardiography, magnetic resonance, and nuclear medicine), electrocardiography, serological assays, and myocardial biopsy; only the appropriate integration of these instruments can reveal the diagnosis to an expert physician. The latest improvements in non-invasive diagnostic techniques with increased diagnostic power have reduced the need for biopsy.

The aim of our study was to assess longitudinal (L), circumferential (C) and radial (R) strain (S) of the left ventricle (LV) in patients with acute myocarditis and preserved LV wall motion. Of the 26 male patients that were enrolled, 13 patients (26+/-8 years) suffered from acute myocarditis and 13 (25+/-2 years) were healthy participants (controls). Both patients and controls underwent cardiac magnetic resonance (CMR) and 2-dimensional S imaging (2D-S) echocardiography on the same day. Myocardial strains (RS, LS and CS) were quantified by 2D-S. In patients with myocarditis, a delayed enhancement (DE) CMR study was performed to identify damaged myocardial segments. In the myocarditis group there was a significant LS reduction compared with controls (-25+/-7 vs -20+/-7, P<0.0001), whereas no difference was found between the 2 groups concerning CS and RS. Subepicardial DE areas were found in 12 of 13 patients. Segments with DE showed a significantly lower LS in comparison with segments without DE (-19+/-4 vs -23+/-6, P<0.0001). In contrast, no difference in CS and RS was found when comparing segments with DE vs segments without DE. In patients with acute myocarditis, evidence of subepicardial damage and no wall motion abnormalities, longitudinal deformation is diffusely impaired, whereas circumferential impairment is regionally sited in the areas of subepicardial damage.