Atrial fibrillation from the pathologist's perspective.
Atrial fibrillation (AF), the most common sustained cardiac arrhythmia encountered in clinical practice, is associated with increased morbidity and mortality. Electrophysiologically, it is characterized by a high rate of asynchronous atrial cell depolarization causing a loss of atrial contractile function and irregular ventricular rates. For a long time, AF was considered as a pure functional disorder without any structural background. Only in recent years, have new mapping and imaging techniques identified atrial locations, which are very often involved in the initiation and maintenance of this supraventricular arrhythmia (i.e. the distal portion of the pulmonary veins and the surrounding atrial myocardium). Morphological analysis of these myocardial sites has demonstrated significant structural remodeling as well as paved the way for further knowledge of AF natural history, pathogenesis, and treatment. This architectural myocardial disarrangement is induced by the arrhythmia itself and the very frequently associated cardiovascular disorders. At the same time, the structural remodeling is also capable of sustaining AF, thereby creating a sort of pathogenetic vicious circle. This review focuses on current understanding about the structural and genetic bases of AF with reference to their classification, pathogenesis, and clinical implications.
Department of Biomedical, Biotechnological, and Translational Sciences (S.Bi.Bi.T.), Unit of Pathology, University of Parma, Parma, Italy. Electronic address: domenico.corradi@unipr.it.
Domenico
D
Corradi
D001281:Atrial Fibrillation / Q000209:etiology / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology / Q000628:therapy; D016275:Atrial Function; D064752:Atrial Remodeling; D020022:Genetic Predisposition to Disease; D006325:Heart Atria / Q000473:pathology / Q000503:physiopathology; D006801:Humans; D009206:Myocardium / Q000473:pathology*; D010641:Phenotype; D011379:Prognosis; D011667:Pulmonary Veins / Q000473:pathology / Q000503:physiopathology; D012307:Risk Factors
Atrial fibrillation; Cardiomyocyte; Fibrosis; Genetics; Structural remodeling; Upstream therapy