Atrial fibrillation is the most common sustained cardiac dysrhythmia leading to an increased risk of heart failure and thromboembolic stroke. It is a multifactorial disease, the incidence of which increases with age and presenceof other comorbidities. Especially in the young it can develop in the absence of known risk factors, and is called idiopathic or ,loneĆ atrial fibrillation, which in a smaller proportion can occur as a familial form. The familial idiopathic atrial fibrillation is a monogenetic disease; mutations found this far mainly cause an altered function of potassium channels. In contrast, the nonfamilial or sporadic form of idiopathic atrial fibrillation is a polygenetic disease where certain polymorphisms increase the risk of developing atrial fibrillation. These polymorphisms encode the subunits of cationic channels and proteins, which participate in inflammation and propagation of depolarisation. With the advances in genetics and discovery of mutations and polymorphisms which increase the risk of developing atrial fibrillation we will discover pathophysiological mechanisms of initiation and chronification of this dysrhythmia. The discoveries could be a basis for the development of new prevention and treatment strategies for atrial fibrillation.

Bibliografija: str. 431-432