Impaired Intracellular Calcium Buffering Contributes to the Arrhythmogenic Substrate in Atrial Myocytes From Patients With Atrial Fibrillation.

Background: Alterations in the buffering of intracellular Ca, for which myofilament proteins play a key role, have been shown to promote cardiac arrhythmia. It is interesting that although studies report atrial myofibrillar degradation in patients with persistent atrial fibrillation (persAF), the intracellular Ca buffering profile in persAF remains obscure. Therefore, we aimed to investigate the intracellular buffering of Ca and its potential arrhythmogenic role in persAF.

Altered atrial cytosolic calcium handling contributes to the development of postoperative atrial fibrillation.

Aims: Atrial fibrillation (AF) is a commonly occurring arrhythmia after cardiac surgery (postoperative AF, poAF) and is associated with poorer outcomes. Considering that reduced atrial contractile function is a predictor of poAF and that Ca2+ plays an important role in both excitation-contraction coupling and atrial arrhythmogenesis, this study aims to test whether alterations of intracellular Ca2+ handling contribute to impaired atrial contractility and to the arrhythmogenic substrate predisposing patients to poAF.

Methods And Results: Right atrial appendages were obtained from patients in sinus rhythm undergoing open-heart surgery.