Excerpt

Atrial fibrillation (AF) is associated with the occurrence of substantial structural changes in atrial tissue. AF is known to induce a cellular calcium-overload due to an increased influx of calcium through L-type calcium channels. Therefore, alterations of intracellular calcium homeostasis with activation of calcium-dependent signalling pathways like calcineurin and calpain appear of particular importance. Whereas calcineurin-dependent signalling contributes to the development of atrial hypertrophy [1‐3], activation of the calcium-dependent protease calpain I may lead to destruction of cellular proteins. The histopathology of fibrillating atria is thought to be similar to chronically ischemic ventricular myocardium. A study by Goette et al. [4] showed that patients with AF have increased expression and activity of calpain I in atrial tissue. The changes in calpain activity were accompanied by reduced amounts of TnT and morphological degradation of myofilaments in fibrillating atria. Aime-Sempe et al. [5] provided evidence of an increased rate of apoptosis in fibrillating human atria. Importantly, inflammatory infiltrates were not observed in that study either. This suggests that non-inflammatory pathways contribute for the described apoptotic cell death in atrial tissue. …