Atrial Myopathy: Its Relationship Between Atrial Fibrillation and Strokes
Atrial myopathy is typically caused by insults such as aging, inflammation, oxidative stress, and stretching of the atria. These myopathic changes alter the properties of myocardial electrophysiology and cardiac autonomic nervous system. They can also lead to architectural structural changes characterized by fibrosis. Furthermore, atrial myopathy results in endothelial dysfunction and stasis, thereby a prothrombotic state. Electrophysiological remodeling and fibrosis facilitate the development of atrial fibrillation, which leads to more inflammation, fibrosis and autonomic remodeling, all of which contribute to a worsening prothrombotic environment, mediated by circulating inflammatory cytokines, chemokines and other molecules such as C-reactive protein (CRP), interleukin (IL)- 2, -6 and -8, tumor necrosis factor (TNF)-α, etc. Atrial fibrillation and thrombosis can develop separately and interact closely to further aggravate the underlying atrial myopathic processes. CRP = C-reactive protein; vWF = von Willebrand's Factor; WBC = white blood cell.