Atrial Myopathy

Central Illustration. 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.

Figure 1. Stages of Atrial Myopathy AF = atrial fibrillation.

Figure 2. Atrial 4D Flow CMR in Patients With AF (A) Atrial 4-dimensional (4D) flow cardiac magnetic resonance (CMR) for 2 patients with AF with comparable left atrial (LA) volume and identical CHA2DS2-VASc scores = 1 indicating low thromboembolic risk. Velocity histograms (C) quantify the LA velocity distribution inside the (B) LA. (D) LA stasis maps depict the relative amount of low LA flow velocities (<0.2 m/s). Note the substantially increased flow stasis (red) in subject #51 compared with subject #35 despite identical CHA2DS2-VASc scores. Ao = aorta; LV = left ventricle; PA = pulmonary artery; RA = right atrium; other abbreviation as in Figure 1.