Characterizing atrial fibrillation substrate via molecular and electrical fingerprint

Atrial fibrillation (AF) is a complex cardiac arrhythmia characterized by irregular rhythm and rapid heart beats. Although fibrosis has been traditionally considered a key factor in AF development, the current research challenges this notion. The findings suggest that lone fibrosis is not the sole culprit in AF trigger and persistence, indicating the involvement of additional and parallel pathophysiological mechanisms. Proteostasis, the maintenance of protein homeostasis, plays a significant role in AF pathogenesis. The present study sheds light to the importance of HSPs as chaperones that maintain proteostasis in atrial cardiomyocyte, and consequently its proper function. It was shown that levels of HSPs, including HSP70, cvHSP, HSP60, and HSP27, can serve as potential indicators of AF stage, recurrence after therapy, and post-operative AF onset. Assessing electrical remodeling through high-resolution epicardial mapping is a promising approach for identifying features of electropathology, and ultimately bio-electrical markers in AF. This methodology provides valuable insights into the correlation between molecular findings and electrophysiological features. By characterizing the molecular mechanisms underlying electrical alterations, clinicians acquire a deeper understanding of AF and tailor treatment strategies accordingly. Furthermore, cytoskeletal proteins, such as desmin, lamin A/C, titin, seem to have an important role driving AF. Genetic variants in these proteins can lead to contractile and electrophysiological atrial abnormalities in cardiomyocytes, associated with AF. In summary, these articles collectively contribute to our understanding of AF by exploring AF substrate under molecular and electrical perspectives.