Figure 1.

A schematic cascade of events from hypothalamus activity and thyroid malfunction to promotion of AF. Pre-clinical and clinical evidence show that hyperthyroidism, and eventually hypothyroidism, are responsible for structural and functional changes affecting cardiac cells, including atrial cardiomyocytes and atrial fibroblasts, leading to the development of arrhythmogenic substrate characterized by electrical conduction slowing, mitochondrial energetic perturbation, and inflammation-induced fibrosis and cardiotoxicity promoting occurrence and maintenance of atrial fibrillation.