LMNA and Myocardial fibrosis: In addition, throughout the disease course, cardiomyocyte loss, likely repaired by replacement fibrosis, may provide a possible substrate for conduction block and re-entrant arrhythmias [42, 43]; this hypothesis is in line with previous studies showing that LMNA mutation carriers with conduction defects and arrhythmias have myocardial fibrosis involving cardiac conduction system, documented by histopathological examinations [21, 36, 41].