Atrial fibrillation (AF), especially persistent and long-standing persistent AF, may result in electro-anatomical changes in the left atrium, resulting in remodeling and deposition of fibrous tissue. There are emerging data that atrial substrate modification may increase the risk of thromboembolic complications, including stroke. Several studies have reported that atrial fibrosis is due to complex interactions among several cellular and neurohumoral mediators. Late gadolinium enhancement MRI has been reported to allow quantitative assessment of myocardial fibrosis in patients at risk of developing a stroke. Current stroke risk stratification criteria for AF do not utilize atrial fibrosis as an independent risk factor despite its association with AF and stroke. Further research is required in developing adequate risk stratification tools for predicting the stroke risk and catheter ablation outcomes in AF.