Atrial fibrillation (AF) causes heart failure, ischemic strokes, and poor quality of life. The number of patients with AF is estimated to increase to 18 million in Europe in 2050. Pharmacological therapy does not cure AF in all patients. Ablative pulmonary vein isolation is recommended for patients with drug-resistant symptomatic paroxysmal AF but is successful in only about 60%. In patients in whom ablative therapy is successful on the long term, recurrence of AF may occur in the first weeks to months after pulmonary vein ablation. The early recurrence (or delayed cure) of AF is not understood but forms the basis for the generally accepted 3-month blinding (or blanking) period after ablation therapy, which is not included in the evaluation of the eventual success rate of the procedures. The underlying pathophysiological processes responsible for early recurrence and the delayed cure are unknown. The implicit assumption of the blinding period is that the AF mechanism in this period is different from the ablation-targeted AF mechanism (ectopy from the pulmonary veins). In this review, we evaluate the temporary and long-lasting pro- and antiarrhythmic effects of each of the pathophysiological processes and interventions (necrosis, ischemia, oxidative stress, edema, inflammation, autonomic nervous activity, tissue repair, mechanical remodeling, and use of antiarrhythmic drugs) occurring in the blinding period that can modulate AF mechanisms. We propose that stretch-reducing ablation scar is a permanent antiarrhythmic mechanism that develops during the blinding period and is the reason for delayed cure.