ACE inhibitors are the most recognized predisposing factors for OA.[7] One hypothesis is a bradykinin-mediated pathway in which RT-PA hydrolyzes plasminogen to plasmin, which in turn activates the kinin pathway and increases bradykinin production.[8] Bradykinin is a potent pro-inflammatory and pro-edematous peptide that increases vascular permeability and vasodilatation, leading to angioedema. Here, ACE is linked to angioedema.