 Aggression or fragilization of the oesophageal mucosa by internal or external factors, and the existence of associated medical comorbidities are recognized predisposing factors.[@ytz069-B7] It has a typical endoscopic presentation, previously described in this case, primarily affecting the distal region of the oesophagus, which is related to the scarce vascularity of this region.[@ytz069-B14] Biopsy is usually unnecessary, but it can be performed specially when it is important to make a differential diagnosis with melanoma, acanthosis nigricans, and pseudo-melanosis of the oesophagus. Treatment of ANE should focus on supportive care to maximize organ perfusion, treatment of underlying medical conditions, and intravenous PPI. Adequate monitoring to detect and properly treat complications is also essential.[@ytz069-B15]

The importance of recognition of this entity is related to the high rate of acute and long-term complications---occurrence of transmural necrosis with perforation, mediastinitis, mediastinal abscess, sepsis, and oesophageal stenosis (10--25% at long-term follow-up). Mortality depends on the underlying condition and it is variably reported in the literature, between 6% to as high as 36%, when associated with other comorbidities.[@ytz069-B10]^,^[@ytz069-B12] There are limited data to guide the management of ANE, and it is largely based upon clinical experience. Repeat endoscopic evaluation should be done to assess mucosal healing. With supportive care, resolution of endoscopic findings occurs in most patients within 72 h to 2 weeks. Symptoms of oesophageal stenosis should be monitored in the long term.[@ytz069-B16]

In this clinical case, the transient low output state during TAVI was probably the ischaemic insult that triggered ANE. The period of hypotension was short (\<4 min), without evidence of other end-organ hypotensive damage. However, the insult of TOE during TAVI and DAPT may have led to oesophageal mucosa fragilization, making it especially vulnerable to the ischaemic injury. Patien