Black esophagus, also known as acute necrotizing esophagitis or acute esophageal necrosis, was first described by Goldenberg et al. [
2] in 1990. Six cases of black esophagus were seen at the Mayo Clinic, Rochester from 1997 through 2003, and 46 cases were reported in the English-language literature from 1963 through 2003 [
3]. Moreto et al. [
4] identified 10 cases of acute esophageal necrosis in a review of more than 80,000 upper endoscopies, with an incidence of only 0.0125%. Grudell et al. [
3] suggested that ischemia is the most common cause of black esophagus. Gurvits et al. [
5] demonstrated that the major risk factors include histories of cardiovascular disease, hemodynamic compromise including shock, and severe third spacing. Neumann et al. [
6] reported a case of black esophagus associated with hypotension that developed during an acute coronary event. Also, he reported that endoscopically, the lesion often appears circumferential and black, with friable or macerated mucosa, usually involving the distal two thirds of the esophagus. Histopathology usually shows necrotic debris and mucosal and submucosal necrosis with a local inflammatory response [
5]. The esophagus receives an intricate segmental vascular supply that separates this organ into three parts: upper, middle, and distal esophagus. The arterial network of the upper esophagus is derived from the descending branches of the inferior thyroid arteries. The mid-esophageal blood supply is derived from the bronchial arteries, right third or fourth intercostal arteries, and numerous small esophageal arteries off the descending aorta. The distal esophagus receives its blood flow from branches off the left gastric artery or left inferior phrenic artery, but variations are common [
7]. Therefore, since the esophagus has a rich intramural arteriovenous network complementing the segmental blood flow, spontaneous esophageal ischemia followed by necrosis is rare [
8]. The overall mortality of acute esophageal necrosis reported in the largest case review to date was high (32%) [
4]. Mortality was most frequently secondary to the seriousness of the comorbid disease state. Our patient had no severe comorbidities except for the underlying coronary three-vessel disease, and the esophageal lesion improved with only conservative treatment using an oral proton-pump inhibitor. Coronary arterial dissection associated with therapeutic coronary intervention occurs in approximately 32% to 41% of cases [
9]. In our case, coronary arterial dissection during the PCI led to sudden hypotension, which was suspected to cause acute esophageal ischemia and then necrosis. Interventional cardiologists should be aware that not only acute coronary events or chronic cardiovascular diseases but also acute hemodynamic changes that can take place during coronary intervention may cause acute esophageal necrosis.