There are many causes of aortic coarctation, but the main causes are hypertension and atherosclerosis. The etiology of atypical aortic coarctation is essentially the same as that of typical aortic coarctation, with the difference that atypical aortic coarctation has the potential for rupture and bleeding of the trophoblastic vessels in the arterial wall. Typical aortic coarctation is most often seen in hypertension and atherosclerosis and is due to rupture of the intima of the aorta and the formation of a coarctation of blood through the rupture into the aortic mesentery under high pressure, resulting in a double-lumen aorta, which shows a typical true and false double-lumen phenomenon on both CT scan and enhancement. Atypical aortic coarctation is caused by intimal damage due to atheromatous plaque or atherosclerotic penetrating ulcers resulting in blood infiltration into the mid-aortic wall, forming an intramural hematoma; another important cause of intramural aortic hematoma formation is due to rupture of the aortic trophoblastic vessels. Unlike typical aortic coarctation, there is no endothelial tear and no traffic with the true lumen of the aorta. On CT scan, the true and false lumen may show different densities, with the false lumen being dense in the acute phase and may be isointense or hypointense in the chronic phase. The aortic wall is crescentic or circumferential thickening with a thickness of more than 5 mm, or the aortic endothelial calcification is displaced into the aortic lumen by more than 5 mm. enhancement scan of the false lumen is not enhanced, therefore, the false lumen and the aortic endothelium of the aortic coarctation cannot be shown, and only a few localized strips of contrast penetrate into the false lumen, indicating the presence of small leaky holes in the aortic endothelium. The pseudolumen is generally hypointense on the enhancement scan. The true lumen is slightly thinned and distorted, and the intima shows smooth and normal. The reason for the non-enhancement of the false lumen in atypical aortic coarctation may be that the false lumen is not communicating with the true lumen, i.e., there is no iatrogenic communication, or when the rupture is occluded, the blood does not flow in the false lumen, and the contrast agent cannot enter the false lumen and does not enhance; if it is due to the rupture and bleeding of the aortic mesenteric or epicardial trophoblastic vessels and the formation of intramural hematoma, there is no communication with the true aortic lumen, and the false lumen does not enter the contrast agent and does not enhance. The following clinical and CT manifestations suggest atypical aortic coarctation: 1. severe chest pain or with abdominal pain; 2. no significant decrease in blood pressure or instead an increase in blood pressure despite signs of shock; 3. sudden onset of aortic closure insufficiency or progressive worsening of heart failure; 4. inconsistent pulsation strength of both carotid, brachial and femoral arteries, or even no pulse. 5, CT scan aortic wall thickening in a semilunar or annular shape, appearing true or false lumen density, false lumen is high or low density; 6, aortic endothelial calcification to the aortic lumen displacement, lumen deformation or narrowing; 7, CT enhanced scan false lumen does not strengthen, does not show the endothelium, visible leakage hole; 8, with pericardial, thoracic and mediastinal effusion (blood).