1.Typing
The most widely used traditional aortic coarctation staging methods are the Stanford staging and the Debakey staging.Debakey divided thoracic aortic coarctation aneurysms into three types: type I, where the thoracic aortic coarctation aneurysm originates from the ascending aorta and involves the abdominal aorta; type II, where the thoracic aortic coarctation aneurysm is limited to the ascending aorta; type III, where the thoracic aortic coarctation aneurysm originates from the thoracic descending Type III, where the thoracic aortic coarctation aneurysm originates in the thoracic descending aorta and does not involve the abdominal aorta downward, is called IIIA, while those involving the abdominal aorta are called IIIB.
Stanford University’s Daily et al. divided thoracic aortic coarctation aneurysms into two types: those involving the ascending aorta, regardless of the origin of the coarctation, are called type A; those originating in the descending thoracic aorta and not involving the ascending aorta are called type B. Stanford type A is equivalent to Debakey types I and II, and Stanford type B is equivalent to Debakey type III. Stanford A is equivalent to Debakey I and II, and Stanford B is equivalent to Debakey III. This guideline considers Stanford typing to be more concise and practical.
2.Grading
Submucosal hemorrhage in the aortic wall, or intermural hematoma formation, as well as ulcer formation of sclerotic plaque in the aortic wall, may be the early stage of entrapment formation, or a subtype of entrapment. On this basis, a 5-level classification of aortic coarctation was proposed.
Grade 1 (typical aortic coarctation with a ruptured and avulsed intimal sheet dividing the aorta into true and false chambers)
The characteristic pathological change in the development of aortic coarctation is a tear in the intima-media of the aorta (usually the tear is located between the outer and inner membranes), which divides the lumen of the aorta into two lumens, a true and a false lumen, which is often larger than the true lumen due to the difference in pressure between the two lumens. However, in some patients with aortic coarctation, no endothelial rupture is found, which is uncommon clinically, but autopsy reports 4% to 12% of endothelial ruptures are not found. The entrapment lesion may begin at the endothelial rupture and progress proximally or distally, and may lead to complications when the lesion involves branches of the aorta.
Grade 2 (aortic mesenteric degeneration with subintimal hematoma formation or subintimal hemorrhage)
Intra-aortic wall hematoma formation may be an early manifestation after aortic mesenchymal degeneration. The different elasticity coefficients of the outer and inner membranes of the aorta may be another cause of intra-aortic wall hemorrhage, and the bleeding vessel may be a trophoblastic artery within the aortic wall. Grade 2 coarctation is found in about 10% to 30% of coarctations on imaging. grade 2 coarctation can be subdivided into two subtypes.
Subtype A shows a smooth aortic wall with an aortic diameter of no more than 3.5 cm and an aortic wall thickness of no more than 0.5 cm. about 1/3 of patients with this subtype can be found to have a hypoechoic zone within the aortic wall on ultrasonography, with no blood flow signal within the hypoechoic take and an average hematoma length of about 11 cm. subtype B occurs in patients with aortic atherosclerosis, with rough atheromatous plaques and calcified areas within the aortic wall. The aortic diameter exceeds 3.5 cm and the aortic wall thickness averages about 1.3 cm. Hypoechoic areas can be detected on ultrasonography in about 70% of patients with this type.
This type of lesion is more likely to occur in the descending aorta than in the ascending aorta. Follow-up data confirm that 28% to 47% of patients with intra-aortic wall hematoma formation or bleeding develop aortic coarctation, 21% to 47% develop aortic dissection, and 10% heal spontaneously.
Grade 3 (small eccentric aortic wall swelling limited to the vicinity of the intimal rupture)
This lesion has been found to have two prognoses at follow-up: incomplete microscopic coarctation if the rupture scar heals, and classic coarctation if the rupture enlarges and blood flow enters the already disrupted mesentery.
Grade 4 (aortic wall ulcer formed by rupture of aortic appendage plaque)
Ulceration of aortic atherosclerotic plaque can be clearly detected by CTA, MRA, and intra-luminal ultrasound. This lesion mainly affects the descending and abdominal aorta, and is generally more limited and does not affect the main branches of the aorta. The continued development of ulcerative lesions can lead to aortic rupture, pseudoaneurysm, or aortic coarctation formation.
Grade 5 (medically or traumatically induced aortic coarctation)
Blunt trauma to the aorta, cardiac catheterization, aortic balloon counterpulsation, and aortic clamp block can cause aortic coarctation. The coarctation caused by catheterization is often a retrograde tear, and follow-up often reveals gradual reduction of the coarctation to complete thrombosis, and most do not require surgical treatment.
3.Stage
Within 14 days of the onset of disease is called the acute phase, and the chronic phase is defined as asymptomatic aortic coarctation found 14 days after acute onset or incidentally during physical examination.
All types and levels of aortic coarctation can be seen in both the acute and chronic phases.