Aortic sandwich – aortic coarctation

The aorta is composed of an intima, a middle elastic lamina, and an epithelium, which normally fit tightly together. Aortic coarctation is a pathologic change in the aorta where the true and false lumens are separated by a rupture of the intima that allows blood to enter the interior of the arterial wall, usually along the long axis. The false lumen communicates with the true lumen through a rupture in the intima. Dangers of aortic dissection The greatest danger of aortic dissection is death. Mortality rates of up to 50% within 1 week and between 60-70% within 1 month have been reported in the literature. In addition, the involvement of aortic coarctation and the corresponding organ supplying arteries can lead to corresponding organ dysfunction, such as acute infarction, intestinal ischemic necrosis, acute renal failure, and the involvement of the aortic valve can occur when the aortic valve closure insufficiency and thus lead to acute left heart failure. Classification1Stanford classification Regardless of the origin of the entrapment, if it involves the ascending aorta, it is called type A. If the entrapment originates in the thoracic and descending aorta and does not involve the ascending aorta, it is called type B. 2DeBakey classification De Bakey type I: endothelial rupture is located in the ascending aorta, and the scope of involvement of all parts of thoracic aorta or even the abdominal aorta, which is the most common type; De Bakey type II: De Bakey type II: the endothelial rupture is located in the ascending aorta, with extension limited to the ascending aorta or the aortic arch; De Bakey type III: the endothelial rupture is located in the descending aorta, with extension to the descending aorta and/or the abdominal aorta, and can be divided into two subtypes, limited and extensive. What are the common causative factors? Aortic coarctation is the result of the interaction between abnormal intima-media structure of the aorta and abnormal hemodynamics. 1. Aortic structural abnormalities. Common factors include Marfan syndrome and Ehlers Danlos syndrome, congenital cardiovascular malformations, idiopathic degenerative changes in the aortic mesentery, aortic atherosclerosis, and inflammatory diseases of the aorta. Patients with Marfan syndrome Patients with Ehlers Danlos syndrome 2. The most common cause of hemodynamic changes is hypertension, and almost all patients with aortic coarctation have poorly controlled hypertension. In other words, the control of hypertension has a comprehensive impact on the prevention, treatment, and prognosis of aortic coarctation, and is the most basic and most important treatment and prevention tool that cannot be ignored. Pregnancy is another high prevalence factor, associated with hemodynamic changes during pregnancy. Among women who develop the disease before the age of 40 years, 50% occur during pregnancy. The male-to-female incidence ratio of aortic coarctation is 2 to 5:1; the common age of onset is 45 to 70 years old, and the youngest patient reported so far is only 13 years old. 3, other trauma and granulomatous arteritis; arterial cannulation and cardiovascular surgery can be caused by a medically induced entrapment tear Clinical manifestations 1, severe chest and back pain: typical patients with acute aortic coarctation tend to manifest sudden, severe, chest and back, tear-like pain. Severe heart failure, fainting, and even sudden death can occur; 2, hypertension: most patients are accompanied by uncontrollable high blood pressure, which is also the most common sign in patients with coarctation; 3, hypotensive shock: in addition to severe chest and back pain, there is also a drop in blood pressure, pallor, and cold sweating when the coarctation ruptures; 4, limb and organ ischemia: aortic branch arterial occlusion can lead to the corresponding brain, limbs, kidneys, and organs, including the brain, kidneys, and organs. Ischemic symptoms of limbs, kidneys, abdominal organs: such as cerebral infarction, oliguria, abdominal pain, pale legs, weakness, maculae, and even paraplegia. 5.Others:peripheral arterial pulsation disappears, hemoptysis and vomiting of blood can appear when the entrapment penetrates the trachea and esophagus; compression of trachea manifests as difficulty in breathing, entrapment involving mesenteric and renal arteries can cause intestinal paralysis or even necrosis and renal infarction and other signs. Pleural effusion is also a common sign of aortic coarctation, mostly on the left side. Ancillary examination CT angiography (CTA) CTA is currently the most commonly used preoperative imaging assessment method, its sensitivity is more than 90%, and its specificity is close to 100%. Magnetic resonance angiography (MRA) has a diagnostic sensitivity and specificity for patients with aortic coarctation that is close to that of CTA, and the enhancers used for MRI are not nephrotoxic; its disadvantage is that the scanning time is longer and it is not suitable for emergency patients with unstable circulatory status, and it is not suitable for patients with magnetic metal implants in the body. Digital Silhouette Angiography (DSA) Although aortic angiography still retains its status as the “gold standard” for the diagnosis of aortic coarctation, it is currently used only in endoluminal repair and not as a preoperative diagnostic tool. The advantages of ultrasonography are that it is non-invasive, does not require contrast media, can localize the endocardial fissure, can show the status of the true and false lumen and the blood flow, and can also show concomitant aortic valve insufficiency, pericardial effusion, and obstruction of the branch arteries of the aortic arch, and so on. Treatment For type A coarctation, surgical treatment is the mainstay. With the rapid development of endovascular interventional techniques (EVAR), EVAR has become the preferred treatment option for type B aortic coarctation. Schematic diagram of open surgery for type A coarctation before and after endovascular intervention for type B coarctation in our department.