Most non-medical people have never heard of aortic dissection, and non-vascular doctors do not know much about the disease, so here is a brief introduction to what aortic dissection is. Aortic dissection (AD) is a catastrophic disease of the cardiovascular system in which blood from the aortic lumen enters the aortic wall through a tear in the aortic intima, causing an entrapment hematoma to form in the middle layer of the aortic wall and expand along the longitudinal axis of the aorta. As a result of the localized tear in the intima, the intima gradually peels off and expands due to the strong blood impact, creating two lumens, true and false, within the artery, which leads to a series of manifestations including tear-like pain. The aorta is the main blood vessel of the body, subject to pressure directly from the beating heart, and has a huge blood flow. Once a tear in the intimal layer occurs, the chance of rupture is very high and the mortality rate is also very high. Cause Degeneration of the middle layer of the aorta The normal human arterial vasculature consists of 3 layers of structures, the intima, the mesima and the epima, which fit closely together and carry the blood flow through them. In contrast, arterial entrapment is a localized tear in the intima, which is subjected to a strong blood shock, and the intima gradually peels off and expands, forming two lumens, a true and a false, within the artery. This leads to a series of manifestations including tear-like pain. Mesenteric degeneration is considered to be the primary predisposing factor. It manifests as degeneration of collagen and fibrous tissue with cystic changes, causing separation of the interstitial layer during chronic irritation of the aortic wall. Marfan and Enler-Danlos syndromes, such as those with inherited connective tissue defects, are seen in young and middle-aged people and often result in proximal entrapment. Hypertension can cause hemodynamic disorders and promote the development of atherosclerosis, which is the most important predisposing factor for AD. Seventy to 90 percent of AD patients have elevated blood pressure. About half of the proximal type and almost all of the distal type of AD have hypertension. Half of the clamping separations in women under 40 years of age in pregnancy occur during pregnancy, typically in the second third of pregnancy, and occasionally in the early postpartum period. Elevated blood volume, cardiac output and blood pressure in late pregnancy are at risk for clamping separation. Other Congenital vascular malformations such as bilobed aortic valves and aortic constriction; medical trauma such as arterial catheterization, intra-aortic balloon pumps, coronary artery bypass and valve replacement; and trauma or cocaine abuse or cellular arteritis triggers are rare. Clinical typing There are two major medical classifications based on the location of the intimal fissure and the extent of entrapment involvement in aortic coarctation. 1965 Professor DeBakey et al, proposed a 3-type classification. Type I: aortic coarctation involving the ascending aorta to the descending aorta and even to the abdominal aorta. Type II: Aortic coarctation involving only the ascending aorta. In 1970, Professor Daily of Stanford University and others proposed another classification based mainly on the location of the proximal endothelial fissure: Type A: all clips involving the ascending aorta, regardless of the site of origin; Type B: all clips not involving the ascending aorta. Stanford type A: equivalent to DeBakey type I and II, and Stanford type B: equivalent to DeBakey type III. Clinical manifestations Chest pain is the most common first symptom, accounting for 74% to 90% of cases. Unbearable tearing-like pain with profuse sweating, nausea, vomiting and syncope, which cannot be relieved by morphine. Sudden death The main cause of early death is AD rupture or obstruction of arteries supplying vital organs, such as coronary arteries, cephalobrachial trunk arteries, or visceral arteries. Sudden death is usually due to acute pericardial tamponade or massive bleeding into the mediastinum or pleural cavity. Neurological symptoms Clinical symptoms such as syncope (9%), cerebrovascular accidents such as hemiparesis, impaired consciousness (5%), and paraplegia can occur and are easily misdiagnosed as cerebrovascular accidents. Syncope without focal neurological signs is often the result of proximal entrapment into the pericardial cavity leading to cardiac tamponade, or occasionally the result of rupture of the descending aorta into the pleural cavity. What tests are performed to confirm the diagnosis of aortic coarctation? The primary adjuncts to diagnose aortic coarctation are CT angiography (CTA), magnetic resonance imaging (MRA) or direct digital silhouette angiography (DSA). For pregnant women MRA can be done without radiation and without any effect on the fetus. Conservative treatment In patients with acute entrapment, whatever the treatment to be taken, the first step should be the appropriate conservative treatment: blood pressure control and pain control. Once the disease is suspected or diagnosed, the patient should be hospitalized for supervised treatment. The goal of treatment is to reduce myocardial contractility, slow left ventricular systolic velocity and peripheral arterial pressure. The goal of treatment is to control the systolic blood pressure at 100-120 mmHg and heart rate at 60-75 beats/min. This can effectively stabilize or abort the continued separation of the aortic coarctation, so that the symptoms can be relieved and the pain can disappear. ①Anti-pain: use morphine with sedatives. ②Replenish blood volume: transfuse blood if there is bleeding into the pericardium: thoracic cavity or aortic dissection. ③Lowering blood pressure: for patients with combined hypertension, lower the blood pressure to the clinical treatment index. Significant reduction or disappearance of pain after blood pressure drop is a clinical indication for the cessation of expansion of the entrapment separation. Surgical treatment After the patient’s condition is appropriately stabilized, the choice of treatment depends mainly on the type of entrapment. For the current state of treatment, for Stanford type B aortic coarctation, minimally invasive endoluminal treatment is the mainstay. The basis for treatment includes the following conditions, or indications for surgery: persistent enlargement of the entrapment, as evidenced by a rapidly increasing diameter and extent of the aortic entrapment, thoracic hemorrhage, and uncontrollable pain; or ischemia of major branches of the aorta, such as the superior mesenteric artery and renal artery. Minimally invasive endoluminal repair of aortic coarctation is performed by hybridization or various endoluminal repair coarctations (chimney, open window, modular branch stenting) to treat Stanford type B aortic coarctation where the main fissure is within 1.5 cm of the left subclavian artery opening. Type B aortic coarctation is the most deadly arterial disease, with a high mortality and complication rate. The primary goal of surgical treatment is to save the patient’s life. Previously, the relatively conservative but simplest and safest treatment was to simply perform an ascending aortic or partial ascending aortic replacement procedure to achieve life-saving results by eliminating the primary rupture. Due to advances in surgical techniques, anesthesia, organ protection, and postoperative care, the scope of surgical aortic vessel replacement has gradually expanded, thereby reducing the incidence of complications in the residual diseased aorta. The current Stanford Type A hybridization technique was used early on with surgical plus artificial vessel implantation into the vascular lumen method.