Although acute aortic syndrome is rare, it is a vicious, serious life-threatening condition with high mortality. The advances in diagnosis and treatment of acute aortic syndrome are a group of relatively uncommon, but it is a serious, life-threatening condition with high mortality. The advances in diagnosis and treatment of acute aortic syndrome Abstract Acute aortic syndrome is a group of relatively rare diseases, but have life- In clinical work, when admissions of patients with acute chest pain, we should take into account the possibility of this In clinical work, when admissions of patients with acute chest pain, we should take into account the possibility of this disease, and rapid diagnose and aggressive treat to prevent complications, reduce mortality.This paper were reviewed in terms of pathophysiology. This paper were reviewed in terms of pathophysiology, clinical features, laboratory examinations selection strategy and the latest treatment progress, so as to enhance clinician awareness of this disease Acute Aortic Syndrome AAS refers to a group of cardiovascular critical emergencies with similar clinical manifestations, but not identical pathogenesis and pathophysiology. The syndrome mainly includes: Aortic Dissection AD, Intramural Aortic Hematoma IMH, and Penetrating Atherosclerotic Aortic Ulcer PAU. This syndrome is relatively rare, but the rapid onset, critical condition, rapid progression, and high mortality of this group of diseases require rapid life-saving measures by clinicians. This group of diseases is now reviewed to improve clinicians’ understanding of this disease, so that they can quickly improve the relevant auxiliary examinations, rapidly confirm the diagnosis, take early and effective treatment plans, and reduce mortality. Pathophysiological changes 1. Aortic dissection (AD) refers to the disruption of aortic endothelial integrity under the action of multiple or one factor. Blood in the aortic lumen enters the aortic wall mesentery through the ruptured endothelial breach and tears along the long axis of the aorta, resulting in the formation of endothelial sheets and the division of the aorta into true and false double-lumen-like structures. The incidence is about 5-10 cases per 1 million and the mortality rate is up to 50% within 48 hours if not treated promptly [1]. There is a clear seasonal pattern in the occurrence of aortic coarctation, and some studies have confirmed that the incidence is much higher in winter than in other seasons [2, 3, 4], which may be related to the cold weather leading to increased sympathetic excitability, which in turn leads to higher blood pressure and increased arterial spasm [4]. The incidence is higher in males than in females, and mostly in middle-aged and elderly people. The common co-morbidities are hypertension, diabetes mellitus and macrovascular disease, and often have obvious triggers, such as sudden change of position, emotional excitement and bending, and some may have no obvious trigger. Most of the current views believe that the mechanism of aortic coarctation may be [5, 6, 7] (1) defects in the aortic wall itself or degenerative necrosis of the aortic mesentery, resulting in reduced adhesion of the intima and mesentery; (2) changes in the geometry of the aorta and oscillation of the aortic root, resulting in changes in the shear stress of the blood flow on the aortic wall; (3) under the action of factors such as hypertension and sudden changes in body position (3) Tearing of the aortic intima caused by high blood pressure, sudden change of position, etc. However, it has also been suggested that pathological changes such as aortic wall elastic fiber rupture, cystic mid-layer degeneration and mid-layer necrosis can occur in the normal population with age-dependent severity and are not specific to patients with aortic coarctation [8], and it has been found that the laceration of aortic coarctation may occur in the normal histology of the aortic wall [9], and it has even been found that most patients with Marfan syndrome present with elastic fiber rupture and severe loss, but only a minority of them had entrapment [10]. They concluded that aortic coarctation has no characteristic histopathological changes as a basis for its pathogenesis and that the possible mechanism is a local injury-repair mechanism. De Bakey type I: the endothelial rupture is located in the ascending aorta and extends to all parts of the thoracic aorta and even the abdominal aorta, which is the most common type; De Bakey type II: the endothelial rupture is located in the ascending aorta and extends to the ascending aorta or the aortic arch; De Bakey type III: the endothelial rupture is located in the descending aorta and extends to the descending aorta or the aortic arch. The extension involves the descending aorta or the abdominal aorta. The common serious complications of aortic coarctation include [6]: coarctation rupture, pericardial effusion and or filling, acute myocardial infarction, ischemic necrosis of abdominal organs, and others such as pleural effusion and pseudoaneurysm formation. 2, Intramural aortic hematoma (IMH) is a hemorrhage in the middle layer of the aorta, resulting in the formation of a hematoma locally or along the long axis of the aorta, but without the formation of an endothelial rupture and endothelial sheet, and the hematoma in the aortic wall does not communicate with the aortic lumen, which is a serious life-threatening acute aortic syndrome [11]. Intra-aortic wall hematomas have been reported in 10-30% of acute aortic syndromes [12]. Although the causative factors of intra-aortic mural hematoma are unknown, hypertension and atherosclerosis play a large role in most patients [13]. The currently accepted cause and mechanism of IMH pathogenesis is rupture of the aortic wall trophoblastic vessels; other causes include pathological vascular proliferation and spontaneous bleeding within the aortic wall atheromatous plaque and thoracic trauma resulting in aortic wall contusions [14, 15].The outcome of IMH includes conditions such as resorption of the hematoma, progression to typical aortic coarctation, and aortic dissection (approximately 15-20% of cases).IMH There are two main types of IMH: Stanford type A: involving the ascending aorta; Stanford type B: confined to the descending aorta, which accounts for about 50-85% of cases, and Stanford type A accounts for about 88% of cases progressing to typical aortic coarctation [16].Complications of IMH include: typical aortic coarctation, pericardial effusion or and tamponade, acute aortic valve closure insufficiency, bloody pleural effusion, acute myocardial infarction, and rupture, which occur by mechanisms similar to those of aortic coarctation complications. 3. Penetrating aortic ulcer (PAU) refers to the formation of atherosclerotic plaque ulcers that penetrate inward into the internal elastic lamina and are accompanied by interstitial aortic wall hematoma formation. In recent years, with the use of multi-row spiral CT in cardiovascular applications, this disease is becoming more and more recognized by radiologists and clinicians. Its prevalence is high in the elderly population, most of whom are asymptomatic, and little is known about its clinical significance and natural course, especially in asymptomatic PAU [17, 18]. the exact incidence of PAU remains unclear, mostly affecting the organism at 70 years of age or older, but the incidence of PAU starting with acute aortic syndrome is about 2.3-7.6%, when it is prone to serious complications such as intra-aortic wall hematoma, pseudoaneurysm, typical aortic coarctation, and even aortic rupture. The pathology is characterized by aortic atherosclerotic plaque ulcerating and eroding the elastic layer within the aortic wall, crossing the intima to the middle layer of the aorta, exposing the middle membrane to the high-speed pulsating aortic blood flow, which can lead to the formation of a localized hematoma within the aortic wall, which can lead to a limited coarctation, or even penetrate the aorta epicardium leading to serious complications such as pseudoaneurysm formation or aortic dissection [19]. Clinical characteristics and strategies for selecting adjunctive tests The above three diseases included in acute aortic syndrome have similar clinical characteristics despite their different pathogenesis [16, 17, 19, 20], mainly including (1) a higher incidence in middle-aged and elderly men; (2) most patients have combined hypertension and often related triggers, with asymmetric bilateral blood pressure or dorsalis pedis artery pulsation; (3) there is often typical tear-like (3) there is often typical tearing or throbbing pain that radiates to both upper extremities, neck, back, lumbar abdomen, and even both lower extremities, and the pain is severe and cannot be relieved for a long time, and nitroglycerin or quick-acting heart pills are ineffective; (4) imaging and histopathological examination show the presence of characteristic aortic lesions. Because of the high mortality rate and serious complication rate of acute aortic syndrome, when acute chest pain caused by other diseases is excluded from clinical work and suspected to be this group of diseases, a rapid and clear diagnosis is needed to arrange the next treatment, and in order to clarify the location and degree of aortic lesions, the diameter of the aortic root and the condition of the aortic valve, the pericardial cavity and the thoracic cavity, transthoracic cardiac ultrasonography and aortic However, because of the long imaging time and the need for prolonged braking, most scholars and myself believe that MR examination should be used when ultrasound and CT examination cannot make a clear diagnosis. However, because of its long imaging time and the need for prolonged braking, most scholars and I believe that MR examination should be used when ultrasonography and CT cannot make a definite diagnosis or for long-term follow-up of the prognosis of this group. The characteristic manifestations of our disease and the differentiation points between the three cases are mainly shown on imaging [5, 11, 16, 18, 21, 22]: (1) the characteristic manifestation of AD is a linear, low-density endothelial sheet in the lumen of the aorta, which can reveal an endothelial tear (i.e., entrance), and most of them can also reveal an endothelial rupture (i.e., exit) distally, forming a double-lumen structure of the aorta; (2) IMH and PAU have no torn endothelium on (2) IMH and PAU are distinguished from AD by the absence of torn endothelial sheets and the absence of pseudoluminal structures; (3) IMH shows crescentic thickening of the aortic wall with a thickness of >7 mm, and the diagnosis can be confirmed with a thickness of >5 mm if the symptoms of chest pain are typical; (4) PAU shows a relative enlargement of the aortic lumen at the lesion and a filling defect outside the lumen. Recent treatment advances For acute aortic syndrome, the disease is mostly combined with hypertension, due to pain stimulation and systemic stress response, resulting in sympathetic nervous system excitation and increased heart rate, so such patients need to strictly control blood pressure (target blood pressure below 120/80 mmHg) and heart rate (target heart rate of about 60 beats/min) to inhibit sympathetic excitation and prevent the progression of the lesion, commonly used vasodilators, The next specific treatment plan is determined according to the patient’s underlying condition and disease type [6, 11, 12, 17, 18, 19]: (1) AD, for De Bakey type I and De Bakey type II, due to their occurrence of aortic valve closure insufficiency, pericardial tamponade In De Bakey III patients, aortic stenting can be performed to seal the endothelial rupture or conservative drug treatment. (2) IMH: The incidence of progression to classic aortic coarctation is higher in Stanford A patients, and sometimes Stanford A aortic coarctation can be misdiagnosed as intra-aortic wall hematoma [23], so surgical treatment is recommended for this type of IMH, and the procedure is basically equivalent to this type of aortic coarctation; conservative pharmacological treatment is recommended for Stanford B IMH patients The patients with Stanford type B IMH should be treated with conservative medication, active control of blood pressure and rhythm, avoiding emotional excitement and activities during the acute period, and bed rest to prevent complications such as aortic dissection, pending hematoma absorption or mechanization. (3) PAU: For PAU involving the ascending aorta, due to its high risk, recanalization therapy is required; for asymptomatic PAU involving the aorta, adequate pharmacological treatment should be given, and changes in the condition should be observed on follow-up; for symptomatic PAU, adequate pharmacological treatment should be given to actively control symptoms, and the next treatment plan should be decided according to the extent of lesion involvement; for lesions involving the abdominal aorta, endovascular recanalization therapy can be given if necessary. Endovascular revascularization treatment can be taken if necessary.