I. Overview of aortic dissection (AD) AD is a catastrophic cardiovascular disease with a very high mortality rate. It is estimated that there are more than 2000 new cases of acute AD in the United States each year; the incidence is estimated to be even higher due to the low awareness, treatment and control of hypertension in our population, as well as the presence of other risk factors. AD is of great concern because of its critical condition, rapid progression and poor prognosis, especially in acute cases. To date, the etiology of AD is not well understood. Although the initiating factor of AD is endothelial rupture, the disease is not an endothelial lesion. Genetic structural abnormalities or other incompletely identified genetic factors that cause lesions in the middle fibers of the vessels, resulting in a lack of elasticity or weakness, may be the underlying cause. The endothelium and basement membrane themselves have no apparent intrinsic tone and in the absence of proper mechanical support of the mid-layer fibers are susceptible to endothelial tears and entrapment formation due to the impact of high velocity blood flow with vascular tension. Atherosclerosis can damage the middle layer of the vessel in different ways; congenital factors such as aortic stenosis and dilatation of the aorta after constriction, weakness and increased tension of the vessel wall, and often accompanied by persistent hypertension. The presence of intrinsic factors such as these, on top of the sudden increase in blood pressure, can also easily cause endothelial rupture. As a result, AD is clinically common in young adults with a history of hypertension, obesity, or “firmness” (although it also occurs in normal blood pressure and lean individuals). According to reports, domestic patients are generally younger than those in Europe, America and Japan, and the incidence of AD seems to be higher in men than in women, and the incidence has been increasing significantly in recent years. The diagnosis of AD is mainly based on history, symptoms and signs, as well as imaging and other examinations to make a clear diagnosis of AD. 1. Pain: Almost all patients have sudden onset of severe chest pain at the time of entrapment. Only in a very small percentage of patients, the pain may be milder in older adults due to atherosclerosis, severe mid-layer degeneration, or delayed (blunted) response. Depending on the development of the pseudocavity, the pain may shift to the back, between the scapulae, and down to the low back or even the groin. Once the pseudocavity has an outlet and the pressure between the real and pseudocavity tends to equalize, the sharp pain may change to a persistent dull pain. This typical pain symptom and nature is the main feature that distinguishes it from other diseases. 2, other clinical manifestations: along with pain symptoms, patients often show irritability, fear, anxiety, frequent death or indifference, sometimes accompanied by general sweating, wet and cold skin, pale face, shortness of breath and fainting and other “body grams” signs. Although there are clinical signs of shock, blood pressure may not drop or may rise; the sudden appearance of low skin temperature at the end of the limbs, varying intensity of arterial pulses or disappearance of one side, and blood pressure discrepancy is another meaningful sign of AD. In addition, symptoms and serious complications associated with poor perfusion occurring with invasion of important branches on the aorta can occur. For younger patients without obvious risk factors for atherosclerosis, AD should be highly suspected when the above symptoms occur. 3. General screening: Including chest X-ray and ECG, although not specific or diagnostic tests, X-ray sometimes shows enlarged heart shadow in case of mediastinal widening, aortic tortuosity and pericardial effusion; ECG may show myocardial ischemia in the lower wall, suggesting entrapment involving the right coronary artery. A normal electrocardiogram with severe chest pain is also a sign in itself. A transthoracic echocardiogram (TTE) showing dilatation of the ascending aorta and root with an endothelial tear in a live valve fragment will suggest a diagnosis of AD. When the quality of the TTE image is poor or difficult to perform, transesophageal echocardiography (TEE) can almost always accurately diagnose AD and its type, but TEE should be performed under anesthesia. 4.Important imaging tests: Computed tomography (CT) can be the first considered test for AD because of its popularity, short time consumption, economy and convenience; its shortcomings are the need for contrast application, poor sensitivity, and additional difficulty in assessing the involvement of supra-aortic branch vessels and endothelial rupture, etc. CT angiography (CTA) can now be the method of choice for AD diagnosis. CTA not only improves the sensitivity and specificity of the diagnosis of AD and makes an accurate diagnosis of AD, but also provides a three-dimensional image reconstruction of the entire aorta and its branches, comprehensively showing the morphological characteristics of the endothelial sheet, true and false lumen and branch vessel involvement, etc., and visually reproducing the extent and degree of the lesion. cTA can be used as the only basis for examination before deciding on the treatment modality. Magnetic resonance imaging (MRI) can also show entrapment, making it a well-established and effective noninvasive technique for the diagnosis of AD, and can be used in cases of allergy to contrast agents or in the presence of renal insufficiency. Due to its not being readily available, time-consuming and high magnetic field technical requirements, MRI should not be used as the preferred diagnostic tool for AD at least. Once AD is diagnosed, the primary treatment should be medical therapy based on pain relief, blood pressure and heart rate control. Therefore, vasodilators alone should not be used, as they may cause a reflex increase in heart rate, increase left ventricular ejection velocity and exacerbate AD enlargement. The ideal and standard approach to disease control is the combination of vasodilators and β-blockers. The vasodilator is better than sodium nitroprusside, which is less toxic and safer; β-blocker is preferred to esmolol. Surgical treatment: Once Stanford type A (i.e. DeBakey type I or II) AD is diagnosed, the patient should be transferred to a hospital where surgery can be performed quickly. The natural prognosis of type A AD is very poor, and the mortality rate of patients with acute type A entrapment is traditionally estimated to be as high as 80% within 48 h of onset. For patients with pericardial tamponade caused by the proximal dissection of the clams; those with myocardial ischemia or myocardial infarction caused by the involvement of coronary arteries; those with aortic regurgitation of moderate degree or above and left heart failure; as well as those with distal dissection of the clams involving the cephalobrachial vessels and abdominal branch vessels, resulting in branch obstruction and perfusion disorders and various complications, all are indications for emergency surgery. 3. Internal or interventional treatment: Compared with type A AD, the risk of type B is much lower, and in the past and even at present, internal or interventional treatment is still the main treatment. This is because the efficacy of surgical repair in patients with type B stability has not been proven to be superior to that of medical or interventional treatment. However, surgical procedures should still be considered for type B entrapment where an aneurysm has formed, with the goal of preventing or mitigating life-threatening complications.