(A) Etiology 1. Cystic necrosis or degenerative changes of the middle layer of the artery is the most common type of anterior thoracic aortic aneurysm when the exact cause is unknown. Associated with a variety of factors, hereditary, infections, smoking, drug abuse, hypertension and aging may lead to degeneration and necrosis of the middle layer of the arterial wall. Typically, it is seen in young and middle-aged men, and its preferred site is the ascending aorta. Severe aortic valve insufficiency may develop due to enlargement of the aortic annulus, which may extend distally to the aortic arch and descending aorta. The histologic manifestations are mainly necrosis and loss of smooth muscle cells, scarce elastic fibers, rupture and cystic gaps filled with mucus, resulting in weakness of the arterial wall and the formation of a special type of cloacal aneurysm.2. Hereditary diseases are represented by and common in Marfon syndrome. Mafang syndrome is an autosomal dominant hereditary connective tissue disease, which is a defect in the protofibronectin gene on chromosome 15, resulting in elastic fibers prone to degeneration and necrosis in early life. 75%-85% of patients with Mafang syndrome are associated with ascending aortic dilatation or aortic root aneurysm. Type IV is often accompanied by spontaneous aortic dissection, familial aneurysm disease, ascending aortic aneurysm and aortic coarctation formation are common, and the etiology is unknown, but some studies have found that metabolic disorders of the arterial wall in this group of patients lead to accelerated arterial degradation and cause aneurysms. 3. Aortic aneurysm due to atherosclerosis is one of the common causes of thoracic aortic aneurysm. Intimal lipid deposition and atheromatous plaque formation in the arterial wall can block the nutrient vessels and cause fracture and necrosis of the elastic fibers in the middle layer of the artery, resulting in weakness of the arterial wall and the formation of aneurysms, which are common in patients aged 50 to 80 years old, more in men than in women. It is often complicated by coronary artery disease and peripheral vascular obstructive disease. Aortic arch and descending aortic aneurysms are more common than ascending aortic aneurysms, and extensive aneurysmal dilatation of the thoracic aorta may also occur. 4, aortic coarctation due to anatomical, pathological or hemodynamic reasons, the aortic intima tears, blood enters the middle layer of the aorta to tear and separate, hematoma or blood flow occurs in the middle layer of the aortic wall, forming a true cavity and a false cavity also known as double cavity aorta. 5, trauma with the rapid development of high-speed transportation, car accidents, air accidents and the subsequent increase in recent years and the trend of increasing, most of the formation of pseudoaneurysm and aortic coarctation. Due to the shear force of acceleration or deceleration and the anatomical characteristics of the thoracic aorta, rupture or tear mostly occurs in the ascending aorta about 2cm below the beginning of the unnamed artery, 3~5cm above the aortic valve ring and the descending aortic isthmus at the beginning of the left subclavian artery. The arch and abdominal aorta are less common.6. Bacterial or fungal infections. Bacteria can directly invade the aortic wall from the tissue adjacent to the aorta, but most are bacteria that enter with the bloodstream. Such bacteria begin to hide in the damaged aortic area to invade. In sepsis, bacteria can also enter the aortic wall through the arterial nutrient vessels and form aneurysms. Most fungal aortic aneurysms are secondary, and occasionally primary fungal aneurysms are seen. Syphilitic aortic aneurysms have been rare; they are a late complication of syphilitic aortitis and usually appear 10 to 20 years after syphilis infection. Syphilitic aortic aneurysm occurs in 50% of ascending aorta, 30%-40% in aortic arch, 15% in descending aorta and 5% in abdominal aorta. In recent years, there is an increasing trend of syphilis infection in patients, which should be alerted clinically. 7, congenital thoracic aortic aneurysm is less common, including aortic sinus aneurysm and thoracic aortic isthmus aneurysm. Patients with congenital thoracic aortic aneurysm are often complicated by congenital aortic stenosis, patent ductus arteriosus and congenital aortic constriction. (B) The prognosis of aortic aneurysm is poor, and the average time to rupture is only 2 years and survival is less than 3 years for patients with diagnosed untreated thoracic aortic aneurysm. 2002 National Center for Health statistics show that there are 67,000 hospitalizations and 16,000 deaths per year due to aortic aneurysm disease. The leading cause of death is thoracic aortic aneurysm rupture or aortic coarctation. According to Laplace’s law, the pressure on the wall is proportional to the blood pressure and the radius of the lumen. The size of aneurysm is closely related to rupture and blood pressure. 1999 Coady study found that patients with aneurysm diameter of 6.0-6.9 cm had 4.3 times more incidence of rupture than patients with diameter of 4.0-4.9 cm. Shimada study found that the average growth of thoracic aortic aneurysm was 2.6 mm/year. The larger the diameter of the thoracic aortic aneurysm, the more rapid the growth. Thoracic aortic diameters less than 40 mm, 40-49 mm, 50-59 mm and greater than 60 mm showed growth rates of 2 mm/year, 2.3 mm/year, 3.6 mm/year and 5.6 mm/year, respectively, with significantly faster growth seen for diameters greater than 50 mm. Considering by site, the aortic arch expanded the fastest (5.6mm/year), followed by the ascending and descending aorta (4.2mm/year), and the abdominal aorta was slower (2.8mm/year). The average diameter of ascending aortic aneurysm rupture or formation of aortic coarctation is about 5.9 cm. The rupture rate of untreated thoracic aortic aneurysm is 42%-70%. Growth of ascending aorta greater than 10 mm/year has the risk of rupture or formation of aortic coarctation and should be promptly treated by surgery. In addition, the natural course of the disease varies with different etiologies. Marfan syndrome can accelerate the growth of aneurysms and form aortic coarctation or rupture at smaller diameters (less than 5 cm), especially in patients with a family history of untreated Marfan syndrome. The average age of death in untreated Marfan syndrome is only 32 years, and the arterial growth rate in patients with familial aneurysms is more than twice as high as normal, and the growth rate of aortic coarctation is 6 times faster. The average survival of syphilitic aneurysms is only 6-8 months after the onset of symptoms, and traumatic aneurysms are more likely to rupture and die if not treated aggressively due to differences in etiology and pathology. If treated surgically, their natural life expectancy can reach the level of a normal person. The 1-year and 5-year survival rates for patients with unoperated thoracic aortic aneurysms after diagnosis are 60% to 70% and 13% to 39%, respectively.