Syphilis spirochetes are mostly infected through sexual contact, and about 30% of untreated patients eventually cause advanced syphilis in cardiovascular, neurological and other organs, while 10% to 12% of syphilis patients can develop cardiovascular syphilis lesions. The incubation period from the beginning of syphilis spirochete infection to the occurrence of cardiovascular disease is mostly 5 to 25 years. There are more men than women with this disease, and the ratio is about 4:1 to 5:1. About 10-25% of cardiovascular syphilis and neurosyphilis coexist. When the syphilis spirochete invades the body from the damaged mucosa, it can invade the lymph nodes and various parts of the body (such as liver, kidney, lung, heart, bone and joint, brain, etc.) after half an hour through the lymphatic vessels, and some of the syphilis spirochetes invade the trophoblastic vessels of the aorta through the lymphatic vessels of the lungs, while the lesions are mostly in the ascending aorta and rarely invade the myocardium, which may be due to the fact that there is more lymphatic tissue in the ascending aorta and very little lymphatic drainage in the myocardium. . After spirochetes invade the ascending aorta, symptoms and signs of lesions usually appear after 10-25 years, but a few may appear within 1 to 2 years. After 8 to 9 weeks of invasion, the spirochetes proliferate in the body and cause secondary lesions in the body. During this time, if not treated effectively, the syphilis spirochetes can produce an immune response in the body and the spirochetes gradually decrease. The immune state produced may include cellular and humoral immunity. The lesions mainly involve the ascending aorta (above the aortic sinus), followed by the aortic arch and thoracic descending aorta, while the innominate artery, common carotid artery and abdominal aorta are rarely involved, and the renal artery is not involved below. When the ascending aortic lesion extends to the root of the aorta, the aortic valve annulus is enlarged and the aortic valve leaflet junction is separated, causing aortic valve insufficiency; when the lesion involves the aortic valve leaflet attachment, it further aggravates the aortic valve insufficiency. The aortic wall becomes progressively thinner with calcium deposition due to lesions in the middle layer of the aorta, resulting in the loss of elasticity or loss of the aortic wall and aortic distension or aortic aneurysm formation. Aortic aneurysms occur mostly in the ascending aorta or aortic arch, are cystic in shape, contain thrombus, and can detach to cause peripheral obstruction or compression of peripheral organ tissues, producing corresponding compression symptoms, but do not cause aortic coarctation separation. When the lesion involves the aortic sinus, it may cause fibrous lesions and scar formation in the aortic wall, resulting in coronary artery stenosis and obstruction. Myocardial involvement is rare, and occasionally dendritic swelling may occur, as well as myocardial hypertrophy, fibrosis, or myocardial ischemia due to incomplete aortic valve closure or coronary artery stenosis. The pathological changes are inflammatory changes and fibrous scar formation in the aorta, especially in the middle layer of the ascending aorta, causing syphilitic aortitis, aortic valve insufficiency, aortic aneurysm, and coronary artery stenosis, while myocardial lesions are rare. The lymphovascular-rich middle layer of the ascending aorta is most susceptible to direct syphilis spirochete invasion. Infiltration of lymphocytes and plasma cells in the trophoblastic vessels of the epicardium leads to obstruction of the trophoblastic vessels, resulting in fibrosis of the arterial epicardium, destruction and necrosis of the middle muscle and elastic fibrous tissue, followed by scar formation. The necrosis and scarring of the middle layer of the aorta leads to a dendritic wrinkling of the intima at the site of the lesion, which is parallel to the long axis of the aorta and covered by a shiny pearl-colored plaque.