Etiology and pathology: Infective endocarditis is an inflammation of the endocardium due to microorganisms, and the causative microorganisms can be bacteria, fungi, rickettsiae, chlamydia, or viruses. In the past, infective endocarditis was thought to occur mostly on the basis of congenital or acquired heart disease, but with the development of modern medicine and the increase in in vivo placement testing and treatment, the incidence of autologous valvular endocarditis has increased significantly. Notably, there has been an increase in recent years in infective endocarditis due to intravenous drug use. The causative organisms have also undergone a major change. Streptococcus straw green as the causative organism has declined at the most marked rate; in contrast, staphylococcal pathogenesis has increased significantly and is seen more often in patients undergoing cardiac surgery and long-term intravenous drug use and drug abuse. The common pathological changes are flab formation and heart valve destruction. The superfluous organisms are easily dislodged to form cerebral emboli or other organ emboli. The clinical manifestations are mainly related to the size of the embolus, the organ involved, the local reaction caused by the embolus and the immune and systemic response of the patient. Involved valves can be perforated by necrosis, causing incomplete valve closure and resulting in hemodynamic changes. The most commonly involved valve is the aortic valve, followed by the mitral valve, with the pulmonary and tricuspid valves being less commonly involved. The pathologic changes in prosthetic endocarditis are more severe than those in autologous endocarditis and vary among valves: infection of mechanical valves often occurs at the interface between the annulus and surrounding tissues and involves the endocardium around the prosthetic valve, resulting in annular ulceration, myocardial abscesses, perivalvular leaks and redundancies, and severe structural damage to the cardiac stent and disruption of the aortic connection to the left ventricle. This change is more common after aortic replacement. The pathology is dominated by hemodynamic changes in valve stenosis due to leaflet thickening and superfluous formation; leaflet perforation and tearing have also been reported. The pathological changes in homologous valve infective endocarditis tend to start with dry valve leaflet tissue, resulting in leaflet destruction and severe valve closure insufficiency. Infection is also less likely to spread to the suture rings and perivalvular tissue. The incidence of infective endocarditis is higher after aortic valve replacement than mitral valve replacement and higher after bivalve valve replacement than univalve valve replacement. Clinical manifestations Fever, malaise, nocturnal sweating, loss of appetite, cardiac enlargement, and anemia remain the main clinical manifestations, while changes in heart murmurs and the appearance of new murmurs strongly suggest infective endocarditis. It may be accompanied by splenomegaly, skin bruising, pestle and toe, 0sler’s node, Janeways node, etc. Complications are more frequent and include heart failure, cerebral embolism, diffuse glomerulonephritis and nephropathy, lower extremity embolism, coronary embolism, and pulmonary embolism, all of which make clinical management very difficult and are important factors in poor prognosis. Prosthetic valve endocarditis mostly has fever as the main symptom, but the symptoms are relatively severe, and there are corresponding clinical manifestations when perivalvular leakage, myocardial abscess, and septal perforation occur. Some patients with infective endocarditis are often admitted to the hospital with symptoms such as pulmonary infection and renal insufficiency, and the diagnosis can be made after a detailed history and physical examination. Laboratory tests Blood cultures are of diagnostic value for infective endocarditis, and multiple cultures of the same bacterial growth are a reliable basis for diagnosis. The culture results will not only help to confirm the diagnosis, but will also be the basis for treatment. Other tests such as blood sedimentation, routine blood count, urine routine and serology are also helpful in clarifying the condition. Echocardiography Echocardiography not only detects the redundancy, but also provides information about valve damage, hemodynamic changes and complications, and becomes one of the main tools to provide a basis for surgery. ECG In patients with suspected infective endocarditis, the presence of partial and complete AV block and premature ventricular contractions indicates the presence of myocarditis or inflammation of the cardiac conduction bundle. The presence of infarction indicates a poor prognosis, and new conduction abnormalities reflecting abscess formation, especially subaortic abscess formation, are indications for surgery. Surgical treatment of infective endocarditis of the heart valves consists of: 1. medical anti-infection. 2.Surgery. 3, systemic nutritional support. In the past, surgical treatment of infective endocarditis was considered to be a rescue measure in case of ineffective medical treatment, but now there is basically a consensus that early diagnosis, aggressive medical treatment combined with surgery are effective means to improve the survival rate of infective endocarditis. Surgical objectives: 1. Complete removal of infected lesions and histopathological changes. 2. To correct the hemodynamic disturbance. Indications for surgery: 1) ultrasound of the heart reveals a superfluous organism with a size of more than 1 cm; 2) destruction or perforation of the valve; 3) abscess formation in the annulus or myocardium; 4) combined with other cardiac lesions requiring surgical management. The timing of surgery is the key to successful surgery and good prognosis. For those who respond well to medical treatment, adequate preoperative preparation can be performed. The advantage is that antibiotic treatment can play the role of killing pathogens in the superfluous and metastatic infected lesions; secondly, effective preoperative treatment of infective endocarditis complications such as sepsis, renal failure, pneumonia, myocarditis and neurological complications can greatly improve the success rate and reduce the risk of surgery; but on the other hand, if the operation is unnecessarily prolonged, the patient may develop serious complications and sudden death, or the timing of surgery may be lost due to deterioration of the disease. Many publications suggest that surgical treatment of infective endocarditis should not be routinely performed after 4-6 weeks of anti-inflammatory treatment, even if the infective endocarditis is still active, and that surgical treatment should be actively performed in cases with uncontrolled fever, ultrasound findings of superfluous organisms, or hemodynamic changes due to valve perforation. Clinical experience shows that early surgery is effective for the following reasons: 1) early valve lesions are mild, providing an opportunity for valvuloplasty; 2) serious complications are avoided, improving long-term survival rates. Surgical modalities: I. Valve repair: for those with mild valve lesions that can be repaired. Valve repair surgical considerations: 1, the debridement should be thorough to prevent recurrence of IE, and the tissue within 1-2 mm of the lesion should generally be removed from the lesioned valve leaflets visible to the naked eye. 2, Thoroughly explore the adjacent myocardial tissue and heart valves for the presence of focal redundancies, the literature reports that patients undergoing tricuspid valve repair have died of postoperative pulmonary embolism because the pulmonary valve redundancy was not explored and cleared. 3, the materials used in repair surgery as far as possible to use autologous materials to prevent recurrence of infection. Second, valve replacement: for those whose valves are not repairable. The aortic valve is less likely to undergo valve repair because of its more serious lesions and hemodynamic aspects. Surgical efficacy: internal application of antibiotics for infective endocarditis is less effective, with a mortality rate of 30% to 50%, mainly because the infection cannot be controlled, leading to multi-organ failure. The mortality rate of surgical procedures is 5%-20%, and the effect of surgical treatment is significantly better than that of medical treatment. After regular combined medical and surgical treatment, the immediate and long-term outcomes of infective endocarditis are satisfactory, and the 5-year and 10-year survival rates are better than those of medical drug therapy alone.