Infective endocarditis definition, active phase definition. Infective endocarditis is caused by infection of the endothelial surface of the heart with microorganisms. The characteristic damage is superfluous, indeterminate masses of platelets and fibrin of variable size with an abundant network of microorganisms and moderate amounts of inflammatory cells. It most often involves heart valves, but can also occur in septal defects, tendons, or mural areas of the endocardium. The main causative organisms are streptococci, staphylococci, enterococci, and anaerobic gram-negative rods; others can be seen as mycobacteria, rickettsia, chlamydia, and histoplasma. Infective endocarditis is clinically classified into active phase, and stable phase according to its response to treatment. The stable phase is generally considered to be 4-6 weeks after completion of a course of antibiotic therapy with a normal clinical temperature and a negative blood culture. There are different definitions of the active phase of infective endocarditis, such as the definition of active endocarditis as positive blood culture, intraoperative finding of active inflammation of the valve and other tissues, and positive culture of the resected material; Sternik et al. considered active IE as the persistent clinical symptoms of infective endocarditis, and the interval between diagnosis of infective endocarditis and surgery was less than 6 weeks; Dreyfus et al. defined the active phase as infective endocarditis is surgery within 6 weeks of the onset of clinical symptoms, or within the full course of antimicrobial therapy regimen. The diagnosis of infective endocarditis is generally considered to be clear, with active inflammation visible on surgical pathology, and the presence of one or more of the following conditions may be considered active: positive blood cultures during the current morbidity period, positive bacterial microbial cultures of cardiac surgical specimens, microorganisms such as bacteria visible on pathological examination of cardiac surgical specimens, embolism or infarction of the body or pulmonary circulation prior to surgery, and persistent fever prior to surgery. Although there have been some improvements in IE diagnosis and treatment strategies in recent years, there have been no major improvements in the last 20 years, and the mortality rate of IE is still as high as 20%. These are partly due to drug resistance of pathogenic microorganisms in IE. Although antimicrobial agents are largely able to treat infective endocarditis, early surgical intervention is often necessary in cases where infective endocarditis has different complications. These complications include refractory heart failure, persistent uncontrolled infection, large, mobile bulky masses, peripheral vascular embolism, and endocarditis with prosthetic valves. Good timing of surgery for endocarditis is effective in reducing early and late mortality from surgery. The American Heart Association recommends that regardless of the cause and mechanism, patients with IE combined with heart failure should be evaluated immediately for the possibility of surgery. IE combined with heart failure predicts a poor prognosis with medical therapy alone and is a strong predictor of poor surgical outcomes. Although surgical treatment of IE combined with heart failure has a high operative mortality rate, surgical treatment significantly reduces the morbidity and mortality rate compared to medical treatment alone. Surgical procedures should be considered in the presence of the following (clall I): mycobacterial IE, IE caused by a highly destructive drug-resistant pathogenic microorganism or one that responds poorly to antibiotics, left heart IE caused by Gram-negative bacteria, infection persisting after one week of negative antimicrobial therapy with blood cultures, and more than one embolic event within the first two weeks of antibiotic therapy. Cardiac ultrasound confirmed valve dehiscence, perforation, rupture, fistula formation, large perivalvular abscesses, and obstructive bulge formation, with surgical treatment considered in these cases (class I). Ultrasound findings suggestive of anterior mitral leaflet flab formation, particularly flab formation larger than 1 mm in diameter, or the persistence of flab after systemic embolization suggest that the patient may require surgery (class IIa). In specific patients with the highest chance of embolization or in combination with other poor prognostic complications (recurrent embolism, congestive heart failure, devastating drug-resistant bacterial infections, PVE), it is important to consider surgical treatment early in the course of IE to maximize the benefit to the patient and prevent embolic events. The most likely scenario for embolism is superfluous formation in the anterior mitral leaflet greater than 10 mm and within 1-2 weeks prior to antimicrobial therapy for IE. Infection extension under the annulus is associated with the development of heart failure and higher mortality, with patients often requiring surgical treatment, and PVE, especially early PVE (less than 12 months), is often due to bacterial infection with Staphylococcus spp. and may lead to serious clinical conditions. For these reasons, PVE is more often treated surgically compared to NVE. Timing of surgery: Treatment of AIE includes both antibiotic anti-infective therapy and surgical procedures. In AIE, the affected valves may become perforated, rupture, and rupture the tendons due to necrosis, resulting in acute hemodynamic disturbances, and if anti-infective therapy is mechanically adhered to, the patient may develop severe complications and die suddenly, or the patient may lose surgery due to deterioration of the disease. Therefore, the timing of AIE surgery is very important. Although there is agreement on the indications for NVE surgery, the appropriate timing of surgery is controversial. Although the incidence of NVE has not changed in recent years, there has been a trend toward aggressive surgical treatment regarding IE treatment in recent years. Good surgical outcomes are reported in some reports, and this is supported in the surgical treatment of active IE. However, multiple parameters of the patient need to be considered to evaluate the patient’s status regarding the type of valve, perivalvular involvement, pathogenic microorganisms, location and nature of the bulge, and status of tethering comorbidities, all of which are necessary to determine the timing of surgery. In the case of cardiac insufficiency after valve injury due to right heart AIE, the body can tolerate it better after the adjustment of medication, and the cardiac function can be in a more stable state, and the surgery can be done after the completion of the course of antibiotic treatment, and the blood culture is negative and the body temperature is normal. However, in the presence of infected lesions, especially in the presence of local pus cavities, it is difficult to control the body temperature to the normal range. Therefore, although cardiac function can be stabilized and the course of antibiotic therapy can be completed in right heart AIE, surgery should be performed decisively for some infections that cannot be controlled by antibiotic therapy. NVE in the left heart can damage normal valves or aggravate existing valve lesions, leading to new regurgitation or worsening the degree of insufficiency. Because of the pressure characteristics of the body circulation, the consequences of valve damage caused by left heart AIE are more severe and have a greater impact on hemodynamics. After drug treatment, some patients are able to control their cardiac function in a more stable state and strive to complete the course of antibiotic therapy, achieve negative blood cultures and normal body temperature before elective surgery. However, in some patients, especially when severe aortic valve insufficiency occurs, the left heart function is in progressive failure. Therefore, the timing of surgery for left heart AIE should mainly depend on the status of the change in cardiac function, and the timing of antibiotic treatment should only be used as a reference factor. The status of the flab attached to the valve in AIE should be used as an indicator for the timing of surgery, and early surgery is recommended when the flab is larger than 10 mm or when the flab is more mobile. PVE is a difficult disease to treat in cardiac surgery, with poor prognosis and high mortality. The bacterial source of early PVE may be related to various aspects of surgery, and the causative organisms of late PVE are similar to those of self valve infection. The incidence of PVE is significantly higher in those with preoperative infective endocarditis and after heart valve replacement, and the mortality rate of PVE surgery has decreased significantly in recent years, but is still as high as more than 15. In patients with early PVE, inflammation often invades the valve annulus, causing perivalvular leaks, and as the disease progresses with pathologic changes, the infection continues to spread, producing cavity leaks or myocardial abscesses, especially in aortic PVE, which in severe cases can invade the aortic root in conjunction with the anterior mitral leaflet. The incidence of myocardial and perivalvular abscesses in patients with PVE with mechanical valve application is 38% and 63%, respectively . Staphylococcal infection of PVE is highly likely to cause perivalvular abscesses. In patients with advanced PVE, inflammation is often confined to the prosthetic valve, especially in patients with biologic and homogeneous valves, and to the valve leaflets. For patients for whom drug therapy alone is not effective, especially early PVE, aggressive early surgical treatment should be taken to reduce mortality, only conservative treatment of PVE mortality can be as high as 33.3 to 66.7%. It is generally believed that early surgery is more risky in IE because there is no sufficient course of antibiotics applied and the local inflammation of the valve is active, making surgical operation difficult. In contrast, recent reports have shown that the duration of preoperative antibiotic application is not associated with perioperative mortality and recurrence of IE. Therefore, early surgery should be considered in case of hemodynamic deterioration, or the appearance of uncontrollable infection, up to and active chase organism formation. Based on the above clinical findings, Olaison L summarized more specific timing of surgery and indications for surgery in active IE. Conditions requiring same-day surgery for confirmed IE: acute aortic regurgitation with early mitral valve closure; coronary sinus rupture into the right heart cavity; or rupture into the pericardium. Conditions requiring surgery within 24-48 hours of diagnosis of IE are: valve obstruction; unstable valve grafts; acute mitral regurgitation or aortic regurgitation with heart failure (NYHA III-IV); septal perforation; annular or aortic abscess formation, aortic sinus or aortic pseudo- or true aneurysm formation, fistula formation, and new conduction block; within 7-10 days of appropriate antibiotic therapy Significant embolic events, superfluous organisms larger than 10 mm in diameter while being active; ineffective or unresponsive to anti-microbial therapy. In the case of early surgery: staphylococcal PVE; early PVE (less than or equal to 2 months after valve replacement); evidence of progressive perivalvular leak; valve malfunction and uncontrolled infection after 7-10 days of appropriate anti-inflammatory therapy (excluding noncardiac causes of fever, bacteremia, etc.); mycobacterial IE due to mold; mycobacterial IE due to yeast; microbial infection that is difficult to treat