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are mainly caused by congestion and may vary from mild dyspnoea to severe and rapidly worsening dyspnoea, orthopnoea, pulmonary oedema, and cardiogenic shock. Factors associated with increased risk of HF complicating the course of IE include older age, presence of NVE with aortic valve involvement, and high comorbidity.420–425 Leaflet perforation and rupture, as well as mitral chordal rupture, lead to new severe valvular regurgitation or worsening of pre-existent valvular regurgitation and subsequent acute HF. Other less common causes of HF include intracardiac fistulae, interference of the vegetation mass with leaflet opening and closure, or myocardial infarction from vegetations embolizing into the coronary arteries. Patients with rightsided IE complicated by HF present with symptoms of right heart congestion, as discussed in Section 12.6. New-onset HF is the predominant clinical presentation in IE patients, whereas worsening of pre-existing HF is less frequent. Cardiogenic shock can be the first presentation in up to 5% of cases, of which half of such patients develop cardiogenic shock within 72 h of admission for IE.424 On imaging tests, patients with IE complicated by HF present more frequently with lower left ventricular ejection fraction, larger vegetation size, perivalvular abscesses, pseudoaneurysms, and valvular regurgitation secondary to leaflet perforation or rupture.420–425 Heart failure complicating IE is independently associated with poor in-hospital and 1-year survival, and surgical treatment is the only effective treatment that is associated with improved survival.420,421,424,426–430 Even though in-hospital mortality rates increase with the severity of HF presentation, the survival benefit of surgical treatment vs. medical therapy is more pronounced among patients with NYHA functional class III–IV symptoms.420 TTE provides important information on the severity of the haemodynamic consequences of valve dysfunction. New onset of elevated filling pressures, pulmonary hypertension, and/or pericardial effusion may lead to urgent or emergency recommendation for surgery.163 Biomarkers such as B-type natriuretic peptide and troponin have been associated with poor prognosis in IE.431,432 Patients who are discharged after treatment of IE require subsequent follow-up (see Section 11). Heart failure is more likely to develop during follow-up in IE patients who are discharged with valvular regurgitation than in those without regurgitation, particularly if mitral regurgitation is present.433

8.2.2 Indications and timing of surgery in the

presence of heart failure in infective endocarditis Timing of surgical intervention in patients with IE (Figure 10) complicated by HF should be decided by the Endocarditis Team, although surgery should not be delayed by Endocarditis Team discussions in patients requiring emergency operations. The presence of HF leads to recommendation for surgery in the majority of patients and is the principal indication for urgent surgery in IE patients.429,434 Emergency surgery should be performed in patients with new-onset NYHA class IV HF symptoms, pulmonary oedema, and/or cardiogenic shock, irrespective of the status of infection or length of antibiotic treatment and when considered non-futile intervention. Urgent surgery is indicated in patients with milder forms of HF (NYHA class II–III) and severe valve regurgitation or echocardiographic signs of haemodynamic compromise (elevated end-diastolic left ventricular pressure, high left atrial pressure, or moderate and severe pulmonary hypertension), or large vegetations. In patients without haemodynamic compromise, i.v. antibiotic therapy and strict clinical and echocardiographic observation are first indicated, and surgery can be temporarily delayed. However, it should be emphasized that early surgery is a good option for patients with surgical indications and low risk of surgery.403,404

8.3 Uncontrolled infection

Uncontrolled infection is one of the most common complications of IE and is the second most frequent indication for surgery.5 Uncontrolled infection is considered to be present when there is: (i) persistent infection or sepsis despite antibiotic therapy; (ii) signs of local infection that do not respond to antibiotic therapy; or (iii) infection with resistant or very virulent organisms.

8.3.1 Septic shock and persistent infection

Septic shock, defined as vasopressor requirement to maintain a mean arterial pressure of 65 mmHg or greater and serum lactate level greater than 2 mmol/L in the absence of hypovolaemia,435 is a highly lethal complication of IE and occurs in ∼5–10% of patients.425,436 Risk factors for septic shock include S. aureus and Gram-negative bacteria, persistent bacteraemia, nosocomial acquisition, acute renal failure, diabetes mellitus, CNS emboli, and large vegetations.147,436 Surgery is associated with a significant reduction in early and 1-year mortality for patients with IE and septic shock.425,436 Urgent surgery is therefore recommended in patients with IE and persistent sepsis or septic shock despite adequate antibiotic therapy, in which surgery is non-futile. The definition of persistent infection is somewhat arbitrary and consists of fever and persistent positive cultures after 7 days of appropriate antibiotic treatment. It has been demonstrated that persistent blood cultures 48–72 h after initiation of antibiotics are an independent risk factor for hospital mortality.437 In many cases of persistent infection, antibiotics alone are insufficient to eradicate the infection. Surgery is therefore indicated for persistent infection when extracardiac abscesses (splenic, vertebral, cerebral, or renal) and other potential causes of positive cultures and fever (infected lines and embolic complications) have been excluded. Persistent fever may also be caused as an adverse reaction to antibiotics.438

8.3.2 Locally uncontrolled infection

Signs of locally uncontrolled infection include increasing vegetation size, abscess formation, the creation of pseudoaneurysms and/or fistulae, and new atrioventricular block (AVB). The incidence of perivalvular extension ranges from 10% to 30% in NVE with higher incidences found in patients with PVE.5,439 Perivalvular complications and abscess formation are more frequent in aortic valve than mitral valve IE, and may be higher in patients with bicuspid vs. tricuspid aortic valves.440 In aortic valve IE, perivalvular extension occurs most frequently in the mitral-aortic intervalvular fibrosa,441 whereas perivalvular abscesses are usually located posteriorly or laterally in mitral valve IE.442 Persistent fever and infection, new AVB, chest pain, new heart murmur, recurrent embolism, or HF may indicate perivalvular extension. The diagnosis should be confirmed by TOE, which is more sensitive and specific than TTE.443 However, mitral annular calcification may obscure small regions of mitral perivalvular extension, particularly in the posterior aspects of the mitral annulus. Cardiac CT has been shown to be an accurate alternative imaging procedure for the evaluation of perivalvular extension of infection, and PET/CT imaging may be particularly helpful in cases of PVE (see Section 5.4.4.

ESC Guidelines                                                                                                                                                                                          3989

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