European Heart Journal (2009) 30, 2369–2413 doi:10.



Guidelines on the prevention, diagnosis, and treatment of infective endocarditis (new version 2009)
The Task Force on the Prevention, Diagnosis, and Treatment of Infective Endocarditis of the European Society of Cardiology (ESC)
Endorsed by the European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and by the International Society of Chemotherapy (ISC) for Infection and Cancer
Authors/Task Force Members: Gilbert Habib (Chairperson) (France)*, Bruno Hoen (France), Pilar Tornos (Spain), Franck Thuny (France), Bernard Prendergast (UK), Isidre Vilacosta (Spain), Philippe Moreillon (Switzerland), Manuel de Jesus Antunes (Portugal), Ulf Thilen (Sweden), John Lekakis (Greece), Maria Lengyel (Hungary), ¨ Ludwig Muller (Austria), Christoph K. Naber (Germany), Petros Nihoyannopoulos (UK), Anton Moritz (Germany), Jose Luis Zamorano (Spain) ESC Committee for Practice Guidelines (CPG): Alec Vahanian (Chairperson) (France), Angelo Auricchio (Switzerland), Jeroen Bax (The Netherlands), Claudio Ceconi (Italy), Veronica Dean (France), Gerasimos Filippatos (Greece), Christian Funck-Brentano (France), Richard Hobbs (UK), Peter Kearney (Ireland), Theresa McDonagh (UK), Keith McGregor (France), Bogdan A. Popescu (Romania), Zeljko Reiner (Croatia), Udo Sechtem (Germany), Per Anton Sirnes (Norway), Michal Tendera (Poland), Panos Vardas (Greece), Petr Widimsky (Czech Republic) Document Reviewers: Alec Vahanian (CPG Review Coordinator) (France), Rio Aguilar (Spain), Maria Grazia Bongiorni (Italy), Michael Borger (Germany), Eric Butchart (UK), Nicolas Danchin (France), Francois Delahaye (France), Raimund Erbel (Germany), Damian Franzen (Germany), Kate Gould (UK), Roger Hall ´ ´ (UK), Christian Hassager (Denmark), Keld Kjeldsen (Denmark), Richard McManus (UK), Jose M. Miro (Spain), ´ ´ Ales Mokracek (Czech Republic), Raphael Rosenhek (Austria), Jose A. San Roman Calvar (Spain), Petar Seferovic (Serbia), Christine Selton-Suty (France), Miguel Sousa Uva (Portugal), Rita Trinchero (Italy), Guy van Camp (Belgium)
The disclosure forms of the authors and reviewers are available on the ESC website
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* Corresponding author. Gilbert Habib, Service de Cardiologie, CHU La Timone, Bd Jean Moulin, 13005 Marseille, France. Tel: þ33 4 91 38 63 79, Email:
The content of these European Society of Cardiology (ESC) Guidelines has been published for personal and educational use only. No commercial use is authorized. No part of the ESC Guidelines may be translated or reproduced in any form without written permission from the ESC. Permission can be obtained upon submission of a written request to Oxford University Press, the publisher of the European Heart Journal and the party authorized to handle such permissions on behalf of the ESC. Disclaimer. The ESC Guidelines represent the views of the ESC and were arrived at after careful consideration of the available evidence at the time they were written. Health professionals are encouraged to take them fully into account when exercising their clinical judgement. The guidelines do not, however, override the individual responsibility of health professionals to make appropriate decisions in the circumstances of the individual patients, in consultation with that patient, and where appropriate and necessary the patient’s guardian or carer. It is also the health professional’s responsibility to verify the rules and regulations applicable to drugs and devices at the time of prescription.

& The European Society of Cardiology 2009. All rights reserved. For permissions please email:


ESC Guidelines

Table of Contents
A. Preamble . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . B. Justification/scope of the problem . . . . . . . . . . . . . . . . . C. Epidemiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . A changing epidemiology . . . . . . . . . . . . . . . . . . . . . Incidence of infective endocarditis . . . . . . . . . . . . . . . Types of infective endocarditis . . . . . . . . . . . . . . . . . . Microbiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . D. Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . The valve endothelium . . . . . . . . . . . . . . . . . . . . . . . Transient bacteraemia . . . . . . . . . . . . . . . . . . . . . . . Microbial pathogens and host defences . . . . . . . . . . . . E. Preventive measures . . . . . . . . . . . . . . . . . . . . . . . . . . Evidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendations Reasons justifying revision of previous ESC Guidelines . . Principles of the new ESC Guidelines . . . . . . . . . . . . . Limitations and consequences of the new ESC Guidelines F. Diagnosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Clinical features . . . . . . . . . . . . . . . . . . . . . . . . . . . Echocardiography . . . . . . . . . . . . . . . . . . . . . . . . . . Microbiological diagnosis . . . . . . . . . . . . . . . . . . . . . . Diagnostic criteria and their limitations . . . . . . . . . . . . G. Prognostic assessment at admission . . . . . . . . . . . . . . . . H. Antimicrobial therapy: principles and methods . . . . . . . . . General principles . . . . . . . . . . . . . . . . . . . . . . . . . . Penicillin-susceptible oral streptococci and group D streptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Penicillin-resistant oral streptococci and group D streptococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Streptococcus pneumoniae, b-haemolytic streptococci (groups A, B, C, and G) . . . . . . . . . . . . . . . . . . . . . . Nutritionally variant streptococci . . . . . . . . . . . . . . . . Staphylococcus aureus and coagulase-negative staphylococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Methicillin-resistant and vancomycin-resistant staphylococci . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Enterococcus spp. . . . . . . . . . . . . . . . . . . . . . . . . . . . Gram-negative bacteria . . . . . . . . . . . . . . . . . . . . . . . Blood culture-negative infective endocarditis . . . . . . . . Fungi . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Empirical therapy . . . . . . . . . . . . . . . . . . . . . . . . . . Outpatient parenteral antibiotic therapy for infective endocarditis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . I. Complications and indications for surgery in left-sided native valve infective endocarditis . . . . . . . . . . . . . . . . . . . . . . . . Part 1. Indications and optimal timing of surgery . . . . . . . . . Heart failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Uncontrolled infection . . . . . . . . . . . . . . . . . . . . . . . Prevention of systemic embolism . . . . . . . . . . . . . . . . Part 2. Principles, methods, and immediate results of surgery . Pre- and peri-operative management . . . . . . . . . . . . . . Surgical approach and techniques . . . . . . . . . . . . . . . . Operative mortality, morbidity, and post-operative complications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 2371 2372 2372 2372 2373 2373 2373 2374 2374 2374 2374 2375 2375 2375 2376 2378 2378 2378 2379 2380 2382 2383 2383 2383 2384 2384 2384 2384 2386 2387 2387 2387 2387 2388 2388 2389 2391 2391 2391 2392 2393 2394 2394 2394 2394

J. Other complications of infective endocarditis Part 1. Neurological complications, antithrombotic therapy . . Part 2. Other complications (infectious aneurysms, acute renal failure, rheumatic complications, splenic abscess, myocarditis, pericarditis) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . K. Outcome after discharge and long-term prognosis . . . . . . Recurrences: relapses and reinfections . . . . . . . . . . . . Heart failure and need for valvular surgery . . . . . . . . . Long-term mortality . . . . . . . . . . . . . . . . . . . . . . . . Follow-up . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . L. Specific situations Part 1. Prosthetic valve endocarditis . . . . . . . . . . . . . . . . . . Part 2. Infective endocarditis on pacemakers and implantable defibrillators . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Part 3. Right-sided infective endocarditis . . . . . . . . . . . . . . . Part 4. Infective endocarditis in congenital heart disease . . . . Part 5. Infective endocarditis in the elderly . . . . . . . . . . . . . Part 6. Infective endocarditis during pregnancy . . . . . . . . . . . M. References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .


2396 2397 2397 2398 2398 2398 2398 2400 2401 2403 2404 2404 2404

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Abbreviations and acronyms
BCNIE CD CDRIE CHD CNS CT ELISA HF IA ICD ICE IE IVDA LDI MBC MIC MRI MRSA MSSA NBTE NVE OPAT PBP PCR PET PMP PPM PVE TEE TTE VISA blood culture-negative infective endocarditis cardiac device cardiac device-related infective endocarditis congenital heart disease coagulase-negative staphylococci computed tomography enzyme-linked immunosorbent assay heart failure infectious aneurysm implantable cardioverter defibrillator International Collaboration on Endocarditis infective endocarditis intravenous drug abuser local device infection minimal bactericidal concentration minimal inhibitory concentration magnetic resonance imaging methicillin-resistant Staphylococcus aureus methicillin-susceptible Staphylococcus aureus non-bacterial thrombotic endocarditis native valve endocarditis outpatient parenteral antibiotic therapy plasma-binding protein polymerase chain reaction positron emission tomography platelet microbicidal protein permanent pacemaker prosthetic valve endocarditis transoesophagal echocardiography transthoracic echocardiography vancomycin-intermediate Staphylococcus aureus

ESC Guidelines

arise during the writing period must be notified to the ESC. The Task Force report received its entire financial support from the ESC and was developed without any involvement of the pharmaceutical, device, or surgical industry. The ESC Committee for Practice Guidelines (CPG) supervises and coordinates the preparation of new Guidelines and Expert Consensus Documents produced by Task Forces, expert groups, or consensus panels. The Committee is also responsible for the endorsement process of these Guidelines and Expert Consensus Documents or statements. Once the document has been finalized and approved by all the experts involved in the Task Force, it is submitted to outside specialists for review. The document is revised, and finally approved by the CPG and subsequently published. After publication, dissemination of the message is of paramount importance. Pocket-sized versions and personal digital assistant (PDA)-downloadable versions are useful at the point of care. Some surveys have shown that the intended users are sometimes unaware of the existence of guidelines, or simply do not translate them into practice. Thus, implementation programmes for new guidelines form an important component of knowledge dissemination. Meetings are organized by the ESC, and directed towards its member National Societies and key opinion leaders in Europe. Implementation meetings can also be undertaken at national levels, once the guidelines have been endorsed by the ESC member societies, and translated into the national language. Implementation programmes are needed because it has been shown that the outcome of disease may be favourably influenced by the thorough application of clinical recommendations. Thus, the task of writing Guidelines or Expert Consensus documents covers not only the integration of the most recent research, but also the creation of educational tools and implementation programmes for the recommendations. The loop between clinical research, writing of guidelines, and implementing them into clinical

A. Preamble
Guidelines and Expert Consensus Documents summarize and evaluate all currently available evidence on a particular issue with the aim of assisting physicians in selecting the best management strategy for an individual patient suffering from a given condition, taking into account the impact on outcome, as well as the risk/ benefit ratio of particular diagnostic or therapeutic means. Guidelines are no substitutes for textbooks. The legal implications of medical guidelines have been discussed previously. A great number of Guidelines and Expert Consensus Documents have been issued in recent years by the European Society of Cardiology (ESC) as well as by other societies and organizations. Because of the impact on clinical practice, quality criteria for development of guidelines have been established in order to make all decisions transparent to the user. The recommendations for formulating and issuing ESC Guidelines and Expert Consensus Documents can be found on the ESC website ( knowledge/guidelines/rules). In brief, experts in the field are selected and undertake a comprehensive review of the published evidence for management and/ or prevention of a given condition. A critical evaluation of diagnostic and therapeutic procedures is performed including assessment of the risk/ benefit ratio. Estimates of expected health outcomes for larger societies are included, where data exist. The level of evidence and the strength of recommendation of particular treatment options are weighed and graded according to predefined scales, as outlined in Tables 1 and 2. The experts of the writing panels have provided disclosure statements of all relationships they may have which might be perceived as real or potential sources of conflicts of interest. These disclosure forms are kept on file at the European Heart House, headquarters of the ESC. Any changes in conflict of interest that

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Table 1

Classes of recommendations


ESC Guidelines

Table 2

Levels of evidence

practice can then only be completed if surveys and registries are performed to verify that real-life daily practice is in keeping with what is recommended in the guidelines. Such surveys and registries also make it possible to evaluate the impact of implementation of the guidelines on patient outcomes. Guidelines and recommendations should help the physicians to make decisions in their daily practice, However, the ultimate judgement regarding the care of an individual patient must be made by the physician in charge of his/her care.

in clinical decision making. These recommendations were obtained by expert consensus after thorough review of the available literature. An evidence-based scoring system was used, based on a classification of the strength of recommendation and the levels of evidence.
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C. Epidemiology
A changing epidemiology
The epidemiological profile of IE has changed substantially over the last few years, especially in industrialized nations.1 Once a disease affecting young adults with previously well-identified (mostly rheumatic) valve disease, IE is now affecting older patients who more often develop IE as the result of health care-associated procedures, either in patients with no previously known valve disease14 or in patients with prosthetic valves.15 A recent systematic review of 15 population-based investigations accounting for 2371 IE cases from seven developed countries (Denmark, France, Italy, The Netherlands, Sweden, the UK, and the USA) showed an increasing incidence of IE associated with a prosthetic valve, an increase in cases with underlying mitral valve prolapse, and a decrease in those with underlying rheumatic heart disease.16 Newer predisposing factors have emerged—valve prostheses, degenerative valve sclerosis, intravenous drug abuse—associated with increased use of invasive procedures at risk for bacteraemia, resulting in health care-associated IE.17 In a pooled analysis of 3784 episodes of IE, it was shown that oral streptococci had fallen into second place to staphylococci as the leading cause of IE.1 However, this apparent temporal shift from predominantly streptococcal to predominantly staphylococcal IE may be partly due to recruitment/referral bias in specialized centres, since this trend is not evident in population-based epidemiological surveys of IE.18 In developing countries, classical patterns persist. In Tunisia, for instance, most cases of IE develop in patients with rheumatic valve disease, streptococci predominate, and up to 50% may be associated with negative blood cultures.19 In other African countries, the persistence of a high burden of rheumatic fever, rheumatic valvular heart diseases, and IE has also been highlighted.20 In addition, significant geographical variations have been shown. The highest increase in the rate of staphylococcal IE has been reported in the USA,21 where chronic haemodialysis, diabetes mellitus, and intravascular devices are the three main factors

B. Justification/scope of the problem
Infective endocarditis (IE) is a peculiar disease for at least three reasons: First, neither the incidence nor the mortality of the disease have decreased in the past 30 years.1 Despite major advances in both diagnostic and therapeutic procedures, this disease still carries a poor prognosis and a high mortality. Secondly, IE is not a uniform disease, but presents in a variety of different forms, varying according to the initial clinical manifestation, the underlying cardiac disease (if any), the microorganism involved, the presence or absence of complications, and underlying patient characteristics. For this reason, IE requires a collaborative approach, involving primary care physicians, cardiologists, surgeons, microbiologists, infectious disease specialists, and frequently others, including neurologists, neurosurgeons, radiologists, and pathologists.2 Thirdly, guidelines are often based on expert opinion because of the low incidence of the disease, the absence of randomized trials, and the limited number of meta-analyses.3,4 Several reasons justify the decision of the ESC to update the previous guidelines published in 2004.3 IE is clearly an evolving disease, with changes in its microbiological profile, a higher incidence of health care-associated cases, elderly patients, and patients with intracardiac devices or prostheses. Conversely, cases related to rheumatic disease have become less frequent in industrialized nations. In addition, several new national and international guidelines or state-of-the-art papers have been published in recent years.3 – 13 Unfortunately, their conclusions are not uniform, particularly in the field of prophylaxis, where conflicting recommendations have been formulated.3,4,6,8 – 13 Clearly, an objective for the next few years will be an attempt to harmonize these recommendations. The main objective of the current Task Force was to provide clear and simple recommendations, assisting health care providers

Causative microorganisms are most often staphylococci. Members of the ‘S. although this higher proportion of men is poorly understood. In an attempt to avoid overlap.28 a.24 – 26 This may reflect methodological differences between surveys rather than true variation. 2010 Types of infective endocarditis IE should be regarded as a set of clinical situations which are sometimes very different from each other. representing 85% of all IE. Infective endocarditis due to streptococci and enterococci Oral (formerly viridans) streptococci form a mixed group of microorganisms. which includes species such as S. the main predisposing factor for S. Of note. the following situations can be identified: community-acquired IE. female patients may have a worse prognosis and undergo valve surgery less frequently than their male counterparts. aureus IE may be intravenous drug abuse. the incidence of IE was very low in young patients but increased dramatically with age—the peak incidence was 14.23 Incidence of infective endocarditis The incidence of IE ranges from one country to another within 3–10 episodes/100 000 person-years. salivarius. by guest on August 31. and S. milleri’ or ‘S. in these surveys. With regard to acquisition.5 episodes/100 000 person-years in patients between 70 and 80 years of age. the male:female ratio is !2:1. Furthermore. right-sided IE. the following four categories of IE must be separated. streptococci. left-sided Table 3 Classification and definitions of infective endocarditis . associated with the development of Staphylococcus aureus endocarditis.oxfordjournals.27 Microbiology According to microbiological findings. according to the site of infection and the presence or absence of intracardiac foreign material: left-sided native valve IE. Infective endocarditis with positive blood cultures This is the most important category. mutans. sanguis.14. the following categories are proposed: 1. S. anginosus. S. and enterococci. and Gemella morbillorum. and IE in intravenous drug abusers (IVDAs).22 In other countries.ESC Guidelines 2373 prosthetic valve IE. mitis. constellatus) must be distinguished since they Downloaded from eurheartj. and device-related IE (the latter including IE developing on pacemaker or defibrillator wires with or without associated valve involvement) (Table 3). intermedius. health care-associated IE (nosocomial and non-nosocomial). In all epidemiological studies of IE. Microorganisms of this group are almost always susceptible to penicillin G.21. S. anginosus’ group (S.

favouring infection by most types of organism. H. in a recent study of 1779 cases of IE collected prospectively in 16 countries. Blood cultures may remain negative for many days after antibiotic discontinuation. durans. are the three species that cause IE. Bartonella. They are usually sensitive to penicillin G. Degenerative valve lesions are detected by echocardiography in up to 50% of asymptomatic patients over 60 years. S. CNS can also cause native valve IE. . promoting IE due to S. mechanical disruption of the endothelium results in exposure of underlying extracellular matrix proteins. fastidious Gram-negative bacilli of the HACEK group (Haemophilus parainfluenzae. Among enterococci. 2010 2. adherent bacteria must escape host defences. However.22 Conversely. Infective endocarditis associated with constantly negative blood cultures They are caused by intracellular bacteria such as Coxiella by guest on August 31. Downloaded from eurheartj. and nurture infected vegetations in which they can survive. which frequently has an aggressive clinical course. aureus trigger their active internalization into valve endothelial cells. and to a lesser extent E. native valve staphylococcal IE is due to S. Chlamydia. staphylococcal prosthetic valve IE is more frequently due to coagulase-negative staphylococci (CNS) with oxacillin resistance. but also as a consequence of chewing and tooth brushing. Following colonization. and K. Actinobacillus actinomycetemcomitans. where they can either persist and escape host defences and antibiotics.) share the ability to adhere to damaged valves. Once adherent.29 – 31 especially S. H. ESC Guidelines D. lugdunensis. including commensal species of the human intestinal tract. Hence.37 They are equipped with numerous surface determinants that mediate adherence to host matrix molecules present on damaged valves (e. H. aureus and other potential intracellular pathogens. aureus and some other IE pathogens carry fibronectin-binding proteins on their surface. Endothelial inflammation without valve lesions may also promote IE. fibrinogen. and one occurring on physically undamaged endothelium. Gram- 4. as in rheumatic carditis. and microthrombi. fibronectin. and Enterococcus spp. the production of tissue factor. usually the diagnosis is eventually considered in the face of relapsing febrile episodes following antibiotic discontinuation. Kingella kingae. aureus. Infective endocarditis with negative blood cultures because of prior antibiotic treatment This situation arises in patients who received antibiotics for unexplained fever before any blood cultures were performed and in whom the diagnosis of IE was not considered.26.35 Of note.34 Thus.10 min]. E. Cardiobacterium hominis. as recently demonstrated. at least in community-acquired IE. Transient bacteraemia The role of bacteraemia has been studied in animals with catheterinduced NBTE. inflammation. aureus was the most frequent cause not only of IE but also of prosthetic valve IE. the agent of Whipple’s disease. and fungi.. Streptococcus spp. Endothelial damage may result from mechanical lesions provoked by turbulent blood flow.36 3. Pathophysiology The valve endothelium The normal valve endothelium is resistant to colonization and infection by circulating bacteria.g. Microbial pathogens and host defences Classical IE pathogens (S. Likewise. trigger local procoagulant activity. b. faecium. and causative organisms are most often oral streptococci or CNS. Tropheryma whipplei.33 and in a similar proportion of elderly patients with IE. Integrins are transmembrane proteins that can connect extracellular determinants to the cellular cytoskeleton. Infective endocarditis frequently associated with negative blood cultures They are usually due to fastidious organisms such as nutritionally variant streptococci. Integrins of the b1 family bind circulating fibronectin to the endothelial surface while S. Local inflammation triggers endothelial cells to express integrins of the b1 family (very late antigen). Both the magnitude of bacteraemia and the ability of the pathogen to attach to damaged valves are important. often requiring a longer duration of antibiotic treatment. Group D streptococci form the ‘Streptococcus bovis/Streptococcus equinus’ complex. there are at least two scenarios for primary valve infection: one involving a physically damaged endothelium. In contrast. Brucella. E. and. S. Such nonbacterial thrombotic endocarditis (NBTE) facilitates bacterial adherence and infection. This might account for the increased risk of IE in the elderly. like oral streptococci. cell culture or gene amplification. Staphylococcal infective endocarditis Traditionally. or multiply and spread to distant organs. which are associated with inflammation. Diagnosis in such cases relies on serological testing. should also be distinguished since they are often tolerant to penicillin [minimal bactericidal concentration (MBC) much higher than the mimimal inhibitory concentration (MIC)].2374 tend to form abscesses and cause haematogenously disseminated infection. microulcers. bacteraemia does not occur only after invasive procedures.32 Overall. and were until recently gathered under the name of Streptococcus bovis. However. when activated endothelial cells bind fibronectin they provide an adhesive surface to circulating staphylococci. Eikenella corrodens. aphrophilus. electrodes or catheters. denitrificans). these account for up to 5% of all IE. paraphrophilus. recently reclassified into other species (Abiotrophia and Granulicatella). platelet proteins) and trigger platelet activation. which is most often susceptible to oxacillin. faecalis. but its high incidence may explain why most cases of IE are unrelated to invasive procedures. aureus. or degenerative changes in elderly individuals. nutritionally variant ‘defective’ streptococci. influenzae. and the deposition of fibrin and platelets as a normal healing process. Such spontaneous bacteraemia is of low grade and short duration [1– 100 colony-forming units (cfu)/ml of blood for .

Preventive measures Evidence justifying the use of antibiotic prophylaxis for infective endocarditis in previous ESC recommendations The principle of prophylaxis for IE was developed on the basis of observational studies in the early 20th century. escaping PMP-induced killing is a typical characteristic of IE-causing pathogens.53 and assumptions on efficacy are based on non-uniform expert opinion. Even strict adherence to generally accepted recommendations for prophylaxis might have little impact on the total number of patients with IE in the community.48 (d) Widespread and often inappropriate use of antibiotics may result in the emergence of resistant microorganisms.43 It therefore appears plausible that a large proportion of IE-causing bacteraemia may derive from these daily routine activities. The incidence after other types of medical procedures is even less well established.46 These estimations demonstrate the huge number of patients that will require treatment to prevent one single case of IE.6. the concept of antibiotic prophylaxis efficacy itself has never been investigated in a prospective randomized controlled trial. in patients with poor dental health. case reports. studies on isolated aspects of the hypothesis. However. or chewing.44 2.oxfordjournals. Risks and benefits of prophylaxis The following considerations are critical with respect to the assumption that antibiotic prophylaxis can efficiently prevent IE in patients who are at increased lifetime risk of the disease: Thus. A better parameter. particularly in patients with predisposing factors.26 Even if effectiveness and compliance are assumed to approximate 100%. In addition. the procedure-related risk. and these results should be interpreted with caution. flossing.49. the Task Force aimed to avoid extensive. which are produced by activated platelets and kill microbes by disturbing their plasma membrane. Recent guideline committees of national cardiovascular societies have re-evaluated the existing scientific evidence in this field. no case of fatal anaphylaxis has been reported in the literature after oral amoxicillin administration for prophylaxis of IE. Incidence of bacteraemia after dental procedures and during daily routine activities The reported incidence of transient bacteraemia after dental procedures is highly variable and ranges from 10 to 100%. The recommendations for prophylaxis are based in part on the results of animal studies showing that antibiotics could prevent the development of experimental IE after inoculation of bacteria. In contrast. no potential index procedure preceding the first clinical appearance of IE can be identified.52 Finally. by guest on August 31.52 to support the necessity of IE prophylaxis.44 positive bacteria are resistant to complement. and rates of post-procedural bacteraemia are higher in this group. they may be the target of platelet microbicidal proteins (PMPs). whereas similar bacteria recovered from patients with other types of infection are susceptible. no sufficient evidence exists from case –control studies36. the extent to which antiobiotic use for IE prophylaxis could be implicated in the general problem of resistance is unknown. E. but to limit prophylaxis to the highest risk patients. non-evidence-based use of antibiotics for all at-risk patients undergoing interventional procedures.47 and (ii) the bacteraemia that causes IE in the majority of patients appears to derive from another source. data from animal experiments. bacteraemia can be observed independently of dental procedures. (2) Prophylaxis should be limited to the highest risk patients (patients with the highest incidence of IE and/or highest risk of adverse outcome from IE). and that prophylactic antibiotics can prevent IE in these patients by minimizing or preventing bacteraemia.9 – 11 Although the individual recommendations of these committees differ in some aspects. ranges from 1:14 000 000 for dental procedures in the average population to 1:95 000 in patients with previous IE. (b) In the majority of patients. However. they did uniformly and independently draw four conclusions: (1) The existing evidence does not support the extensive use of antibiotic prophylaxis recommended in previous guidelines. The main reasons justifying the revision of previous recommendations are the following: 1. this observation leads to two conclusions: (i) IE prophylaxis can at best only protect a small proportion of patients. Lack of scientific evidence for the efficacy of infective endocarditis prophylaxis Studies reporting on the efficacy of antibiotic prophylaxis to prevent or alter bacteraemia in humans after dental procedures are contradictory. and contradictory observational studies. transient bacteraemia is reported to occur frequently in the context of daily routine activities such as tooth brushing.39 The basic hypothesis is based on the assumption that bacteraemia subsequent to medical procedures can cause IE.50 and so far there are no data demonstrating that reduced duration or frequency of bacteraemia after any medical procedure leads to a reduced procedure-related risk of IE.ESC Guidelines 2375 (a) Increased lifetime risk of IE is not an ideal measure of the extent to which a patient may benefit from antibiotic prophylaxis for distinct procedures.41 This may be a result of different analytical methods and sampling procedures. or by altering bacterial properties leading to reduced bacterial adherence on the endothelial surface. Bacteria recovered from patients with IE are consistently resistant to PMP-induced killing. (3) The indications for antibiotic prophylaxis for IE should be reduced in comparison with previous recommendations. However.40 Downloaded from eurheartj. These findings emphasize the importance of good oral hygiene and regular dental review to prevent IE. 2010 Reasons justifying revision of previous ESC Guidelines Within these guidelines. Similarly. (c) Antibiotic administration carries a small risk of anaphylaxis.

54. Level of evidence. 2010 a b Class of recommendation. b a .org by guest on August 31.oxfordjournals. Principles of the new ESC Guidelines Although recent guidelines proposed limitation of prophylaxis to patients at increased risk of adverse outcome of IE6 or even complete cessation of antibiotic prophylaxis in any patient groups.55 Table 4 Cardiac conditions at highest risk of infective endocarditis for which prophylaxis is recommended when a high risk procedure is performed Downloaded from eurheartj. Table 5 Recommendations for prophylaxis of infective endocarditis in highest risk patients according to the type of procedure at risk Class of recommendation. Patients with the highest risk of infective endocarditis (Table 4) They include three categories of patients: (a) Patients with a prosthetic valve or a prosthetic material used for cardiac valve repair: these patients have a higher risk of IE. please refer to text. but 1.12 the Task Force decided: – to maintain the principle of antibiotic prophylaxis when performing procedures at risk of IE in patients with predisposing cardiac conditions.2376 (4) Good oral hygiene and regular dental review are of particular importance for the prevention of IE. – ESC Guidelines to limit its indication to patients with the highest risk of IE (Table 4) undergoing the highest risk procedures (Table 5). *For management when infections are present. a higher mortality from IE and more often develop complications of the disease than patients with native valves and an identical pathogen. Level of evidence.

the Task Force recommends prophylaxis for the first 6 months after the procedure until endothelialization of the prosthetic material occurs. consultation with an infectious diseases specialist is recommended. dermatological or musculoskeletal procedures Downloaded from eurheartj. amoxicillin. particularly for those individuals with CHD who are at increased susceptibility for the acquisition of IE. e. Education of patients at risk of IE is paramount. Currently no data are available on (a) the incidence of IE after such procedures and (b) the efficacy of antibiotics for prevention.58. angio-oedema. ampicillin. in particular those with complex cyanotic heart disease and those who have post-operative palliative shunts. the probability of IE from dental origin is extremely low in these patients.g. Although AHA guidelines recommend prophylaxis in cardiac transplant recipients who develop cardiac valvulopathy. higher mortality and incidence of complications than patients with a first episode of IE. Vancomycin or clindamycin may be used in patients unable to tolerate a b-lactam. * Alternatively cephalexin 2 g i. Vancomycin should be given to patients unable to tolerate a b-lactam. Table 6 summarizes the main regimens of antibiotic prophylaxis recommended before dental procedures. or 50 mg/kg i.ESC Guidelines 2377 cause IE. In addition. Other at-risk procedures There is no compelling evidence that bacteraemia resulting from either respiratory tract procedures. aureus (MRSA).v. for children.g. ii. Dermatological or musculoskeletal procedures.6 this is not supported by strong evidence.g.62. In the case of an established infection or if antibiotic therapy is indicated to prevent wound infection or sepsis associated with a gastrointestinal or genitourinary tract procedure in patients described in Table 4. (b) Patients with previous IE: they also have a greater risk of new IE. or vancomycin. b. Body piercing and tattooing. Patients listed in Table 4 who undergo an invasive respiratory tract procedure to treat an established infection. Highest risk procedures (Table 5) a. Vancomycin should only be administered to patients unable to tolerate b-lactams. Fluoroquinolones and glycopeptides are not recommended due to their unclear efficacy and the potential induction of resistance. Respiratory tract procedures. 2. or musculoskeletal tissue. 2010 Table 6 Recommended prophylaxis for dental procedures at risk Cephalosporins should not be used in patients with anaphylaxis. gastrointestinal or genitorurinary procedures. e. The main targets for antibiotic prophylaxis in these patients are oral streptococci. Vancomycin or another suitable agent should be administered if the infection is known or suspected to be caused by a methicillin-resistant strain of S. These growing social trends are a cause for concern. Dental procedures Procedures at risk involve the manipulation of the gingival or periapical region of teeth or perforation of the oral mucosa (including scaling and root canal procedures). it is reasonable that the therapeutic regimen contains an agent active against staphylococci and b-haemolytic streptococci.v. should receive an antibiotic regimen which contains an anti-staphylococcal penicillin or cephalosporin. cefazolin or ceftriaxone 1 g i. The impact of increasing resistance of these pathogens for the efficacy of antibiotic prophylaxis is unclear. skin structure. Prophylaxis should only be considered for patients described in Table 4 undergoing any of these procedures.56.57 (c) Patients with congenital heart disease (CHD). Prophylaxis is not recommended for any other form of native valve disease (including the most commonly identified conditions.59 After surgical repair with no residual defects. and piercing and tattooing procedures should be discouraged.oxfordjournals. an anti-staphylococcal penicillin or cephalosporin. Thus. For patients described in Table 4 undergoing surgical procedures involving infected skin (including oral abscesses). for adults or 50 mg/kg i. Case reports of IE after piercing and tattooing are increasing. and is not recommended in other situations. . although the risk of adverse outcome is high when IE occurs in transplant patients.v. or other prostheses. Gastrointestinal or genitourinary procedures.v. bicuspid aortic valve.60 The ESC Task Force does not recommend prophylaxis in such by guest on August 31. mitral valve prolapse. iii. conduits. If infection is caused by a known or suspected strain of resistant enterococcus.61 particularly when piercing involves the tongue. it is reasonable that the antibiotic regimen includes an agent active against enterococci. for children. iv. If undertaken. vancomycin or another suitable agent should be administered. i. If the infection is known or suspected to be caused by MRSA. e.63 although publication bias may overestimate the problem since millions of people are tattooed and pierced around the world and CHD concerns only 1% of the general population. drainage of an abscess. procedures should be performed under strictly sterile conditions though antibiotic prophylaxis is not recommended. prophylaxis is not recommended in patients undergoing these procedures. and calcific aortic stenosis). or urticaria after intake of penicillin and ampicillin.

and their patients. thus representing an important health problem.oxfordjournals. The early involvement of a cardiologist and an infectious disease specialist to guide management is highly recommended. 2010 Limitations and consequences of the new ESC Guidelines The Task Force understands that these updated recommendations dramatically change long-established practice for physicians. Aseptic measures are mandatory during venous catheters manipulation and during any invasive procedures in order to reduce the rate of health care-associated IE F. Cardiac or vascular surgery. Heart Downloaded from eurheartj. poor appetite. the Task Force strongly recommends prospective evaluation in the wake of these new guidelines to evaluate whether reduced use of prophylaxis is associated with a change in the incidence of IE. after antibiotic pre-treatment. the Task Force proposes limitation of antibiotic prophylaxis to patients with the highest risk of IE undergoing the highest risk dental procedures. Prophylaxis should be started immediately before the procedure. unless the latter procedure is urgent. In summary.66 Finally. aseptic measures during the insertion and manipulation of venous catheters and during any invasive procedures are mandatory to reduce the rate of this infection.2378 v. but also as a subacute or chronic disease with low grade fever and non-specific symptoms which may thwart or confuse initial assessment. and terminated 48 h afterwards. Good oral hygiene and regular dental review have a very important role in reducing the risk of IE. and weight loss. often associated with systemic symptoms of chills. Up to 90% of patients present with fever. rapidly progressive infection. and these views should be respected. Ethically. by guest on August 31. aureus. In patients undergoing implantation of a prosthetic valve or intravascular prosthetic or other foreign material. Practitioners may also have a reasonable fear of litigation should prophylaxis be withdrawn. these practitioners need to discuss the potential benefit and harm of antibiotic prophylaxis with their patients before a final decision is made.1 year after surgery) prosthetic valve infections are CNS and S. and the mode of presentation. The most frequent microorganisms underlying early (. cardiologists. Following informed review and discussion. in the immunocompromised patient and in IE involving less virulent or atypical organisms. IE should be suspected in a variety of very different clinical situations (Table 7). rheumatological and autoimmune disease.64 Although routine antimicrobial prophylaxis administered before most invasive procedures is not recommended. It may present as an acute. ESC Guidelines neither the previous guidelines nor the current proposed modifications are based on strong evidence. vi. the presence or absence of pre-existing cardiac disease. Patients may therefore present to a variety of specialists who may consider a range of alternative diagnoses including chronic infection. or malignancy. repeated if the procedure is prolonged. Thus. They represent up to 30% of all cases of IE and are characterized by an increasing incidence and a severe prognosis. As Table 7 Clinical presentation of infective endocarditis *NB: Fever may be absent in the elderly.65 though unnecessarily so since adherence to recognized guidelines affords robust legal protection. Procedures causing health care-associated IE. many may wish to continue with routine prophylaxis.67 The clinical history of IE is highly variable according to the causative microorganism. It is strongly recommended that potential sources of dental sepsis are eliminated at least 2 weeks before implantation of a prosthetic valve or other intracardiac or intravascular foreign material. Diagnosis Clinical features The diverse nature and evolving epidemiological profile of IE ensure it remains a diagnostic challenge. but reflect an expert consensus of opinion. peri-operative antibiotic prophylaxis should be considered due to the increased risk and adverse outcome of an infection. the current recommendations are not based on appropriate evidence. .

although peripheral stigmata of IE are increasingly uncommon elsewhere.70 Echocardiography must be performed rapidly. b a murmurs are found in up to 85% of patients.7 Atypical presentation is common in elderly or immunocompromised patients. 2010 Class of recommendation. as soon as IE is suspected. TEE ¼ transoesophageal by guest on August 31. aureus Figure 1 Indications for echocardiography in suspected infective endocarditis. TEE ¼ transoesophageal echocardiography. . A high index of suspicion and low threshold for investigation to exclude IE are therefore essential in these and other high-risk groups. vascular and immunological phenomena such as splinter haemorrhages. anaemia. Classic textbook signs may still be seen in the developing world. such as elevated C-reactive protein or sedimentation rate. TTE ¼ transthoracic echocardiography. *TEE is not mandatory in isolated right-sided native valve IE with good quality TTE examination and unequivocal echocardiographic findings. Level of evidence.69 in whom fever is less frequent than in younger individuals.ESC Guidelines 2379 Table 8 Role of echocardiography in infective endocarditis Downloaded from eurheartj.oxfordjournals. these lack specificity and have not been integrated into current diagnostic criteria. leukocytosis. and microscopic haematuria. The utility of both modes of investigation is diminished when applied indiscriminately. as patients generally present at an early stage of the disease. lung or spleen occur in 30% of patients and are often the presenting feature. IE ¼ infective endocarditis. and follow-up (Table 8) of IE is clearly recognized. Roth spots. however.68 In a febrile patient. management.3 However. Echocardiography Transthoracic and transoesophageal echocardiography (TTE/TEE) are now ubiquitous and their fundamental importance in diagnosis. An exception is the patient with S. and emboli to the brain. However. the diagnostic suspicion may be strengthened by laboratory signs of infection. and glomerulonephritis remain common. TTE ¼ transthoracic echocardiography. and appropriate application in the context of simple clinical criteria improves diagnostic yield71 (Figure 1).

73 However. positron emission tomography (PET). prosthetic valves). Although IE caused by anaerobes is uncommon. particularly at the earliest stage of disease. magnetic resonance imaging (MRI). typically staphylococcal) and misleading findings. and (2) virtually all blood cultures (or a majority of them) are positive. diagnosis may be particularly challenging in IE affecting intracardiac devices. and rheumatoid disease.oxfordjournals. When cultures remain negative at 5 days. chordal rupture. and in non-vegetant IE. cultures should be incubated in both aerobic and anaerobic atmospheres to detect organisms such as Bacteroides or Clostridium species. or even earlier in case of S.75 However. follow-up echocardiography to monitor complications and response to treatment is mandatory (Table 8). with little additional information derived after the second or third assessment. Blood cultures Positive blood cultures remain the cornerstones of diagnosis and provide live bacteria for susceptibility testing. a single positive blood culture shoud be regarded cautiously for establishing the diagnosis of IE. degenerative calcified lesions. if vegetations are very small (. Three sets (including at least one aerobic and one anaerobic). Additional echocardiographic study is seldom helpful. The use of harmonic imaging has improved study quality. although surveys of contemporary practice reveal frequent violations of this by guest on August 31.72 Three echocardiographic findings are major criteria in the diagnosis of IE: vegetation.13.77 Microbiological diagnosis 1. even with use of TEE. as compared with TEE. and in the presence of a prosthetic device (especially in the mitral position). repeat TTE/TEE must be performed 7–10 days later if the clinical level of suspicion is still high. As a result. and new dehiscence of a prosthetic valve (see Table 9 for anatomical and echocardiographic definitions). 2010 bacteraemia where routine echocardiography is justified in view of the frequency of IE in this setting and of the virulence of this organism. Identification of vegetations may be difficult in the presence of preexisting severe lesions (mitral valve prolapse.76 while the roles of three-dimensional echocardiography and other alternative modes of imaging [computed tomography (CT). Similarly. subculture onto chocolate agar plates may . particularly for the assessment of the perivalvular extent of abscesses and pseudoaneurysms. in the post-operative period. Appearances resembling vegetations may be seen in degenerative or myxomatous valve disease. each containing 10 mL of blood obtained from a peripheral vein using meticulous sterile technique. especially for potentially ‘contaminants’ such as CNS or corynebacteria. aureus infection. Other advances in imaging technology have had minimal impact in routine clinical practice. which has two implications: (1) there is no rationale for delaying blood sampling to coincide with peaks of fever. and radionuclide scanning] have yet to be evaluated in IE.74 In cases with an initially negative examination. is virtually always sufficient to identify the usual microorganisms—the diagnostic yield of repeated sampling thereafter is low.79. valvular thrombus. and its devastating effects once intracardiac infection is established.80 In IE. The sensitivity of TTE ranges from 40 to 63% and that of TEE from 90 to 100%.2 mm).2380 ESC Guidelines Table 9 Anatomic and echocardiographic definitions Downloaded from eurheartj. not yet present (or already embolized). systemic lupus (inflammatory Libman –Sacks lesions). Multislice CT has recently been shown to give good results in the evaluation of IE-associated valvular abnormalities. and in association with small intracardiac tumours (typically fibroelastomata). small abscesses may be difficult to identify. The need for culture prior to antibiotic administration is self-evident.78 Sampling from central venous catheters should be avoided in view of the high risk of contaminants (false positives. abscess. bacteraemia is almost constant. advanced malignancy (marantic endocarditis). primary antiphospholipid syndrome.

81 A proposed scheme for the identification of microorganisms in culture-positive and culture-negative IE is provided in Figure 2. Early consultation with an infectious disease specialist is recommended. IE ¼ infective endocarditis. and immunocompromised states (Table 10). often delaying diagnosis and the initiation of treatment. renal failure. Culture-negative infective endocarditis and atypical organisms Blood-culture negative IE (BCNIE) occurs in 2. indwelling venous lines. underlying the need for withdrawing antibiotics and repeat blood Downloaded from eurheartj.ESC Guidelines 2381 cultures in this situation. consider antibiotic withdrawal and repeat blood cultures. 2. Table 10 Investigation of rare causes of culture-negative infective endocarditis PCR ¼ polymerase chain reaction. Histological/immunological techniques Pathological examination of resected valvular tissue or embolic fragments remains the gold standard for the diagnosis of IE and may also guide antimicrobial treatment if the causative agent can be identified allow identification of a fastidious organism. 2010 Figure 2 Microbiological diagnosis in culture-positive and culture-negative infective endocarditis. *If the organism remains unidentified and the patient is stable.5– 31% of all cases of IE. An increasingly common scenario is infection by fastidious organisms with limited proliferation under conventional culture conditions. with profound impact on clinical outcome. and alternative techniques (or an alternative diagnosis) should be considered at this stage. or requiring specialized tools for identification (see Section C). PCR ¼ polymerase chain reaction. Prolonged culture is associated with rising likelihood of contamination. .org by guest on August 31.82 BCNIE arises most commonly as a consequence of prior antibiotic administration. pacemakers.83 These organisms may be particularly common in IE affecting patients with prosthetic valves.oxfordjournals. 3.

Corey GR.84 Immunological analysis of urine may allow detection of microorganism degradation products. Sexton DJ. Bashore T.94 . and recent data demonstrate similar utility for staphylococci. and ELISA detection of Legionella species has been described using this technique.2382 ESC Guidelines Table 11 Modified Duke criteria for the diagnosis of infective endocarditis (adapted from Li et al.92 based upon clinical. and microbiological findings provide high sensitivity and specificity (80% overall) for the diagnosis of IE. The presence of a positive PCR at the time of pathological examination of the excised valve is not synonymous with treatment failure unless valve cultures are positive. Indeed. and persistent positivity despite clinical remission. Diagnostic criteria and their limitations The Duke criteria.30:633 –638.86 Although there are several advantages. Ryan T. Fowler VG. 2010 Adapted from Li JS. and the resultant so-called modified Duke criteria are now recommended for diagnostic classification (Table 11). Jr. false negatives due to the presence of PCR inhibitors in clinical samples.85 The technique has been validated using valve tissue from patients undergoing surgery for IE. PCR of excised valve tissue or embolic material should be performed in patients with negative blood cultures who undergo valve surgery or embolectomy. Electron microscopy has high sensitivity and may help to characterize new microorganisms. Clin Infect Dis 2000. Molecular biology techniques The polymerase chain reaction (PCR) allows rapid and reliable detection of fastidious and non-culturable agents in patients with IE.88 Improvements (including the availability of real-time PCR and a wider range of comparator gene sequences)89 and availability of other emerging technologies90 will address many of these deficiencies. Incorporation of these methods into accepted diagnostic criteria awaits prospective validation.oxfordjournals. by means of special stains or immunohistological techniques. inherent limitations include the lack of reliable application to whole blood samples. Mick N. but is time consuming and expensive. 94) Downloaded from eurheartj. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. but results still require careful specialist interpretation. 4. risk of contamination. Recent amendments recognize the role of Q-fever (a worldwide zoonosis caused by Coxiella burnetii). Although PCR positivity has been proposed as a major diagnostic criterion for IE. and widespread use of TEE.87. Nettles R. Coxiella burnetii and Bartonella species may be easily detected by serological testing using indirect immunofluorescence or enzyme-linked immunosorbent assay (ELISA).91 the technique seems unlikely to supersede blood cultures as a prime diagnostic tool. positive PCR can persist for months after successful eradication of infection. echocardiographic. increasing prevalence of staphylococcal infection.. including extreme by guest on August 31. inability to provide information concerning bacterial sensitivity to antimicrobial agents.93.

it should be kept in mind that these modifications await formal validation and that the original criteria were initially developed to define cases of IE for epidemiological studies and clinical trials. 2010 H. and echocardiographic parameters. and when IE affects the right heart95 (particularly in IVDAs). Clear deficiencies remain and clinical judgement remains essential.96 When three of these factors are present. Quick identification of patients at highest risk of death may offer the opportunity to change the course of the disease and improve prognosis. TTE must be performed first. but both TTE and TEE should ultimately be performed in the majority of cases of suspected or definite IE. and the presence of stroke are also predictors of poor in-hospital outcome. However. and should be used to choose the best therapeutic option.oxfordjournals. G. A high degree of co-morbidity.15 In summary.102 – 104 Nowadays. persistent infection and renal failure are predictors of by guest on August 31.105. the infecting organism. aureus infection are at highest risk of death and need for surgery in the active phase of the disease. In summary. insulin-dependent diabetes. urgent surgery). both in animal experiments and in humans. This explains why bactericidal regimens are more effective than bacteriostatic therapy. Prognosis in IE is influenced by four main factors: patient characteristics.14. The Duke criteria are useful for the classification of IE but do not replace clinical judgement.109 Table 12 Predictors of poor outcome in patients with IE .g. echocardiography and blood cultures are the cornerstone of diagnosis of IE.100. Prognostic assessment at admission The in-hospital mortality rate of patients with IE varies from 9. and/or S. especially in settings where sensitivity of the modified criteria is diminished.108. microbiological.97 – 99.96. when blood cultures are negative. periannular complications.97 Patients with heart failure (HF).96 Therefore. the presence or absence of cardiac and non-cardiac complications.96 – 102 but differs considerably from patient to patient. Surgery contributes by removing infected material and draining abscesses.6 to 26%. patients with an indication for surgery who cannot proceed due to prohibitive surgical risk have the worst prognosis. e.ESC Guidelines 2383 assessed according to these variables. prognostic assessment at admission can be performed using simple clinical. and echocardiographic findings (Table 12). depressed left ventricular function. 50% of patients undergo surgery during hospitalization.14.106 In those patients who need urgent surgery. the risk reaches 79%. Host defences are of little help. when infection affects a prosthetic valve or pacemaker lead. The risk of patients with left-sided IE has been formally Downloaded from eurheartj. Antimicrobial therapy: principles and methods General principles Successful treatment of IE relies on microbe eradication by antimicrobial drugs.68.107 Predictably. It will also allow identification of patients with the worst immediate outcome who will benefit from closer follow-up and a more aggressive treatment strategy (eg. these patients should be followed up closely and referred to tertiary care centres with surgical facilities.

and should be replaced with ceftriaxone or cefotaxime alone or in combination with vancomycin. Nutritionally variant streptococci They produce IE with a protracted course. Ceftriaxone alone or combined with gentamicin or netilmicin given once a day is particularly convenient for outpatient therapy. only limited retrospective studies have assessed its efficacy in streptococcal117 and enterococcal118 IE. Compiling four of them.126 Group A streptococci are uniformly susceptible to b-lactams. In NVE needing valve replacement by a prosthesis during antibiotic therapy. whereas other serogroups may display resistance. Recent large strain collections report . However. Little experience exists with highly resistant isolates (MIC . oralis. in penicillin-resistant cases aminoglycoside treatment may be prolonged to 3 –4 weeks and short-term therapy regimens are not recommended. which is associated with higher rates of complications and treatment failure (up to 40%). i. Enterococcus spp. After surgery.oxfordjournals.2 mg/L). S.125 IE due to group A.118. Treatment guidelines for penicillin-resistant streptococcal IE rely on retrospective series.124 which requires special consideration in cases with penicillin resistance. and some with either clindamycin or aminoglycosides alone. Drug treatment of PVE should last longer (at least 6 weeks) than that of native valve endocarditis (NVE) (2–6 weeks).g. e. Teicoplanin has been proposed as an alternative3 and requires loading doses (6 mg/kg/12 h for 3 days) followed by 6–10 mg/kg/day. except for staphylococcal PVE where the regimen should include rifampin whenever the strain is susceptible.113.110 – 112 Cure rate is expected to be .122 Treatment outcome was similar in PVE and NVE.126 Mortality of Group B PVE is very high and cardiac surgery is recommended. However. Loading is critical because the drug is highly bound to serum proteins (!98%) and penetrates slowly into vegetations.95%. IE due to group B streptococci was once associated with the peripartum period. C. Slow-growing and dormant microbes display phenotypic tolerance towards most antimicrobials (except rifampin to some extent).4 mg/L)—vancomycin might be preferred in such circumstances. 2010 Streptococcus pneumoniae.5 mg/L as fully resistant. Bactericidal drug combinations are preferred to monotherapy against tolerant organisms. Death was not related to resistance.114 The latter two studies demonstrated that gentamicin and netilmicin can be given once daily in patients with IE due to susceptible streptococci and normal renal function. In non-complicated cases.7. milleri produce abscesses and thus may require adjunctive surgery.g. and G) IE due to S. not for PVE. but now occurs in other adults.3. but is otherwise similar. antibiotic therapy for penicillin-resistant and penicillin-susceptible oral streptococci is qualitatively similar (Table 13). Antibiotic recommendations include penicillin G.128 possibly due to delayed diagnosis and treatment. B. milleri group (S. oral streptococci) and eradicate problematic organisms (e. They are present in vegetations and biofilms.121 Hence. the post-operative antibiotic regimen should be that recommended for NVE. or G streptococci—including the S.99% of group D streptococci remain penicillin susceptible. B. Penicillin-susceptible oral streptococci and group D streptococci Recommended regimens against susceptible streptococci (penicillin MIC 0. combined with an aminoglycoside for at least the first 2 by guest on August 31.0. In cases with meningitis.3. It is associated with meningitis in up to 30% of cases. Some bacteria carry mutations rendering them tolerant during both active growth and stationary (dormant) phases.g. Group B. constellatus. One major hindrance to drug-induced killing is bacterial antibiotic tolerance.125 –2 mg/L) and fully-resistant (MIC . but escape drug-induced killing and may resume growth after treatment discontinuation.120 – 123 Most penicillin MICs were !1 mg/L.). they are still susceptible to growth inhibition by the drug. and S.119 Conversely. b-lactams and glycopeptides) for bactericidal activity and are useful to shorten the duration of therapy (e. in prosthetic valve endocarditis (PVE).1 mg/L) without meningitis. Treatment of penicillin-susceptible strains (MIC 0.109a the choice of antibiotic being based on the susceptibility of the latest recovered bacterial isolate. 47/60 (78%) patients were treated with penicillin G or ceftriaxone mostly combined with aminoglycosides. which has not been formally investigated.1 mg/L) is similar to that of oral streptococci (Table 13). some guidelines consider a MIC .e.113 – 115 Patients allergic to b-lactams should receive vancomycin.127 Antibiotic treatment is similar to that of oral streptococci (Table 13). b-haemolytic streptococci (groups A. ceftriaxone or vancomycin for 6 weeks. In both NVE and PVE.30% of relatively and fully . not on the day of surgery. anginosus.110 Such resistant streptococci are increasing. Penicillin-resistant oral streptococci and group D streptococci Penicillin-resistant oral streptococci are classified as relatively resistant (MIC 0. Fifty patients (83%) were cured and 10 (17%) died.125 mg/L) are summarized in Table 13. .7. a new full course of treatment should only start if valve cultures are positive. C. C.2384 Aminoglycosides synergize with cell wall inhibitors (i.e. Downloaded from eurheartj. except that short-term therapy is not recommended. penicillin must be avoided because it poorly penetrates the cerebrospinal fluid. One recent study reported on eight cases of successful treatment with penicillin G or ceftriaxone plus gentamicin. intermedius)—is relatively rare. and G streptococci and S. the duration of treatment is based on the first day of effective antibiotic therapy. especially the elderly. pneumoniae has become rare since the introduction of antibiotics.10 mm) and underwent surgery. except for the use of short-term 2-week therapy. but to patients’ underlying conditions. ESC Guidelines resistant S. and justify the need for prolonged therapy (6 weeks) to sterilize infected heart valves fully. mitis and S.116 However.129 Seven patients had large vegetations (. shortterm 2-week therapy can be administered by combining penicillin or ceftriaxone with gentamicin or netilmicin. The same holds true for penicillinresistant strains (MIC . Tolerant microbes are not resistant.

org by guest on August 31. h Renal function and serum gentamicin concentrations should be monitored once a week. Preferred in patients . g Only if non complicated native valve IE. f Paediatric doses should not exceed adult doses. c 6-week therapy in PVE. same dosages as amoxicillin. b a . 2010 See text for other streptococcal species.112 i Serum vancomycin concentrations should achieve 10 –15 mg/L at pre-dose (trough) level and 30 –45 mg/L at post-dose level (peak. e Preferred for outpatient therapy. 1 h after injection) serum concentrations should be 10 –12 mg/L.oxfordjournals.ESC Guidelines 2385 Table 13 Antibiotic treatment of infective endocarditis due to oral streptococci and group D streptococcia Downloaded from eurheartj. When given in a single daily dose. 1 h after infusion is completed). pre-dose (trough) concentrations should be . d Or ampicillin.65 years or with impaired renal function.1 mg/L and post-dose (peak.

Its use is associated with increased toxicity and is therefore optional. to minimize the risk of resistant mutant selection.1 mg/L and post-dose ( by guest on August 31.2386 ESC Guidelines Staphylococcus aureus and coagulase-negative staphylococci Staphylococcus aureus is usually responsible for acute and destructive IE.112 b a . When given in three divided doses. Paediatric doses should not exceed adult doses. Of note. 1 h after injection) concentrations should be between 3– 4 mg/L. lugdunensis and some cases of S.131 Table 14 summarizes treatment recommendations for methicillinsusceptible and methicillin-resistant S. Renal function and serum gentamicin concentrations should be monitored once/week (twice/week in patients with renal failure). e Although the clinical benefit of gentamicin has not been demonstrated. Rifampin is believed to play a special role in prosthetic device infection because it helps eradicate bacteria attached to foreign material.135 Rifampin should always be used in combination with another effective antistaphylococcal drug. the benefit of additional Table 14 Antibiotic treatment of infective endocarditis due to Staphylococcus spp. it remains recommended for PVE. capitis). whereas CNS produce more protracted valve infections (except S. Downloaded from eurheartj. 2010 The clinical benefit of gentamicin addition has not been formally demonstrated. d Rifampin increases the hepatic metabolism of warfarin and other drugs.130. c Serum vancomycin concentrations should achieve 25 –30 mg/L at pre-dose (trough) levels. pre-dose (trough) concentrations should be .oxfordjournals. aureus and CNS in both native and prosthetic valve IE.

Ciprofloxacin (2 Â 400 mg/day i. Enterococcal IE is primarily caused by Enterococcus faecalis (90% of cases) and.146 Fully penicillin-susceptible strains (penicillin MIC 8 mg/L) are treated with penicillin G or ampicillin (or amoxicillin) combined with gentamicin.139.152 Treatment options are summarized in Table 16.145 Such cases warrant collaborative management with an infectious diseases specialist.137 Downloaded from eurheartj. vancomycin-intermediate S.132.147 This option might be considered in cases where prolonged treatment is limited by toxicity. faecium.138 Moreover. enterococci are highly tolerant to antibiotic-induced killing. However.142. more prolonged courses of b-lactams or vancomycin should be considered. linezolid. A further recently described option against gentamicin-resistant E.oxfordjournals. One study reported success with shortcourse administration of aminoglycosides (2 – 3 weeks) in 74 (81%) of 91 episodes of enterococcal IE. and eradication requires prolonged administration (up to 6 weeks) of synergistic bactericidal combinations of cell wall inhibitors with aminoglycosides (Table 15). b-lactam might be used against vancomycin-resistant strains and vice versa. quinupristin – dalfopristin with or without b-lactams. definitive studies are missing. aureus IE is not formally demonstrated.45%)134 and often requires early valve replacement. faecalis is the combination of ampicillin and ceftriaxone. although treatment may be associated with microbial resistance. by Enterococcus faecium or other species. and are associated with IE treatment failures. Importantly. leaving only vancomycin to treat severe infections. Prolonged courses of gentamicin require regular monitoring of serum drug levels and renal and vestibular function. First. and the addition of rifampin.133 It is optional for the first 3 – 5 days of therapy in NVE. and aminoglycosides should not be used in such conditions. b-Lactam and vancomycin resistance are mainly observed in E. and recommended for the first 2 weeks in PVE. Secondly. in four or six doses) plus gentamicin (3 mg/kg/ day divided in two or three doses) for 4 weeks is an option. Gram-negative bacteria 1.143 b-lactams plus oxazolidinones. Short-term (2 week) and oral treatment have been proposed for uncomplicated rightsided IE (see also Section L). they are susceptible to ceftriaxone. daptomycin needs to be administered in appropriate doses to avoid further resistance. adding rifampin in the treatment of staphylococcal PVE is standard practice. but with subpopulations growing at higher concentrations) have emerged worldwide. these conditions should be managed with the input of an infectious diseases specialist. daptomycin. they may be resistant to multiple drugs. and quinolones—the standard treatment is ceftriaxone 2 g/day for 4 weeks. They are usually resistant to multiple antibiotics. High-level gentamicin resistance is frequent in both E. Staphylococcus aureus PVE carries a very high risk of mortality (. and drug interactions. b-lactams (via PBP5 modification and sometimes b-lactamases). If they do not produce b-lactamase.139 Observational studies suggest that daptomycin might also be considered in leftsided IE and may overcome methicillin and vancomycin resistance.v. HACEK-related species HACEK Gram-negative bacilli are fastidious organisms needing specialized investigations (see also Section C).149. faecium. other third-generation cephalosporins. requiring new approaches to treatment. more rarely.v. and vancomycin.8%) of IE cases.v.136 Although the level of evidence is poor. Again.144 and b-lactams plus vancomycin. but these regimens are invalid for left-sided IE. Because of their rarity and severity. Streptomycin may remain active in such cases and is a useful alternative. Non-HACEK species The International Collaboration on Endocarditis (ICE) reported non-HACEK Gram-negative bacteria in 49/2761 (1. New lipopeptide daptomycin (6 mg/kg/day i. Other differences in comparison with NVE include the overall duration of therapy. In vitro bactericidal tests and monitoring of serum antibiotic concentrations may be helpful. Some HACEK group bacilli produce b-lactamases.146 An aminoglycoside MIC . hepatotoxicity. or 1000 mg/day orally) is a less well validated option. standard MIC tests may be difficult to interpret.140 However. prolonged additional use of aminoglycosides.151 Recommended treatment is early surgery plus long-term (!6 weeks) therapy with bactericidal combinations of b-lactams and aminoglycosides. faecalis and E. these situations require the expertise of an infectious diseases specialist. aureus (VISA) (MIC 4 – 16 mg/L) and hetero-VISA (MIC 2 mg/L. Conversely. which confers cross-resistance to most b-lactams. Ampicillin (or amoxicillin) might be preferred Blood culture-negative infective endocarditis The main causes of BCNIE are summarized in Section F. Enterococcus spp.153 . Because they grow slowly.141 Other choices include newer b-lactams with relatively good PBP2A affinity. including aminoglycosides. and tigecycline. Varying results have been reported with quinupristin–dalfopristin. some highly vancomycinresistant by guest on August 31. and ampicillin is therefore no longer the first-line option. aureus have been isolated from infected patients in recent years. Use of the latter is based on its success in treatment of infected orthopaedic prostheses135 (in combination with quinolones) and in the prevention of re-infection of vascular prostheses. They pose two major problems.ESC Guidelines 2387 since MICs are 2 – 4 times lower. aminoglycoside in S. aureus bacteraemia and right-sided IE. Since dual resistance is rare.500 mg/L is associated with loss of bactericidal synergism with cell wall inhibitors.) was recently approved for S.148 which synergize by inhibiting complementary PBPs. 2010 Methicillin-resistant and vancomycin-resistant staphylococci MRSA produce low-affinity plasma-binding protein (PBP) 2A. Otherwise.150 2. sometimes with additional quinolones or cotrimoxazole. intravenous ampicillin (12 g/day i.

predominate. Three sets of blood cultures should be drawn at 30 min intervals before initiation of . e Monitor serum levels of aminoglycosides and renal function as indicated in Table 13.50%).155. The combination of ampicillin with ceftriaxone was recently suggested for gentamicin-resistant E. c Multiresistance to aminoglycosides. (ii) if due to PBP5 alteration. Suggested regimens are summarized in Table 17. antibiotics. b b-Lactam resistance: (i) if due to b-lactamase production. faecalis 148 (IIa. (iii) b-lactam combinations including imipenem plus ampicillin or ceftriaxone plus ampicillin for !8 weeks (IIb. replace ampicillin with ampicillin –sulbactam or amoxicillin with amoxicillin –clavulanate (I. and vancomycin: suggested alternatives are (i) linezolid 2 Â 600 mg/day i. although recent case reports describe successful therapy with the new echinocandin caspofungin. Empirical therapy Treatment of IE should be started promptly. A).500 mg/L): if susceptible to streptomycin. use more prolonged course of b-lactam therapy.2388 ESC Guidelines Table 15 Antibiotic treatment of infective endocarditis due to Enterococcus spp.156 Suppressive treatment with oral azoles is often maintained long term and sometimes for life.3 months symptoms and in PVE. the latter resulting in BCNIE. HACEK species. f Paediatric doses should not exceed adult doses. Monitor serum vancomycin concentrations as indicated in Table 13.v. and Bartonella spp.154 Most cases are treated with various forms of amphotericin B with or without azoles. especially for antibiotic resistance and specific genuine culture-negative pathogens (Table 16). Otherwise. B). if so. use vancomycin-based regimens. a Fungi Fungi are most frequently observed in PVE and in IE affecting IVDAs and immunocompromised patients. by guest on August 31.oxfordjournals. when surgery was performed (early vs. late PVE) and (iii) knowledge of local epidemiology.5 mg/kg/day for !8 weeks (IIa. and treatment necessitates dual antifungal administration and valve replacement. 2010 High level resistance to gentamicin (MIC . Mortality is very high (. NVE and late PVE regimens should cover staphylococci. Downloaded from eurheartj. C). (ii) quinupristin–dafopristin 3 Â 7. Candida and Aspergillus spp. g In b-lactam allergic patients. d 6-week therapy recommended for patients with . or orally for !8 weeks (IIa.157 The initial choice of empirical treatment depends on several considerations: (i) whether the patient has received prior antibiotic therapy or not (ii) whether the infection affects a native valve or a prosthesis (and. Early PVE regimens should cover methicillin-resistant staphylococci and ideally non-HACEK Gramnegative pathogens. C). replace gentamicin with streptomycin 15 mg/kg/day in two equally divided doses (I. C) (monitor haematological toxicity). C). streptococci.

161 . monitoring of efficacy and adverse effects.1 year) cotrimoxazole therapy. Table 18 summarizes the salient questions to address when considering OPAT for IE.250 000 patients/year in the USA. and a second continuation phase (beyond 2 weeks therapy) where OPAT may be feasible. Dosages are as for streptococcal and enterococcal IE (Tables 13 and 15). paramedic and social support. f Treatment of Whipple IE remains highly empirical.153 Due to the lack of large series. If problems arise. optimal duration of treatment of IE due to these pathogens is unknown. perivalvular abscesses. Legionella spp. d Several therapeutic regimens were reported. the patient should be directed towards informed medical staff familiar with the case and not an anonymous emergency department. OPAT performs equally well independently of the pathogen and clinical context. g-Interferon plays a protective role in intracellular infections and has been proposed as adjuvant therapy in Whipple’s disease.160. Under these conditions.ESC Guidelines 2389 Table 16 Antibiotic treatment of blood culture-negative infective endocarditis Downloaded from eurheartj.386 a Outpatient parenteral antibiotic therapy for infective endocarditis Outpatient parenteral antibiotic therapy (OPAT) is used in . b Addition of streptomycin (15 mg/kg/24 h in two doses) for the first few weeks is optional..385. Successes have been reported with long-term (.158 For IE.159 Logistic issues are critical and require patient and staff education to enforce compliance. it should be used to consolidate antimicrobial therapy once critical infection-related complications are under control (e. c Doxycycline plus hydroxychloroquine (with monitoring of serum hydroxychloroquine levels) is superior to doxycycline alone and to doxycycline þ fluoroquinolone. 2010 Adapted from Brouqui and Raoult. Two different phases may be separated during the course of antibiotic therapy—a first critical phase (the first 2 weeks of therapy).oxfordjournals. including aminopenicillins and cephalosporins combined with aminoglycosides. septic emboli. doxycycline.g. acute heart by guest on August 31. and stroke). during which OPAT has a restricted indication.384 e Newer fluoroquinolones are more potent than ciprofloxacin against intracellular pathogens such as Mycoplasma spp. and Chlamydia spp. vancomycin.. and easy access to medical advice. and quinolones.383. The presented durations are based on selected case reports.

org by guest on August 31. (before or without pathogen identification) Downloaded from eurheartj.159 .b Monitoring of gentamicin and vancomycin dosages is as in Table 13 and Table 14. 2010 a.oxfordjournals.2390 ESC Guidelines Table 17 Proposed antibiotic regimens for initial empirical treatment of infective endocarditis. Table 18 Criteria which determine suitability of outpatient parenteral antibiotic therapy (OPAT) for infective endocarditis Adapted from Andrews and von Reyn.

Heart failure in infective endocarditis HF is the most frequent complication of IE and represents the most frequent indication for surgery in IE. and prevention of embolic events (Table 19) by guest on August 31. b a . are to avoid progressive HF and irreversible structural damage caused by severe infection and to prevent systemic embolism. Level of evidence.79 HF is observed in 50 –60% of cases overall and is more often present when IE affects the aortic (29%) rather than the mitral (20%) valve. Surgery is justified in patients with high-risk features which make the possibility of cure with antibiotic treatment unlikely and who do not have co-morbid conditions or complications which make the prospect of recovery remote. surgery can be postponed to allow 1 or 2 weeks of antibiotic treatment under careful clinical and echocardiographic observation before an elective surgical procedure is performed. # Surgery may be preferred if procedure preserving the native valve is feasible.e.7 HF can be caused by severe aortic or mitral insufficiency. Age per se is not a contraindication to surgery. urgent surgery: within a few days.98.79 Reasons to consider early surgery in the active phase. Identification Heart failure 1. while the patient is still receiving antibiotic treatment.162 – 165 On the other hand. uncontrolled infection. intracardiac Downloaded from eurheartj.165 In some cases. Frequently.167 The three main indications for early surgery in IE are HF. i. the need for surgery will be determined by a combination of several high-risk features. irrespective of the duration of antibiotic treatment.166 Early consultation with a cardiac surgeon is recommended in order to determine the best therapeutic approach. Each case must be individualized and all factors associated with increased risk identified at the time of diagnosis. In other cases. Indications and optimal timing of surgery Surgical treatment is used in approximately half of patients with IE because of severe complications. Complications and indications for surgery in left-sided native valve infective endocarditis Part 1.165. surgery needs to be performed on an emergency (within 24 h) or urgent (within a few days) basis.7. I. 2010 Table 19 Indications and timing of surgery in left-sided native valve infective endocarditis Class of recommendation. elective surgery: after at least 1 or 2 weeks of antibiotic therapy. surgical therapy during the active phase of the disease is associated with significant risk. *Emergency surgery: surgery performed within 24 h.ESC Guidelines 2391 of patients requiring early surgery is frequently difficult.

Clinical presentation of HF may include severe dyspnoea. while the sensitivity of TTE is . The most characteristic lesion leading to HF in NVE is valve destruction causing acute regurgitation. depending on tolerance of the valve lesion and according to the recommendations of the ESC Guidelines on the Management of Valvular Heart by guest on August 31.165 Surgery is indicated in patients with HF caused by severe aortic or mitral insufficiency.2392 fistulae. An ECG should therefore be performed frequently during follow-up. perivalvular abscesses are usually located posteriorly or laterally. and aneurysms are best assessed using TEE. infected lines. In patients with well tolerated severe valvular insufficiency and no other reasons for surgery. TEE is the technique of choice for the diagnosis and follow-up of all perivalvular complications. and research for intracardiac or extracardiac focus of infection.92 which may occur as a result of mitral chordal rupture.3 Management of persisting fever includes replacement of intravenous lines.7 Moderate-to-severe HF is the most important predictor of in-hospital and 6-month mortality.179 – 181 and very frequent in PVE (56–100%). small abscesses can be missed. TTE is of crucial importance for initial evaluation and follow-up.176 In summary. and locally uncontrolled infection. 2. particularly those in a mitral location when there is co-existent annular calcification. perivalvular extension occurs most frequently in the mitral –aortic intervalvular fibrosa.7 In mitral IE. particularly in aortic IE. S. starting with aortic root wall thickening and extending to the development of fistulae. It must be performed on an urgent basis when HF is less severe. HF is the most frequent and severe complication of IE.68. Echocardiography is also of more general value for haemodynamic assessment of valvular dysfunction.175 2.178.170 The suspicion of valve obstruction is raised by an elevated transvalvular gradient on TTE.178 Perivalvular abscess is more common in aortic IE (10–40% in native valve IE)3. Surgery must be performed on an emergency basis. infection due to resistant organisms. or.50%179 – 183 (see Section F). Persisting infection Persisting fever is a frequent problem observed during treatment of IE. Perivalvular complications include abscess formation. Resultant aneurysm formation on the atrial aspect of the mitral leaflet may later lead to mitral perforation.74 Downloaded from eurheartj. and assessment and monitoring of left ventricular systolic function and left and right heart filling pressures.3. aortic location. 2010 .184 In one study.7–10 days).173 HF may progress from mild to severe during treatment. the most important risk factors for perivalvular complications were prosthetic valve. measurement of pulmonary artery pressure. Surgery should be subsequently considered after healing of IE. hospital mortality remains high (41%). aureus being the most commonly associated organism (46%).183 Serial echocardiographic studies have shown that abscess formation is a dynamic process. leaflet rupture (flail leaflet). Usually. Unless severe co-morbidity exists. intracardiac fistulae. perivalvular extension is frequently discovered on a systematic TEE. when a large vegetation partially obstructs the valve orifice. more rarely.181 Pseudoaneurysms and fistulae are severe complications of IE and frequently associated with very severe valvular and perivalvular damage. In IE with acute regurgitation. and two-thirds of these cases occur during the active phase of the disease. However. 1. Persisting fever may be related to several reasons. Surgery is also indicated in patients with severe acute aortic or mitral regurgitation without clinical HF but with echocardiographic signs of elevated left ventricular enddiastolic pressure (premature closure of the mitral valve).7. and cardiogenic shock. secondary mitral lesions. and fistulae (Table 9). ESC Guidelines the presence of HF indicates early surgery in patients with NVE. even using TEE. Chamber size is usually normal. blood cultures and echocardiography.174. and acute coronary syndrome.185 – 188 The frequency of fistula formation in IE has been reported to be 1.171. when patients are in persistent pulmonary oedema or cardiogenic shock despite medical therapy. or interference of the vegetation mass with leaflet closure.6%. or moderate or severe pulmonary hypertension.169. Perivalvular extension in infective endocarditis Perivalvular extension of IE is the most frequent cause of uncontrolled infection and is associated with poor prognosis and high likelihood of need for surgery.177. In addition to clinical findings. A special situation is secondary infection168 of the anterior mitral leaflet associated with primary aortic IE with aortic regurgitation.oxfordjournals. regurgitant flow velocities are frequently low with a short deceleration time since pressures in the left atrium (mitral regurgitation) or left ventricle (aortic regurgitation) equalize rapidly. third degree atrioventricular block. and infection with CNS. Uncontrolled infection Uncontrolled infection is the second most frequent cause for surgery79 and encompasses persisting infection (. irrespective of the status of infection. embolic complications or extracardiac site of infection. leaflet perforation.177. by valve obstruction.98. pseudoaneurysms.107.182 In aortic IE. medical management with antibiotics is recommended under strict clinical and echocardiographic observation.188 Despite high rates of surgery in this population (87%). high left atrial pressure. Indeed. Indications and timing of surgery in the presence of heart failure in infective endocarditis (Table 19) The presence of HF indicates surgery in the majority of patients with IE7 and is the principal indication for urgent surgery.189 Perivalvular extension should be suspected in cases with persistent unexplained fever or new atrioventricular block. or by valve obstruction caused by vegetations.172 Brain natriuretic peptide (NT-proBNP) has potential use in the diagnosis and monitoring of HF in IE. including inadequate antibiotic therapy. Valve perforation. repeat laboratory measurements. locally uncontrolled infection. and adverse reaction to antibiotics. resistant organisms. temperature normalizes within 5– 10 days under specific antibiotic therapy. pulmonary oedema.186 – 188 Other complications due to major extension of infection are less frequent and may include ventricular septal defect.

195 The best means to reduce the risk of an embolic event is the prompt institution of appropriate antibiotic therapy. systematic abdominal and cerebral CT scan may be helpful.68 Patients with vegetations length .10 mm) following one or more clinical or silent embolic events despite appropriate antibiotic therapy.7/1000 patient days in the second week and further thereafter. . particularly if the vegetation is located on the mitral valve. Several factors are associated with increased risk of embolism.155 Surgery is indicated in IE due to multiresistant organisms. cerebral. persistent infection despite appropriate antibiotic therapy. especially those affecting the splenic or cerebral circulation. the risk of new events (occurring after initiation of antibiotic therapy) is only 6–21%. particularly beyond 2 weeks.194 Conversely.195.209 Among these.200. The main indications and timing of surgery to prevent embolism in NVE are given in Table 19. Indications and timing of surgery to prevent embolism in infective endocarditis (Table 19) Avoiding embolic events is difficult since the majority occur before admission. Rarely. vertebral.186. vegetation size was one of the reasons for surgery in 54% of patients with NVE and in 25% of those with PVE.68 Surgery undertaken for the prevention of embolism must be performed very early.10 mm are at higher risk of embolism.196. Surgery is indicated in patients with large vegetations (.210 although some risk persists indefinitely whilst vegetations remain present.68.ESC Guidelines 2393 2. although this decision is more difficult and must be very carefully individualized. Downloaded from eurheartj.193 In summary.195 Whilst promising. the benefits of surgery to prevent embolism are greatest during the first week of antibiotic therapy. Overall embolic risk is very high in IE.200.204.15 mm) and mobile vegetations.165 The overall benefits of surgery should be weighed against the operative risk and must consider the clinical status and co-morbidity of the patient.8/1000 patient days in the first week of therapy.g. and the duration of antibiotic therapy. false aneurysms or the creation of fistulae. with embolic events occurring in 20 –50% of patients. embolic events may be totally silent in 20% of patients with IE.oxfordjournals. and can be diagnosed by non-invasive imaging. aureus. falling to 1. Unless severe co-morbidity exists.200 It must be re-emphasized that the risk of new embolism is highest during the first days following initiation of antibiotic therapy and rapidly decreases thereafter.207 particular microorganisms (staphylococci. while pulmonary embolism is frequent in native right-sided and pacemaker lead IE.211. previous embolism. contrast media should be used with caution in patients with renal failure or haemodynamic instability because of the risk of worsening renal impairment in combination with antibiotic nephrotoxicity. Embolic events in infective endocarditis Embolic events are a frequent and life-threatening complication of IE related to the migration of cardiac vegetations. abscess). In NVE caused by S. when embolic risk peaks. and also in the rare infections caused by Gramnegative bacteria. For this reason.208 Candida spp.213 The exact role of early surgery in preventing embolic events remains controversial.203 and this risk is even higher in patients with very large (. MRSA or vancomycin-resistant enterococci. Indications and timing of surgery in the presence of uncontrolled infection in infective endocarditis (Table 19) Persistent infection In some cases of IE. surgery is indicated in patients with large vegetations (. according to the probability of conservative surgery.134.200 Streptococcus bovis. especially in staphylococcal IE affecting the mitral valve. Infection by microorganisms infrequently cured by antimicrobial therapy Surgery is indicated in fungal by guest on August 31.68. Thus. and surgery is recommended as soon as possible. Signs of locally uncontrolled infection These include increasing vegetation size.199 – 207 the location of the vegetation on the mitral valve. the size and mobility of the vegetations are the most potent independent predictors of a new embolic event.68. during the first few days following initiation 3. the presence of a large vegetation favours earlier surgery.16.190.15 mm) isolated vegetations on the aortic or mitral valve.212 the addition of antiplatelet therapy did not reduce the risk of embolism in the only published randomized study.68 In the absence of embolism.79 but was rarely the only reason. the decision to operate early for prevention of embolism must take into account the presence of previous embolic events. other complications of IE. 3. In these situations. or renal) and other causes of fever have been excluded. abscess formation. when there are no other reasons for surgery and fever is easily controlled with antibiotics. antibiotics alone are insufficient to eradicate the infection. The value of early surgery in this situation has never been proven.199 and biological markers. small abscesses or false aneurysms can be treated conservatively under close clinical and echocardiographic follow-up. In the Euro Heart Survey.154. e. The brain and spleen are the most frequent sites of embolism in left-sided IE.195 – 203 However. the presence of locally uncontrolled infection indicates early surgery in patients with NVE. 2010 Prevention of systemic embolism 1. and other predictors of a complicated course (HF.199 – 203 the increasing or decreasing size of the vegetation under antibiotic therapy. Surgery may be considered in patients with very large (. Stroke is a severe complication and is associated with increased morbidity and mortality. uncontrolled infection is most frequently related to perivalvular extension or ‘difficult-to-treat’ organisms. including the size and mobility of vegetations. the size and mobility of the vegetation.196. Surgery is indicated when fever and positive blood cultures persist for several days (. the likelihood of conservative surgery.191 Persistent fever is also usually present.7–10 days) despite an appropriate antibiotic regimen and when extracardiac abscesses (splenic. surgery is indicated if a favourable early response to antibiotics is not achieved.10 mm).68. Predicting the risk of embolism Echocardiography plays a key role in predicting embolic events.200 – 205 although prediction remains difficult in the individual patient.200 multivalvular IE.192.200 A recent study from the ICE group204 demonstrated that the incidence of stroke in patients receiving appropriate antimicrobial therapy was 4. However.).195 Thus.195.

215. Mechanical and biological prostheses have similar operative mortality. type of microorganism. Extracardiac infection If a primary focus of infection likely to be responsible for IE has been identified. high-resolution CT may be used to rule out significant coronary artery disease. and post-operative complications Peri-operative mortality and morbidity vary according to the type of infective agent. assess the result. However. with improved durability. Currently. In complex cases with locally uncontrolled infection. acute renal failure requiring haemodialysis.237 Immediate post-operative complications are relatively common.229 In experienced hands. Risk is increased with large (>10 mm) vegetations and particularly high with very mobile and larger (>15 mm) vegetations. Principles. to guide surgery.226 – 228 Homografts or stentless xenografts may be preferred in PVE or in cases where there is extensive aortic root destruction with aorto-ventricular discontinuity. successful valve repair can be achieved by experienced teams in up to 80% of patients. valve repair is favoured whenever possible. re-exploration of the chest for bleeding or tamponade. any method to repair or replace the valve may be used. 2010 Operative mortality.235. unless valve surgery is urgent. and stroke. Governing factors include size and mobility of the vegetation.176 2. coagulopathy.216 Perforations in a single valve cusp or leaflet may be repaired with an autologous glutaraldehyde-treated or bovine pericardial patch. annular.40 years. respectively.225 However. Where infection is confined to the valve cusps or leaflets.224. a prosthetic valve then being secured to the reconstructed/reinforced annulus. methods. but larger cavities should be allowed to drain into the pericardium or the circulation. it must be eradicated prior to cardiac surgical intervention. The use of foreign . embolism is very frequent in IE.214 material should be kept to a by guest on August 31. a recent study showed that in-hospital mortality is 15%.217 Therefore. Mitral subannular.223 but their application is limited by poor availability and difficulty of the surgical technique. and in patients with at least one cardiovascular risk factor or a history of coronary artery disease.2394 of antibiotic therapy (urgent surgery).227. operative mortality in IE lies between 5 and 15%. Exceptions arise when there are large aortic vegetations which may be dislodged during catheterization. pneumonia. mortality should be similar to routine valve surgery. mechanical prostheses and xenografts compare favourably. but the main reasons are multiorgan failure.222.219 – 221 The use of mitral valve homografts and pulmonary autografts (Ross procedure) has been suggested. In these situations. or supraannular tissue defects are preferably repaired with autologous or bovine pericardium. and help in early post-operative follow-up. the Ross procedure may be used in children or adolescents to facilitate growth and in young adults for extended durability. and immediate results of surgery Pre. complicating 20 –50% of cases of IE.218 Residual mitral regurgitation should be assessed using intra-operative TEE.224. The use of cryopreserved or sterilized homografts has been suggested to reduce the risk of persistent or recurrent infection. ESC Guidelines Part 2. as the risk of embolism is highest at this time.104 Surgical approach and techniques The two primary objectives of surgery are total removal of infected tissues and reconstruction of cardiac morphology.234 – 239 When surgery must be performed within the first week of antimicrobial therapy.and peri-operative management 1. the extent of destruction of cardiac structures. The decision to operate on early to prevent embolism is always difficult and specific for the individual patient. if necessary. and atrioventricular block following radical resection of an aortic root abscess with need for pacemaker implantation. The risk of embolism is the highest during the first 2 weeks of antibiotic therapy and is clearly related to the size and mobility of the vegetation. the degree of left ventricular dysfunction. including repair or replacement of the affected valve(s). falling to 6 –21% after initiation of antibiotic therapy. with risks of recurrence and non-infective post-operative valvular dysfunction of 12 and 7%. previous embolism.225. where disease is limited to the valve structures alone allowing complete excision of infected tissue. stroke. Small abscesses can be closed directly.231 A monoblock aorto-mitral homograft has been suggested as a surgical option for extensive bivalvular IE. intractable sepsis. replacement of the aortic valve using a mechanical or biological prosthesis is the technique of choice.233 Downloaded from eurheartj. although such excellent results may not be matched in non-specialist centres. HF. Intra-operative echocardiography Intra-operative TEE is most useful to determine the exact location and extent of infection. and duration of antibiotic therapy. morbidity. Among the most frequent are severe coagulopathy requiring treatment with clotting factors.239 In less complex cases. In aortic IE.oxfordjournals. or when emergency surgery is necessary. The choice of technique depends on the vertical extension of the lesion/tissue defect. 3. low cardiac output syndrome. The cause of death is often multifactorial. and the patient’s haemodynamic condition at the time of surgery. total excision of infected and devitalized tissue should be followed by valve replacement and repair of associated defects to secure valve fixation.232 Cardiac transplantation may be considered in extreme cases where repeated operative procedures have failed to eradicate persistent or recurrent PVE. In mitral valve IE.237 A pre-operative ECG demonstrating left bundle branch block predicts the need for a post-operative permanent pacemaker.68.200 In summary. Coronary angiography Coronary angiography is recommended according to the ESC Guidelines on the Management of Valvular Heart Disease176 in men . particularly when IE affects the mitral or tricuspid valve. the Task Force does not favour any specific valve substitute but recommends a tailored approach for each individual patient and clinical situation. in post-menopausal women.

cardiac surgery is not contraindicated unless the neurological prognosis is judged to poor (Figure 3). uncontrolled infection. Level of evidence.194. After an ischaemic by guest on August 31. MR ¼ magnetic resonance.246.242 – 246 If cerebral haemorrhage has been excluded by cranial CT and neurological damage is not severe (i.oxfordjournals.ESC Guidelines 2395 and can be performed with a relatively low neurological risk (3– 6%) and good probability of complete neurological recovery. silent cerebral embolism.247 Conversely. After a neurological event. particularly in the case of stroke.e. neurological prognosis is worse and surgery must be postponed for at least 1 month. 2010 Figure 3 Therapeutic strategy for patients with infective endocarditis and neurological complications. transient ischaemic attack. or persistent high embolic risk should not be delayed Downloaded from eurheartj. meningitis.194. abscess. including ischaemic or haemorrhagic stroke.194 The risk of post-operative neurological deterioration is low after a silent cerebral embolism or transient ischaemic attack.98. antithrombotic therapy Neurological complications Neurological events develop in 20–40% of all patients with IE and are mainly the consequence of vegetation embolism. surgery indicated for HF. most patients still have at least one indication for cardiac surgery. A neurologist/neurosurgeon should always be involved in the management of these patients.194 Rapid diagnosis and initiation of appropriate antibiotics are of major importance to prevent a first or recurrent neurological complication. Neurological complications. toxic encephalopathy.240. in cases with intracranial haemorrhage. symptomatic or asymptomatic infectious aneurysm. Table 20 Management of neurological complications Class of recommendation.240 They are associated with an excess mortality. CT ¼ computed tomography. and seizure.241 The clinical spectrum of these complications is wide. b a .242 If urgent cardiac surgery is needed. Evidence regarding the optimal time interval between stroke and cardiac surgery is conflicting because of lack of controlled studies. coma). brain abscess.194. close cooperation with the neurosurgical team is mandatory. Table 20 and Figure 3 J.194 and surgery is recommended without delay if an indication remains. Staphylococcus aureus causes higher overall rates of neurological complications. Other complications of infective endocarditis Part 1.

249 – 251 no strong evidence exists on its beneficial effect in clinical practice because of conflicting data. and the experience of the medical team. In summary.252 Besides.259 serial imaging is required. Although initial experimental studies showed a beneficial impact of aspirin therapy on the risk of an embolic event in S.213. In cases with large. splenic abscess. seizures) and imaging should be performed to detect intracranial IAs in any case of IE with neurological symptoms. myocarditis. neurological events develop in 20 –40% of all patients with IE and are mainly the consequence of embolism.oxfordjournals. rheumatic complications.248 The recommendations for the management of the anticoagulant therapy are based on low level of evidence (Table 21).258 by guest on August 31. acute renal failure. In patients already taking oral anticoagulants. To prevent this complication.252 from subsequent spread of infection through the intimal vessels. 2010 summarize the recommended management of neurological complications in IE.213. headache. Antithrombotic therapy There is no indication for the initiation of antithrombotic drugs (thrombolytic drugs.263 but acute renal failure is often reversible. No randomized trials exist to guide management. Stroke is associated with excess mortality. vancomycin (synergistic toxicity with aminoglycosides).255 Clinical presentation is highly variable256 (focal neurological deficit. Ruptured IAs have a very poor prognosis. but no predictors of this complication have been identified to date. or after cardiac surgery B Antibiotic toxicity (acute interstitial nephritis).257.255. and even high dose penicillin B Nephrotoxicity of contrast agents used for imaging purposes. and therapy must be tailored to the individual patient.260 The choice between these options will depend on the presence and size of the haematoma. CT and magnetic resonance angiography both reliably diagnose IAs with high sensitivity and specificity. some studies showed a non-significant increase of major bleeding episodes.261 Causes are often multifactorial:262 B Immune complex and vasculitic glomerulonephritis B Renal infarction B Haemodynamic impairment in cases with HF or severe sepsis. anticoagulant or antiplatelet therapy) during the active phase of IE.253.aureus IE. Acute renal failure Acute renal failure is a common complication of IE which occurs in 30% of patients and predicts poor prognosis. confusion. Downloaded from eurheartj. Other complications (infectious aneurysms. Haemodialysis may be required in some patients. Rapid diagnosis and initiation of appropriate antibiotics are of major importance to prevent a first or recurrent neurological complication. notably related to aminoglycosides. enlarging. Level of evidence. aureus PVE and those with a previous neurological event.212.254 An intracranial location is most frequent. there is a risk of intracranial haemorrhage which seems to be highest in patients with S. conventional angiography remains the gold standard and should be performed when non-invasive techniques are negative and suspicion remains. pericarditis) Infectious aneurysms Infectious (mycotic) aneurysms (IAs) result from septic arterial embolism to the intraluminal space or vasa vasorum. most patients still have an indication for surgery which is generally not contraindicated. neurosurgery or endovascular therapy is indicated. After a first neurological event. antibiotic Part 2. Since many unruptured IAs may resolve during antibiotic treatment. or ruptured IAs.2396 ESC Guidelines Table 21 Management of antithrombotic therapy in infective endocarditis a b Class of recommendation. or . and the reported frequency of 2 –4% is probably an underestimate since some IAs are clinically silent.

Outcome after discharge and long-term prognosis Late complications occurring after the initial infection contribute to the poor prognosis of IE.271 Rarely. or ultrasound. Persistent or recurrent fever and bacteraemia suggest the diagnosis. the main complications include recurrence of infection.3 Myocardial involvement is best assessed using TTE. and should be performed before valvular surgery unless the latter is urgent. Ventricular arrhythmias may indicate myocardial involvement and imply a poor prognosis.oxfordjournals. Treatment consists of appropriate antibiotic regimens. In these cases. back pain) are frequent during IE.ESC Guidelines 2397 doses should be adjusted for creatinine clearance with careful monitoring of serum levels (aminoglycosides and vancomycin). 2010 Splenic abscess Although splenic emboli are common.275 For these purposes. need for valve surgery. and death. although variable. Regional myocardial infarction may be caused by coronary embolism or compression.270. and a persistent focus of infection (e. Reinfection is more Downloaded from eurheartj.273 – 275 In a recent large series with mean 5-year follow-up. Imaging with nephrotoxic contrast agents should be avoided in those with haemodynamic impairment or previous renal insufficiency. the time between episodes is usually shorter for relapse than for reinfection—in broad terms.g.3. MRI. storage of endocarditis isolates for at least 1 year is recommended. Following in-hospital treatment. IE was diagnosed in 30.105.56 Factors associated with an increased rate of relapse are listed in Table 22. splenic abscess is rare. Patients with previous IE are at risk of reinfection. Conversely. The term ‘relapse’ refers to a repeat episode of IE caused by the same microorganism as the previous episode. aureus infection. the rate of recurrence in non-IVDAs was 1.57.235 – 237. and these patients should be evaluated by abdominal CT. suboptimal choice of initial antibiotics. HF.273 Rheumatic complications Musculoskeletal symptoms (arthralgia.268.56 When the same species is isolated during a subsequent episode of IE.274 and prophylactic measures should be very strict.272 Although not systematically differentiated in the literature.5%. ‘reinfection’ is primarily used to describe infection with a different microorganism. K. Peripheral arthritis occurs in 14% and spondylodiscitis in 3–15% of cases. Recurrences: relapses and reinfections The risk of recurrence amongst survivors of IE varies between 2. periprosthetic abscess). Table 22 Factors associated with an increased rate of relapse . an episode of IE caused by the same species within 6 months of the initial episode represents relapse.7 and 22. echocardiography may be performed in patients with a definite diagnosis of pyogenic spondylodiscitis and underlying cardiac conditions predisposing to endocarditis. myocarditis. ruptured pseudoaneurysms or fistulae may communicate with the pericardium. molecular methods including strain-typing techniques should be employed. the timing of the second episode of IE may be used to distinguish relapse from reinfection. Relapses are most often due to insufficient duration of original treatment. myalgia. and rheumatic complications may be the first manifestations of the disease.56 In contrast. pericarditis Cardiac failure may also be due to myocarditis which is frequently associated with abscess formation. Splenectomy may be considered for splenic rupture or large abscesses which respond poorly to antibiotics alone. there are two types of recurrence: relapse and reinfection. Thus. or bacteraemia often as a result of S. Percutaneous drainage is an alternative for high-risk surgical candidates.8% of patients with pyogenic spondylodiscitis and was more common in cases of streptococcal infection and predisposing heart conditions.267 MRI or CT of the spine should be performed in IE patients with back pain. there is often uncertainty as to whether the repeat infection is a relapse of the initial infection or a new infection (reinfection).3 Pericarditis may be associated with an abscess. Purulent pericarditis is rare and may necessitate surgical drainage. whereas later events suggest reinfection.264 – 266 In one study.3.3% per patient-year.56. When the duration of therapy has been insufficient or the choice of antibiotic by guest on August 31. with dramatic and often fatal consequences.56 When these techniques or the identity of both isolates are unavailable. Prolonged antibiotic therapy is generally required in definite spondylodiscitis. relapse should be treated for a further 4 –6 weeks depending on the causative microorganism and its susceptibility (remembering that resistance may develop in the meantime).272.269 Myocarditis.

57.1. dehiscence. while the microbiology of late PVE mirrors that of NVE.236. In cases with perioperative contamination.273 and in those with multiple risk factors for IE. However.105.253.106 The pathogenesis of PVE differs according to both the type of contamination and the type of prosthetic valve. diagnosis of PVE is mainly based on the results of echocardiography and blood cultures.2398 frequent in IVDAs (especially in the year after the initial episode).236. large vegetations may cause prosthetic valve obstruction. resistant microorganisms. and perforation.176 As a consequence of increasing rates of operation during the active phase of the infection. Heart failure and need for valvular surgery Progressive HF can occur as a consequence of valve destruction. recommendations for surgery follow conventional guidelines. as compared with NVE. After discharge. Streptococcus bovis. As in NVE.285 Although TEE is mandatory in suspected PVE (Figure 1). Clinical presentation is frequently atypical. and 12 months during the first year following completion of treatment. principal factors which determine long-term mortality are age.281.284 However. Downloaded from eurheartj. What is important is not the time from the surgical procedure to the onset of IE. and late PVE beyond 1 year. relapse and reinfection are rare following IE. Preventive measures should be applied in these patients who are a high risk group (see Section E). because of significant differences between the microbiological profiles observed before and after this time point.273. but the Task Force recommend clinical evaluation. in late bioprosthetic PVE. patients with IE must be informed of the risk of recurrence and educated about how to diagnose and prevent a new episode of IE. cusp rupture.oxfordjournals.235. and poor prognosis. chills. infection is frequently located on the leaflets of the prosthesis. Prosthetic valve endocarditis PVE is the most severe form of IE and occurs in 1– 6% of patients with valve prostheses279—an incidence of 0. but may be caused by inadequate initial antibiotic therapy. A negative echocardiogram is frequently observed in PVE2 and does not exclude the diagnosis. and Gram-negative bacilli are the main causes of early PVE. They should be aware that recurrence can occur in IE and that new onset of fever. .277 in patients undergoing chronic dialysis. In summary.3 Patients with reinfection are at higher risk of death and need for valve replacement. In PVE. 6. PVE was observed in 16% of cases in the French Survey. leading to vegetations. oral streptococci. staphylococcal and fungal infections are more frequent and streptococcal infection less frequent than in NVE. more probably due to community-acquired infections. fungi.2% per patientyear. blood cultures are more frequently negative in PVE.273 Definition and pathophysiology Early PVE is defined as occurring within 1 year of surgery. even when infection is healed. Less frequently.106 PVE is still associated with difficulties in diagnosis.280 – 284 It accounts for 10 –30% of all cases of IE280 and affects mechanical and bioprosthetic valves equally. and by guest on August 31. or intravenous drug abuse.106.236.274 Information concerning longer follow-up is scarce.235.273 Following the in-hospital phase.3 –1. There is no evidence base to guide the optimal monitoring of these patients.3. Similarly. particularly during the first year of follow-up. or other signs of infection mandate immediate evaluation.57. in which fever and inflammatory syndromes are common in the absence of IE. For example. 2010 Long-term mortality Long-term survival is 60 –90% at 10 years.276 in PVE.278 ESC Guidelines L. including the procurement of blood cultures before empirical use of antibiotics. determination of the optimal therapeutic strategy. To monitor the development of secondary HF. Diagnosis Diagnosis is more difficult in PVE than in NVE. ranging from 3 to 7% in the most recent series. Staphylococci. the need for late valve surgery is low. its diagnostic value is lower than in NVE.3.272.225. which can be diagnosed by fluoroscopy and/or TEE.275 The type of valve implanted has no effect on the risk of recurrent IE. pseudoaneurysms. but whether IE is acquired peri-operatively or not and which microorganism is involved. the same and other mechanisms may exist. The consequence of PVE is usually new prosthetic regurgitation. leading to perivalvular abscess. 3. A survival at 15 –20 years of 50% has been reported. persistent focus of infection. blood samples (white cell count.101. and fistulae.235. A recent large prospective multicentre international registry found that 37% of PVE were associated with nosocomial infection or non-nosocomial health care-associated infections in outpatients with extensive health care contact. this is an artificial distinction. with staphylococci.237 Aortic valve and root replacement with a prosthetic conduit yields results comparable with those of homograft root replacement. particularly when surgery has not been performed. C-reactive protein) and TTE at 1. the infection usually involves the junction between the sewing ring and the annulus. particularly in the early post-operative period.1. IE was the cause of the late mortality in only 6. an initial clinical evaluation and baseline TTE should be performed at the completion of antimicrobial therapy and repeated serially. and enterococci being the most frequent organisms.5% of patients who died.273 In a recent series.188.275. After completion of treatment. co-morbidity. both are more frequently negative in PVE. Specific situations Part 1.282 In late PVE. suggesting that long-term mortality is related to the underlying conditions rather than IE itself.272.272 Follow-up Patients should be educated about the signs and symptoms of IE after discharge.14 in 26% of cases inthe Euro Heart Survey.79 and in 20% of 2670 patients with definite IE in the ICE Prospective Cohort Study.

Radical debridement in these cases means removal of all foreign material.288.295 However.106.294. Alternatively. Although surgical treatment is frequently necessary in PVE. An exception is S. or autografts may be Downloaded from eurheartj.e. HF. it was performed in only 50% of patients with PVE in the Euro Heart Survey. The need for surgery should be considered in all cases of early PVE. and these patients need aggressive management.263. most cases referred for surgery represent uncontrolled PVE and are treated accordingly. aureus PVE. prognostic assessment is of crucial importance in PVE. stentless xenografts. patients with uncomplicated nonstaphylococcal and non-fungal late PVE can be managed conservatively. PVE complicated by HF. Several factors have been associated with poor prognosis in PVE.oxfordjournals. Antimicrobial therapy for PVE is similar to that for NVE.291 Conversely. which requires a more prolonged antibiotic regimen (particularly aminoglycosides) and frequent use of rifampin (see Section H). b a . or persistent fever. complicated PVE and staphylococcal infection are the most powerful markers. with a sensitivity of 70 –80%. elective surgery: after at least 1 or 2 weeks of antibiotic therapy.279. and intracardiac abscess. because of their lower sensitivity in this setting.283. abscess. a valved Dacron conduit278 can be used.ESC Guidelines 2399 considered in aortic PVE. and any calcium remaining from previous surgery. Similarly.285 but are less useful in PVE. early PVE. The Duke criteria have been shown to be helpful for the diagnosis of NVE. 2010 Table 23 Indications and timing of surgery in prosthetic valve infective endocarditis (PVE) Class of recommendation.283 Although no evidence-based data exist.287 Prognosis and treatment A very high in-hospital mortality rate of 20 –40% has been reported in PVE. Surgery for PVE follows the general principles outlined for NVE. including the original prosthesis. and homograft or xenograft root replacement is indicated for any abnormality of the aortic root that distorts the aortic sinuses.280 As in NVE. stroke. the best therapeutic option is still debated. patients who are initially treated medically require close follow-up. severe prosthetic dysfunction. because of the risk of late events.286. staphylococcal infection. urgent surgery: within a few days.283.79 similar to patients with NVE. Among these. Level of evidence.288 – 290 including age. since most are caused by staphylococci or other aggressive organisms. early surgery is frequently needed in early staphylococcal PVE134. Homografts. since it allows identification of high-risk subgroups of patients in whom an aggressive strategy may be necessary. *Emergency surgery is surgery performed within 24 h. a surgical strategy is recommended for PVE in high-risk subgroups identified by prognostic assessment.134.290 or PVE caused by fungi or other highly resistant organisms.13.92.291 – 295 Although surgery is generally considered the best option when PVE causes severe prosthetic dysfunction or HF. i. Similar data have been reported by others. By by guest on August 31. Table 23 summarizes the main indications and proposed timing of surgery in PVE.

wound by guest on August 31. Attempts to treat these patients with antibiotic alone have been proposed in the case of negative TEE.314 when percutaneous extraction is technically impossible.302. non-staphylococcal late PVE can be managed conservatively with close follow-up. The reported incidence of PPM infection varies widely among studies.303 Then.9 per 1000 device-years and a higher probability of infection after ICD as compared with PPM. use of temporary pacing before Treatment (Table 24) In the majority of patients. fluctuance.305 Some authors recommend surgery to be performed in patients with very large vegetations. and a normal echographic examination does not rule out CDRIE. particularly in elderly patients.296.305 as well as local signs of infection. Fever is frequently blunted. Patients with non-complicated. Antibiotic prophylaxis is protective in this indication. it is recommended to perform both in suspected CDRIE.297 A recent populationbased study found an incidence of CD infection of 1. warmth. Duration of therapy should be 4–6 weeks in most cases. but also on the mural endocardium of the right atrium and right ventricle. staphylococcal PVE. When performed. Infective endocarditis on pacemakers and implantable defibrillators Infection of cardiac devices (CDs). medical therapy alone has been associated with high mortality and risk of recurrence. PVE represents 20% of all cases of IE with increasing incidence. Complicated PVE. with predominant respiratory or rheumatological symptoms. in the case of definite CDRIE. Several factors have been associated with CD infections.302. LDI is defined as an infection limited to the pocket of the CD and is clinically suspected in the presence of local signs of inflammation at the generator pocket. CDRIE must be treated by prolonged antibiotic therapy associated with device removal. and early reimplantation. which can be found anywhere from the subclavian vein to the superior vena cava. tenderness. echocardiography and blood cultures are the cornerstone of diagnosis. Echocardiography plays a key role in CDRIE and is helpful for the diagnosis of both lead vegetation and tricuspid involvement. these episodes are frequently asymptomatic.305 – 308 and is cost-effective. Other possible mechanisms of CDRIE include haematogenous seeding from a distant focus of infection. CD removal is recommended in all cases of proven CDRIE and should also be considered when CRDIE is only suspected.304 Diagnosis CDRIE is one of the most difficult forms of IE to diagnose. Pulmonary embolism as a result of vegetation displacement during extraction occurs frequently.296. and early PVE are associated with worse prognosis.305 to include local signs of infection and pulmonary embolism as major criteria.310 Antimicrobial therapy for PPM infections should be individualized and based on culture and susceptibility results if possible. or endocardial surface.296. Downloaded from eurheartj. including permanent pacemakers (PPMs) and implantable cardioverter defibrillators (ICDs). and must be managed aggressively. on the tricuspid valve. cardiac valve leaflets.301 culture of intravascular lead segments was positive in 72% of 50 patients with manifestations strictly limited to the implantation site.305 The Duke criteria are difficult to apply in these patients because of lower sensitivity.302 It has recently been proposed that positive lead cultures can be used as a sign of CDRIE only in the absence of pocket infection or when the leads were removed using a remote incision from the pocket or surgical extraction. Preliminary experience with intracardiac echocardiography has recently been reported. and follow-up after lead extraction. Part 2.302. including fever within 24 h before implantation. A distinction should be made between local device infection (LDI) and cardiac device-related IE (CDRIE).298 Overall incidence lies between that of NVE in the general population and that of PVE.302. Clinical presentation is frequently misleading. 2010 Definition and pathophysiology of cardiac device infections. aureus being predominant in the acute forms of PPM infection.309 Blood cultures are positive in 77% of cases of CDRIE.305 Finally.3 on the electrode lead. the infection can spread along the electrode to the endocardium and the electrode tip. or when severe tricuspid valve IE is associated. or purulent drainage.299 Both diagnosis and therapeutic strategy are particularly difficult in these patients. ESC Guidelines implantation. CDRIE must be suspected in the presence of unexplained fever in a patient with a CD. However.313 However. is a severe disease associated with high mortality. Diagnosis is more difficult than in NVE. As in other forms of IE. erosion.oxfordjournals. percutaneous extraction may be more difficult when the CD has been implanted for several years. in the case of occult infection without any other apparent source than the device. lung CT and lung scintigraphy are both useful to detect pulmonary septic embolism.302 For this reason.302 Staphylococci are the most frequent pathogens. Although TEE has superior sensitivity and specificity to TTE. including erythema. sizing of vegetations. and percutaneous extraction remains the recommended method even in cases of large vegetations.296 The rising number of patients with an implanted CD explains the increasing frequency of IE in these patients. However. Modifications of Duke criteria have been proposed.300 CDRIE is defined as an infection extending to the electrode leads. Septic pulmonary embolism is a very frequent complication of CDRIE.313 since overall risks are even higher with surgical extraction. In one study.305. surgery requires good exposure under . S. if treated without surgery.311 However. the possibility of intra-operative contamination of the lead tip cannot be excluded in these patients. both TTE and TEE may be falsely negative in CDRIE.302 The main mechanism of CDRIE is contamination by local bacteriological flora at the time of device implantation.2400 In summary. differentiating LDI and CDRIE is frequently difficult.297. particularly when vegetations are large.297 The consequence may be formation of vegetations. quantification of tricuspid regurgitation. However. However.312 CD extraction can be performed percutaneously without need for surgical intervention in the majority of patients.

particularly those with advanced immunosuppression.316 In patients with NVE or PVE and an apparently non-infected PPM. In other by guest on August 31. antibiotic prophylaxis is usually recommended before implantation. device extraction may be considered. CDRIE must be treated by prolonged antibiotic therapy and device removal.300.304 If reimplantation is performed. a new transvenous system is usually implanted on the contralateral side. and must be suspected in the presence of frequently misleading symptoms. Level of evidence.317 Although there are no large controlled studies on this topic. not least because of its frequent occurrence in elderly patients with associated co-morbidity. 2010 a b Class of recommendation.321 This disease occurs more frequently in IVDAs who are HIV seropositive.320.ESC Guidelines 2401 Table 24 Cardiac device-related infective endocarditis (CDRIE): treatment and prevention Downloaded from eurheartj. Excision of all infected contact lesions at the level of the tricuspid valve. and distal superior vena cava is essential. or CHD. reimplantation can be postponed for a few days or weeks. reassessment may lead to the conclusion that reimplantation is unnecessary in a number of patients. extracorporeal circulation to allow complete removal of all foreign material.14.323 Whilst the tricuspid valve is the usual site of infection in IVDAs.318 In summary. The exact incidence of IE in IVDAs is unknown. However. In the majority of patients. right atrium. Temporary pacing is not recommended because it has been shown to be a risk factor for subsequent CD infection. pulmonary and eustachian valve infection may also be observed. and left-sided IE is not . contaminated drug solutions.310. and this decision must be adapted to the individual patient. Finally. Right-sided infective endocarditis Epidemiology Right-sided IE accounts for 5 –10% of cases of IE. with reduced infectious risk.322 Damage to the right-sided valves from injected particulate matter associated with poor injection hygiene. Immediate reimplantation should be avoided owing to the risk of new infection. There is no clear recommendation concerning the optimal timing and site of reimplantation.319. and abnormalities of immune function are some of the pathophysiological hypotheses underlying right-sided IE in IVDAs. particularly in elderly patients. central venous catheter.320 Although it may occur in patients with a PPM. CDRIE is one of the most difficult forms of IE to diagnose. epicardial implantation is a possible alternative. this situation is most frequently observed in IVDAs. Part 3.306. ICD. Prognosis is poor. If immediate reimplantation is necessary. mortality associated with surgical removal is high315 in these frequently elderly patients with associated co-morbidities. but some recent data show an increasing number of hospitalizations for intravenous drug abuse-related IE. right ventricular free wall.

349 (e) associated left-sided IE.327 and Pseudomonas aeruginosa.340. Right-sided S.10%. an antipseudomonas agent should be added. aureus and 3 Good response to treatment and .343. antibiotic treatment should include cover against streptococci and enterococci. S.338 If an IVDA uses brown heroin dissolved in lemon juice.334 Once the causative organisms have been isolated. Although the full implications of HIV infection for the medical and surgical therapy of IE in IVDAS are not yet fully known.333 – 335 Vegetation length . the choice of initial empiric antimicrobial therapy depends on the suspected microorganism.344. and multiple septic pulmonary emboli.343. Candida spp.350 For organisms other than MSSA. vegetations .334 In right-sided NVE. streptococci.352. e. and increased drug clearance in IVDAs. aureus. but should be considered in the following situations (Table 25): (a) right HF secondary to severe tricuspid regurgitation with poor response to diuretic therapy.) provided that the strain is fully susceptible to both drugs and patient adherence is monitored carefully.g. Cardiac surgery in HIV-infected IVDAS with IE does not worsen the prognosis of either the IE or the HIV.200 cells/mL has a high prognostic value.356 and (3) if valve replacement is Downloaded from eurheartj.200 CD4 cells/mm3) with or without AIDS.335 In HIV-infected patients.339 More conventionally. therapy has to be adjusted.335. Treatment will include either penicillinase-resistant penicillins or vancomycin.20 mm which persist after recurrent pulmonary emboli with or without concomitant right HF. albicans) should be considered and antifungal treatment added. persistent fungi). paradoxical embolism or associated left-sided IE should be by guest on August 31.345 Indications for surgery and the peri-operative approach in IVDAS are the same as for non-addicts but should be more conservative overall since IVDAS have a much higher incidence of recurrent IE.329 – 331 However.d. and associated left-sided involvement.353 usually due to continued drug abuse.352 (c) Tricuspid valve vegetations . or extracardiac complications. TEE is more sensitive in the detection of pulmonary vegetations332 and abscesses (particularly those adjacent to the membranous septum).333. the type of drug and solvent used by the addict. Surgery Surgical treatment should generally be avoided in right-sided native IE. and polymicrobial infections also occur less frequently. aeruginosa) despite adequate antimicrobial therapy. enterococci. S. acute respiratory failure.324 – 326 Staphylococcus aureus is the dominant organism (60– 90%).20 mm and fungal aetiology were the main predictors of death in a recent large retrospective cohort of right-sided IE in IVDAs.) plus rifampicin (300 mg b. Antimicrobial therapy On admission. acute renal failure.i. P. fungi. depending on the local prevalence of MRSA.320.354.200 cells/mL) with or without AIDS.341 Two-week treatment with oxacillin (or cloxacillin) with or without gentamicin is possible if all the following criteria are fulfilled: 3 Methicillin-susceptible S. poor penetration into vegetations. or haemoptysis.355 Current strategies for surgery of tricuspid valve IE should be based on the following three principles: (1) debridement of the infected area or ‘vegetectomy’. TTE usually allows assessment of tricuspid involvement because of the anterior location of this valve and usual large vegetations. glycopeptides should not be used in a 2-week treatment. with an in-hospital mortality rate . a 2-week course of antimicrobial therapy is unsuitable. aureus IE in IVDAs may also be successfully treated with oral ciprofloxacin (750 mg b. septic metastatic foci outside the lungs (including empyema).336. 2010 Prognosis and treatment Prognosis of right-sided NVE is relatively good. but can be caused by the increase of pulmonary pressures or severe right-sided valvular regurgitation or obstruction. bacteraemia.345 (c) therapy with antibiotics other than penicillinase-resistant penicillins. aureus must always be covered. abscess.96 h) to antibiotic therapy.d.322 1.347 (d) IVDA with severe immunosuppression (CD4 count . with clear data demonstrating that penicillinase-resistant penicillin regimens are superior to glycopeptide-containing regimens.348. Pulmonary septic emboli may be complicated by pulmonary infarction. The standard 4–6 week regimen must be used in the following situations: (a) slow clinical or microbiological response (.2402 unusual in this group. the standard therapy for IE due to MSSA is appropriate.20 mm. ESC Guidelines Diagnosis and complications The usual manifestations of right-sided IE are persistent fever. When systemic emboli occur.344. which may manifest with chest pain. Because of limited bactericidal activity.327. and purulent pulmonary effusion. and the location of cardiac involvement.344 (b) right-sided IE complicated by right HF. particularly in IVDAs or venous catheter-related infection. a CD4 count of . therapy in IVDAs does not differ from that in non-addicts.342. (not C. in IVDAs with underlying valve lesions and/or left-sided involvement. avoiding artificial material. In IVDAs. cough.337 If the patient is a pentazocine addict. 20 mm vegetation and 3 Absence of severe immunosuppression (.333. (b) IE caused by organisms which are difficult to eradicate (e.341 There are also consistent data showing that a 2-week treatment may be sufficient341 – 343 and that the addition of an aminoglycoside may be unnecessary. 3 Absence of metastatic sites of infection or empyema and 3 Absence of cardiac and extracardiac complications and 3 Absence of associated prosthetic valve or left-sided valve infection and 3 .g. (2) valve repair whenever possible.328 Right HF is rare. other Gramnegative organisms.i.346.g.351 2. pneumothorax. or bacteraemia for at least 7 days (e.

However. particularly in the adult group. Infective endocarditis in congenital heart disease The population of children and adults with CHD is expanding. there is also an educational by guest on August 31. However.368 The importance of good oral.363 – 365 with a consistent minor male dominance.g. In summary. if unavailable. However. TTE is of major value in these patients. use of a pulmonary homograft (or. after multiple pulmonary emboli.362. in other cases when artificial valve substitutes are implanted. provided there is no residual lesion. and antibiotic prophylaxis is indicated in high-risk groups as defined in Section E. and selection bias associated with studies from highly specialized centres hampers universal application. Prognosis is better than in other forms of IE. but may be associated with severe post-operative right HF. between 2 and 18%.370 However.ESC Guidelines 2403 Table 25 Indications for surgical treatment of right-sided infective endocarditis a b Class of recommendation.358 Cryopreserved mitral homografts have been used for management of persistent tricuspid endocarditis. CHD often consists of multiple cardiac lesions. a xenograft valve) is preferred. There are no scientific data justifying cardiac surgery or percutaneous interventions (e.371 Cardiac repair as a secondary preventive measure to reduce the risk of recurrent IE has been described but not systematically studied. Primary prevention is vital. but the valve should be subsequently replaced once cure of infection has been achieved. thus favouring the addition of TEE. streptococci and staphylococci being the most common strains. excision of the tricuspid valve with prosthetic valve replacement. The superiority of TEE over TTE has not been systematically studied in this setting. For example. Complex anatomy makes echocardiographic assessment difficult.366 This better prognosis in comparison with acquired heart disease may reflect the higher proportion of right heart IE. closure of a patent ductus arteriosus) with the sole purpose of eliminating the risk of IE.367 The distribution of causative organisms does not differ from the pattern found in acquired heart disease. and awareness of the risk of IE and need for preventive measures are not satisfactorily spread in the population with CHD.362 However. It may be performed in extreme cases. particularly in patients with elevated pulmonary arterial pressure. In summary. at least involving the tongue and mucous membranes. Despite relatively low in-hospital mortality.360 Pulmonary valve replacement is best avoided—if judged necessary.g. Diagnostic features include respiratory symptoms and fever.359. However. right-sided IE has a high risk of recurrence in IVDAs and a conservative approach to surgery is recommended in this group.58. 2010 . the incidence of IE is considerably higher in patients with a ventricular septal defect when there is associated aortic regurgitation.362 The reported proportion of CHD in patients with IE varies. each contributing to the total risk of IE. our knowledge of IE in this setting is limited since systematic studies are few and often retrospective.366 Some simple lesions. right-sided IE is most frequently observed in IVDAs and CHD.362. complex anatomy and the presence of artificial material may reduce the rate of detection of vegetations and other features of IE. and skin hygiene has already been emphasized. complications.364. and when there is a high risk of devastating septic embolism.58. Cardiac surgery is appropriate when medical therapy fails. right-sided IE is more frequent in CHD than in acquired cardiac disease. Part 4.357 Valvectomy without prosthetic replacement has been advocated. Surgical repair of CHD often reduces the risk of IE. probably due to selection bias.62. the procedure may increase the overall risk of IE. Downloaded from eurheartj. Preventive measures and patient education are of particular importance in this population. with a mortality rate <10%.366 The principal symptoms.369 Cosmetic piercing. Treatment of IE in CHD follows general principles.58. a negative study does not exclude the diagnosis. IE in CHD carries a mortality of 4–10%. unavoidable. However. and this is the major substrate for IE in younger patients. carry a low risk of IE. such as secundum atrial septal defect and pulmonary valve disease. dental. when serious haemodynamic complications arise. and basis for diagnosis do not differ from IE in general.361. Level of evidence. IE in CHD is rare and more frequently affects the right heart.oxfordjournals. should be discouraged in this group. The reported incidence of IE in CHD is 15 –140 times higher than that in the general population (the highest estimate originating from a highly specialized unit). e.

91:715 –718. von Graevenitz A. Delahaye F. Endocarditis. and the Council on Clinical Cardiology. Smiseth OA. Takahashi M. Perry JD. Roberts GJ. 10. Lengyel M. Lode H. Horstkotte D.69 Finally. Block M. ¨ ¨ Handrick W.378 However. Fernandez Burgos E. in which colonic lesions are frequent and may cause occult bleeding. the vegetations in the elderly have been reported to be smaller375 and to carry a lower embolic risk. Oto A. 9. Goff D. IE in pregnancy is extremely rare. which is an institution of the European Union of Medical Specialists (UEMS). Wilson WR. Steckelberg JM.166. Kern P.382 Therefore.189:301 –302. Levison ME. Takahashi M. Niebel J. Kramer HH. Moulds RF. ¨ . Becker HJ. Morais J. Schmaltz AA. 8. Gardner T.70 years) is increasingly frequent and associated with specific features. Rowley AH. Maternal mortality approaches 33%. Shulman ST. Burns JC.escardio.372 Negative blood cultures were recently observed in 16. Naber CK.372.25:267 –276. Lekakis J. Taubert KA. the task force on infective endocarditis of the European society of cardiology. 2010 The CME Text ‘Guidelines on the prevention. bovis) are an increasingly frequent cause of IE. Erbel R. Bolger AF. all authors participating in this programme have disclosed potential conflicts of interest that might cause a bias in the article. and the Quality of Care and Outcomes Research Interdisciplinary Working Group. Bayer AS. Garcia MA. Ferrieri P. Carabello BA. O’Rourke RA. Al-Nawas B. Fluckiger U.80 In the French surveys. Council on Cardiovascular Disease in the Young. Horstkotte D. Bolger A. M. 3. Seifert H. Lockhart PB. Gewitz MH.50 years old and peaked at 145 cases per million between 70 and 80 years of age. Bonow RO. Shah PM. Shulman ST. Guidelines for the prevention of endocarditis: report of the Working Party of the British Society for Antimicrobial Chemotherapy. Endocarditis. Rapid detection of IE and appropriate treatment is important in reducing the risk of both maternal and foetal mortality. Watkin RW. Int J Antimicrob Agents 2007.7% of elderly patients with IE. Erbel R. ACC/AHA 2008 Guideline Update on Valvular Heart Disease: Focused Update on Infective Endocarditis. Ertl G. Baddour LM.208. Pavie A. Cowie M. O’Gara PT. Baltimore RS. CME questions for this article are available at: European Heart Journal http://cme. Freed MD. Cabell CH.379 Part 6. Duval X. Antibiotic prophylaxis against infective endocarditis: time to rethink. Falace DA. Aldershvile J. Dean V. Levison M. Lancet 2004. Baddour LM. Elliott TS. Follath F.ehj and European Society of Cardiology http://www. and Cardiovascular Surgery and Anesthesia. Heying R. Que YA. antimicrobial therapy. Fowler VG Jr. Infective endocarditis: diagnosis. 57:1035 – Moreillon P. diagnosis.006%. Tani LY. Graninger R. Rosenhek R. Gerber MA. multiple valve involvement. Lindahl B. the incidence of IE increased between 1991 and 1999 among patients . Jeyasingham MS. Gould Filipatos G. and high embolic risk. diagnosis and treatment of infective endocarditis executive summary.381 The incidence of IE during pregnancy has been reported to be 0. ¨ Mugge A. Moreillon P. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever. Guidelines on prevention. Mehlhorn U. Kuhl S. Leport C. and to a higher incidence of more aggressive pathogens in this cohort.166.166. while foetal mortality is 29%. and Kawasaki Disease Committee. Circulation 2008. Council on Cardiovascular Disease in the Young. Jaussi A. Mazzotta G. Strom BL. Durack DT. Habib G.111:e394 –e434. and Kawasaki Disease. Gattringer R. 11.374. Lepper PM. Tong DC. Circulation 2007. Infective endocarditis during pregnancy A challenge for the physician during pregnancy in the cardiac patient is the changing cardiovascular physiology which can mimic cardiac disease and confuse the clinical picture. with the same indications as for younger patients. Heart 2005.372. Leyh RG. American Heart Association: endorsed by the Infectious Diseases Society of America. Gohlke-Barwolf C.374. Infective endocarditis in the elderly IE in the elderly (. Newburger JW. Baltimore RS. Working Party of the British Society for Antimicrobial C. Burns JC.208 Enterococcal IE has also been shown to be more frequent in older patients. 5. older age has been associated with poor prognosis in the majority of recent studies.374.2404 ESC Guidelines Part 5. Parkhomenko A. and the Councils on Clinical Cardiology. Pallasch T. Naber CK. Gewitz M. and treatment of infective endocarditis (new version 2009)’ is accredited by the European Board for Accreditation in Cardiology (EBAC).372 The relative incidence of IE affecting the elderly was 26% in the Euro Heart Survey. Newburger JW. most deaths relating to HF or an embolic event. Blanc JJ. Baumgartner B. Budaj A. Gerber M. Sandoe JA. Danchin N. Wilson W.376 and have been associated with colonic disease.375 A gastrointestinal source of infection has been described more commonly in elderly patients. Fulford M. Nishimura RA. Foweraker J. Infective endocarditis. Prophylaxis of infective endocarditis: French recommendations 2002.382 Close attention should be paid to any pregnant woman with unexplained fever and a cardiac murmur. Stroke. Med J Aust 2008.208 In some studies. Gutschik E. and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever.oxfordjournals. Baddour LM. Faxon DP. Thiene G. Herrmann M. Taubert KA. Peters G. Horstkotte D.118:887 –896. though not consistently. Franzen D. probably in relation to a higher operative risk related to advanced age and frequent co-morbidity. Oto A. Soler-Soler J. Heart 2006.363:139 –149. References by guest on August 31. In compliance with EBAC/EACCME guidelines. The Organizing Committee is responsible for ensuring that all potential conflicts of interest relevant to the programme are declared to the participants prior to the CME activities. A Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Priori SG. EBAC works according to the quality standards of the European Accreditation Council for Continuing Medical Education (EACCME). Lytle BW. and is either a complication of a pre-existing cardiac lesion or the result of intravenous drug abuse. Pallasch TJ. 4.14 Previous reports have shown. Tani LY. New guidelines for infective endocarditis: a call for collaborative research. Mutters R. 7. 6. Lekakis J. Circulation 2005.382 Downloaded from eurheartj. Vardas P. especially in the elderly.375 This more severe clinical course has been related to insidious initial symptoms and delayed diagnosis in elderly people. Vahanian A.116:1736 –1754. bovis IE.373 and 33% of patients were older than 67 years in a French registry. Management of infective endocarditis. Deckers J.377 Fever is less frequent374 and anaemia more common in elderly patients. 2. Council on Cardiovascular Surgery and Anesthesia.29: 615 –616.92:124 –130. Eur Heart J 2004. Group D streptococci (S. surgical treatment appears as a reasonable option in the elderly. probably related to the high proportion of S.oxfordjournals.380.375 Fewer elderly patients are treated by surgery. Ferrieri P. J Antimicrob Chemother 2006. that IE in advanced age is associated with poor prognosis and with a high complication rate.

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