1. 1
    Current Diagnosis

    • Infective endocarditis should be considered as a diagnosis in the setting of fever and heart murmur.

    • Health care–associated interventions and resulting infections are an increasingly noted cause of IE, changing the epidemiology of this disease.

    • Blood cultures show growth in approximately 90% of cases, and multiple sets should be obtained before initiating antibiotics to improve diagnostic yield.

    • Echocardiography, particularly transesophageal echocardiography, improves diagnostic sensitivity for infective endocarditis as well as its complications (e.g., intracardiac abscess, fistula).

    • The diagnosis of complications, including heart failure, embolic events, and abscess, requires close surveillance, particularly during the first week of therapy, and has adverse prognostic implications.

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  2. 2
    Current Therapy

    • Because of changes in the epidemiology of infective endocarditis (IE), empiric antibiotic therapy for Staphylococcus aureus should be considered before results of blood cultures are available.

    • Prompt initiation of antibiotic therapy is important, because the rate of complications such as embolization decreases rapidly within several days.

    • Multidisciplinary care for the patient with IE should include evaluation by specialists in infectious diseases, cardiology, and cardiothoracic surgery, especially in cases of complicated IE.

    • Surgery for IE has not been studied in randomized, controlled trials compared to medical therapy alone. Surgery should be considered for IE complicated by heart failure, embolism, intracardiac abscess, or persistent bacteremia.

    • Although stroke due to embolism is not uncommon in IE, data do not suggest a benefit in delaying cardiac surgery after cerebral infarction if surgery is otherwise indicated.

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  3. 3

    Infective endocarditis (IE) is a microbial infection of the valves or endocardium of the heart.

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  4. 4
    Epidemiology and Risk Factors

    The incidence of IE varies regionally from 2.6 per 100,000 population reported in France to 11.6 per 100,000 population in urban areas of the United States. This range of incidence has been attributed to differences in predisposing cardiac conditions or risk factors, such as use of injection drugs. The incidence of IE is also affected by age and sex. The incidence of native valve IE increases with age and exceeds 30 per 100,000 after 30 years of age. The average age of the patient with IE has increased over time, likely related to the decreased prevalence of rheumatic heart disease and increased prevalence of degenerative valvular disease in the aging population. IE is more commonly diagnosed in men, with studies showing male-to-female ratios as high as 9:1.

    In earlier eras, streptococcal species were the predominant cause of native valve IE. However, changes in the delivery of health care, with increasing exposure to invasive procedures and devices, and the changing demographics of patients and their risk factors for IE have led to major changes in the microbiologic causes of endocardits. There is an increasing incidence of health care–associated IE, including nosocomial infection and infection related to ambulatory care, which accounts for approximately 25% of IE cases. For example, in one large multinational study, the International Collaboration on Endocarditis (ICE) registry (N = 2781 patients with definite native or prosthetic endocarditis), 31% of cases were attributable to Staphylococcus aureus, 17% to viridans streptococci, 11% to enterococci, 10% to coagulase- negative staphylococci, 12% to other streptococcal species, 2% to the HACEK (Haemophilus spp., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, Kingella spp.) group, 2% to non-HACEK Gram-negative bacteria, and 2% to fungi. Among those with S. aureus endocarditis, health care–associated infection accounted for 39% of cases.

    Predisposing cardiac conditions to the development of IE include degenerative valve disease (in approximately 40% of cases of mitral and 25% of aortic valve IE), presence of prosthetic valve, injection drug use, and rheumatic heart disease.

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  5. 5

    A preexisting valvular or endocardial condition, such as mitral valve prolapse with regurgitation, degenerative aortic valve disease (including bicuspid aortic valve), or congenital heart disease, is a major host factor related to development of IE. Endothelial damage and denudation of the endothelium exposes the underlying basement membrane and fosters platelet and fibrin deposition, a process that occurs spontaneously in persons with valvular heart disease. These deposits are called nonbacterial thrombotic endocarditis and form the nidus for vegetation to begin in the setting of bacteremia. The classic lesion of IE, the vegetation, is made up of fibrin, platelets, inflammatory cells, and microorganisms adherent to the endothelium of the heart.

    The degree of mechanical stress exerted on the valve might contribute to endothelial denudation and the location of vegetation formation, with left-sided IE more common than right-sided IE. Endocarditis involving the nonvalvular endocardium of the heart similarly occurs at sites of endothelial damage due to mechanical stress, such as the left ventricular outflow tract in patients with hypertrophic obstructive cardiomyopathy and congenital heart defects (ventricular septal defects and patent ductus arteriosus).

    The adhesion of bacteria to the denuded endothelium might depend on specific properties of the bacteria. Cell surface characteristics of the organism promote its adherence. For example, the adherence of S. aureus to a traumatized animal heart valve has been found to be reduced in the setting of impaired fibronectin binding. Similarly, the ability of bacteria to form biofilm may be associated with their ability to form localized clusters of infections that can make these clusters more resistant to killing by the host immune system and antimicrobial therapy.

    With the progressive development of a vegetation, function of the specific heart valve is impaired. Regurgitation or insufficiency of the affected valve most commonly results, leading predominantly to volume overload of the ventricular chamber. In the setting of acute or rapid development of regurgitation, there may be no ventricular adaptation to this volume overload; as a result, acute, severe pulmonary edema and cardiogenic shock may quickly ensue. Less commonly, a large vegetation can result in stenosis of the valve orifice and pressure overload of the proximal or upstream cardiac chamber. As infection extends, destruction of other cardiac tissue, including myocardium and fibrous structures, can occur and result in intracardiac abscess or fistula formation between cardiac chambers.

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  6. 6

    The efficacy of antimicrobial prophylaxis in preventing IE continues to be debated. Current recommendations are generally based on the likelihood of bacteremia occurring as a result of the procedure, the potential for adverse outcome as related to the predisposing cardiac condition, and the level of evidence for antibiotic prophylaxis as effective for the prevention of IE. The American Heart Association has published updated guidelines for IE prophylaxis with a continued trend toward fewer indications for prophylaxis.

    Based on an extensive review of published literature and expert consensus, these guidelines have concluded that IE is more likely to result from bacteremia associated with daily activities than with a dental procedure. Antibiotic prophylaxis, even if 100% effective, is estimated to prevent only an extremely small number of cases of IE. These recommendations concluded that antibiotic prophylaxis should not be prescribed solely on the basis of an increased lifetime risk of IE but on the basis of cardiac conditions associated with highest risk of an adverse outcome from IE.

    Conditions that warrant IE prophylaxis before dental procedures and procedures on respiratory tract, skin, and musculoskeletal structures are listed in Box 1 and Table 1. The American Heart Association no longer recommends prophylaxis before gastrointestinal or genitourinary procedures solely for the prevention of IE.

    Box 1

    Prophylaxis Against Infective Endocarditis

    Procedures Warranting Prophylaxis

    Dental procedures that involve manipulating gingival tissue or the periapical region of teeth

    Dental procedures that involve perforating the oral mucosa

    Cardiac Conditions with High Risk of Adverse Outcome

    Prosthetic heart valve or prosthetic material used for valve repair Previous infective endocarditis

    Congenital heart disease including unrepaired cyanotic lesions, palliative shunts or conduits, previous repair with residual defect at site of prosthetic patch or device, and recent repair (<6 months) involving prosthetic device or material

    Cardiac transplant with valve regurgitation due to structurally abnormal valve

    Table 1

    Regimens for Dental Procedure

    Adapted from Bonow RO, Carabello BA, Kanu C, et al: ACC/AHA 2006 guidelines for the management of patients with valvular heart disease: A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to revise the 1998 Guidelines for the Management of Patients with Valvular Heart Disease): Developed in collaboration with the Society of Cardiovascular Anesthesiologists: Endorsed by the Society for Cardiovascular Angiography and Interventions and the Society of Thoracic Surgeons.  Circulation 2006;114(5):e84–e231.

    Note: The antibiotic agent is administered as single dose 30–60 minutes before the procedure.


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  7. 7
    Clinical Manifestations and Diagnosis

    The diagnosis of IE depends on findings of bacteremia with an organism associated with IE and evidence of endocardial involvement. Because these objective findings may not be sought unless the possibility of IE is considered, careful attention to the patient’s history and physical examination is critical to the eventual diagnosis. The clinical presentation of IE is highly variable and can range from chronic fatigue with low-grade fever to acute heart failure due to new, severe valvular regurgitation. Although the virulence of the organism can influence acuity of presentation, the onset of infection is generally followed by the onset of symptoms within 2 weeks of bacteremia. Four processes contribute to the clinical presentation of IE: infection on the valve, including the local intracardiac complications; septic or aseptic embolization to distant organs; continuous bacteremia, often with metastatic foci of infection; and circulating immune complexes and other immunopathologic factors.

    Approximately 85% of patients present with fever, although this finding might not be present in immunosuppressed states and in patients who have previously been on antibiotic therapy. Nonspecific signs and symptoms such as chills, sweats, anorexia, weight loss, malaise, dyspnea, and cough are common but generally occur in less than half of patients with IE. In addition, predisposing conditions or risk factors for the development of IE, including a history of structural heart disease, injection drug use, or recent invasive procedure, should be sought in the patient’s history.

    Evidence of a new or changing regurgitant murmur in the presence of fever of undetermined origin should prompt additional, timely evaluation for possible IE. Because of the lack of ventricular adaptation to acute volume overload and the resulting hemodynamic changes (tachycardia, hypotension), the murmur in acute aortic insufficiency may be poorly audible. Embolic phenomena, a common extracardiac complication of IE, can manifest with localizing symptoms such as focal neurologic deficit due to stroke or left upper abdominal pain due to splenic infarction. The patient should be carefully examined for any peripheral stigmata of IE such as petechiae, splinter hemorrhages, Janeway lesions, Osler nodes, and Roth spots. Many of these findings are immune-mediated yet infrequently present. Although Janeway lesions, Osler nodes, and Roth spots are more specific abnormalities for IE, they can occur in other conditions and their low incidence in cases of proven IE limits their diagnostic utility.

    Blood Cultures

    Blood cultures are the definitive microbiologic procedure for the diagnosis of IE. Continuous and low-grade bacteremia makes it unnecessary to await fever spikes or chills to obtain blood cultures, and the first two blood cultures yield an etiologic agent in 90% of cases. In patients who have not received antibiotics recently, it is recommended that at least three blood culture sets from separate venipunctures should be obtained over the first 24 hours, which will increase the yield to more than 95% in cases of untreated IE with continuous bacteremia. Each culture media bottle should be inoculated with at least 10 mL of blood to increase the number of colony-forming units per culture. The results of blood cultures should be interpreted based on the specific microorganisms identified as well as the recognized, constant nature of bacteremia in IE.

    Other laboratory data may provide clues to the diagnosis yet lack specificity for IE. Hematologic parameters are often abnormal. A normocytic, normochromic anemia (70%–90%), thrombocytopenia (5%–15%), and leukocytosis (30%) are common findings. The erythrocyte sedimentation rate (ESR) and C-reactive protein concentrations are usually elevated. Similarly, the C-reactive protein concentration is also elevated in IE but is a nonspecific finding.

    Rheumatoid factor assay is positive in up to half of the cases, especially if the illness is protracted. Urinalysis might demonstrate microscopic hematuria and mild proteinuria. Red blood cell casts and heavy proteinuria can be seen in patients with immune complex glomerulonephritis.


    Although the electrocardiogram (ECG) lacks sufficient sensitivity and specificity for the diagnosis of IE, ECG abnormalities commonly occur in patients with IE and are associated with invasive infection and increased in-hospital mortality. The presence of atrioventricular heart block in a patient with IE is diagnostic of the presence of a ring abscess, typically of the aortic valve, with invasion posteriorly toward the atrioventricular conduction system. One single-center study found that 53% of patients with invasive infection had ECG changes and about a third of the patients with ECG conduction abnormalities died during hospitalization in their cohort of 137 patients with definite IE.

    Echocardiography and Diagnostic Criteria

    The diagnosis of IE is based upon clinical suspicion derived from signs and symptoms and, most importantly, the demonstration of associated bacteremia. Given the nonspecific nature of findings from history, physical examination, and even blood cultures, the inclusion of echocardiographic findings has improved the sensitivity of diagnostic criteria for this condition (see modified Duke criteria, Box 2).

    Box 2
    The Modified Duke Criteria and Case Definitions of Infective Endocarditis
    Modified Duke
    Criteria Major Criteria

    Positive blood cultures

    •   Typical microbes consistent with IE from two separate blood cultures: viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; community-acquired enterococci in absence of another focus


    • Microrganisms consistent with IE from persistently positive blood cultures defined as follows: at least 2 blood cultures drawn more than 12 hours apart or all of three or a majority of more than four separate blood cultures

    • Single positive blood culture for Coxiella burnetti or antiphase IgG antibody titer >1:800

    Evidence of endocardial involvement

    Echo findings of IE, defined as:

    •   Oscillating intracardiac mass on valve or supporting structure

    •   Abscess

    •   New partial dehiscence of prosthetic valve

    •   New valvular regurgitation

    Minor Criteria

    Predisposition: predisposing heart condition or injection drug use Fever, temperature >38°C

    Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhage, and Janeway lesions

    Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor

    Microbiologic evidence: positive blood cultures but does not meet a major criterion as noted above, or serologic evidence of active infection with organism consistent with causing IE

    Case Definitions

    Definite Infective Endocarditis

    Presence of any pathologic criteria:

    • Microorganisms demonstrated by culture or histologic examination of a vegetation, a vegetation that has embolized, or an intracardiac abscess specimen


    • Pathologic lesions; vegetation or intracardiac abscess confirmed by histologic examination showing active endocarditis

    If there are no pathologic criteria, then clinical diagnosis of definite IE:

    •   Two major criteria


    •   One major and three minor criteria


    •   Five minor criteria

    Possible Infective Endocarditis

    One major criterion and one minor criterion


    Three minor criteria


    Firm alternative diagnosis explaining evidence of IE


    Resolution of IE syndrome with antibiotic therapy for ≤4 days


    No pathologic evidence of IE at surgery or autopsy, with antibiotic therapy for <4 days


    Does not meet criteria for possible IE, as above.

    Adapted from Li JS, Sexton DJ, Nettles R, et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2003;30(4):633–638. Abbreviations: HACEK = Haemophilus spp., Aggregatibacter spp., Cardiobacterium hominis, Eikenella corrodens, Kingella spp.; IE = infective endocarditis; Ig =  immunoglobulin.

    ECG findings provide specific evidence of IE that include vegetations, evidence of periannular tissue destruction (abscess), aneurysm, fistula, leaflet perforation, and valvular dehiscence. Box 3 outlines specific definitions of these characteristic findings.

    Box 3
    Echocardiographic Findings in Infective Endocarditis

    Irregularly shaped, discrete echogenic mass

    Adherent to but distinct from endocardial surface or intracardiac device

    Oscillation of mass (supportive, not mandatory)


    Thickened area or mass within the myocardium or valve annulus Evidence of flow into region (supportive, not mandatory)


    Echolucent space with thin surrounding tissue


    Blood flow between two distinct cardiac blood spaces or chambers through an abnormal path or channel

    Leaflet perforation

    Defect in body of valve leaflet with flow through defect

    Valve dehiscence

    Prosthetic valve with abnormal rocking motion/excursion >15 degrees in at least one direction

    Adapted from Sachdev M, Peterson GE, Jollis JG: Imaging techniques for diagnosis of infective endocarditis. Cardiol Clin  2003;21:185–195.

    The diagnostic utility of transthoracic echocardiogram (TTE) for suspected IE is highest in patients with intermediate to high likelihood of this disease (e.g., a patient with a new or changed heart murmur and bacteremia). Hence, TTE should be performed in all patients with suspected IE. However, the diagnostic sensitivity of TTE for the visualization of an intracardiac vegetation or abscess is limited, ranging from 40% to 80%, and thus the diagnosis of IE cannot be ruled out on the basis of a negative study. The absence of five clinical criteria has been associated with zero probability of a TTE showing evidence of IE: positive blood cultures, presence of central venous access, recent history of injection drug use, presence of prosthetic valve, and vasculitic or embolic phenomena.

    Transesophageal echocardiography (TEE) has greater spatial resolution compared to TTE and so is more sensitive than TTE for detecting intracardiac vegetations (sensitivity, 87%; specificity, 95%). As a result, TEE should be performed in patients with a high likelihood of IE and a negative TTE. Although TTE and TEE have been found to have concordant results in approximately half of patients with suspected IE, TEE provides additional diagnostic information in a high percentage of patients, particularly those with prosthetic valves. Specific subsets of patients in whom TEE should be performed, even as the primary imaging modality (without TTE), include patients with prosthetic heart valves and suspected IE and patients with persistent staphylococcal bacteremia without known source or nosocomial infection. In addition, TEE should be performed in patients with IE when paravalvular abscess is suspected.

    Other Cardiac Imaging Modalities

    Cardiac magnetic resonance imaging with contrast appears promising for detecting paravalvular abscesses, thrombus associated with vegetations, valvular complications, and aortocameral fistulas, although temporal resolution might limit its use for detecting vegetation. Cardiac computed tomography has also been used to detect aortic root abscess. However, clinical experience with these techniques in IE patients is limited and their sensitivities and specificities in comparison to echocardiography are not well defined. Positron emission tomography-computed tomography (PET-CT) scans have been used to evaluate prosthetic devices, including cardiac implanted electronic devices, for inflammation localized to these devices, and may help differentiate post-surgical changes from active infection.

    Routine coronary angiography is recommended in patients older than 55 years and in those at high risk for coronary artery disease before surgery for IE.

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  8. 8
    Differential Diagnosis

    Given the protean manifestations of IE, the differential diagnosis includes a number of systemic conditions: systemic lupus erythematosus, acute rheumatic fever, atrial myxoma, vasculitis, and renal cell carcinoma.


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  9. 9
    Treatment, Complications, and Outcome

    Multidisciplinary care of the patient with IE, involving cardiologists, infectious disease specialists, and cardiac surgeons, improves the outcome of IE by optimizing appropriate antibiotic treatment and assessment for surgical indications and operative risk. Antibiotic therapy has improved survival in IE by 70% to 80% and has been shown to reduce the incidence of complications of IE. Detailed descriptions of antibiotic regimens for specific causative organisms are found in guidelines by the American Heart Association (updated in 2015) and the European Society of Cardiology (also updated in 2015). Recommended antimicrobial regimens against typical organisms causing IE are outlined in Table 2. Although the choice of antimicrobial therapy is mainly guided by the infecting organism and its antibiotic susceptibilities, there are three basic principles of antibiotic treatment for the eradication of native valve infection.

    Table 2

    Antimicrobial Regimens against Typical Infective Endocarditis Organisms

    Abbreviation: max = maximum.

    1  Not FDA approved for this indication.

    First, a prolonged course of antibiotic treatment (4 to 6 weeks) is necessary to eradicate infection because bacterial concentration within vegetations is high and organisms deep within vegetations are inaccessible to phagocytic cells. Repeat sets of blood cultures after antibiotic initiation should be obtained every 24 to 48 hours until the resolution of bacteremia is confirmed. If surgery for IE is performed, completion of the 4- to 6-week course of antibiotic therapy is generally favored to reduce the risk of recurrent IE.

    Second, parenteral administration of antibiotic therapy is necessary to achieve adequate drug levels required to eradicate infection.

    Parenteral therapy is typically initiated in the hospital setting, and the patient may receive outpatient parenteral treatment for the remaining duration after an initial period of observation to assess for clinical response to therapy (e.g., clearance of bacteremia and absence of complications).

    Third, because of the need for prolonged therapy and rising antimicrobial resistance among organisms, combination therapy typically involving a β-lactam and aminoglycoside antibiotic is recommended. Combination therapy has been shown to reduce the duration of bacteremia in S. aureus endocarditis, although this more- rapid resolution of bacteremia was not associated with an improved clinical response or outcome. Both antibiotics should be given temporally close together so that maximum synergistic microcidal effect is obtained. In addition, the dosage and kidney function should be monitored carefully, because combination therapy has been associated with a higher rate of kidney dysfunction.

    IE can progress to the development of various intracardiac and extracardiac complications before or despite effective treatment. Heart failure or pulmonary edema is a common complication, occurring in about one third to one half of patients with IE, and it is the most common indication for urgent surgery. Valvular destruction and ensuing insufficiency can result in volume overload and heart failure; in rare cases of large vegetations, heart failure may be a result of valvular stenosis. Heart failure complicates aortic valve IE more often than mitral or tricuspid IE and can result in the setting of moderate, rather than severe, regurgitation, because the left ventricle is unable to compensate for the acute increase in preload and afterload in this condition.

    Medical therapy alone is generally insufficient in managing IE complicated by heart failure, particularly in the setting of severe or progressive valvular regurgitation. Surgery should be prompt, and unnecessary delays should be avoided.

    Para-valvular abscess complicates 30% to 40% cases of IE and is a result of invasive infection that spreads generally along contiguous tissue planes, particularly with aortic valve infection. In the International Collaboration on Endocarditis (ICE) cohort, 22% cases of definite aortic valve IE were complicated by a periannular abscess.

    These patients were more likely to have prosthetic valves and coagulase-negative staphylococcal infection. TEE is the diagnostic test of choice when an abscess is suspected clinically. An abscess is diagnosed by TEE as the visualization of a periannular area of thickening or mass with a heterogeneous echogenic or echolucent appearance. Rarely, antibiotic therapy alone may be used to treat an intracardiac abscess, though this treatment alone is generally reserved for patients who are poor surgical candidates. The vast majority of patients with an intracardiac abscess require cardiac surgery for débridement. In addition, surgery represents the gold standard for the diagnosis of abscess.

    Embolic phenomena often complicate the clinical course in IE. Although clinical signs of embolization occur in approximately one third of patients with IE, at least another third of patients have silent embolism. In the majority of cases, embolic events occur before antibiotic therapy is initiated. The most frequent sites of embolic events were the central nervous system (approximately 40% of embolic events), lungs (approximately 20%), spleen (20%), peripheral artery (approximately 15%), and kidney (10%).

    Factors including vegetation size, mobility, and location as well as the causative organism have been associated with the likelihood of embolic event. Vegetations larger than 10 mm in greatest diameter are associated with an increased risk of embolization. Causative organisms such as S. aureus and Streptococcus bovis confer an independent risk of embolization. Embolism also occurs with greater frequency in IE caused by enterococci, fastidious gram-negative organisms (HACEK), and fungi as compared to streptococcal IE. In addition to causing infarction of distal vascular beds, embolic events can result in metastatic sites of infection.

    Cerebral embolization occurs in 10% to 35% of cases and is at times complicated by meningitis, brain abscess, or intracerebral hemorrhage. The risk of stroke dramatically decreases with initiation of antibiotic therapy. Findings from the ICE merged database suggested a 65% reduction in stroke incidence by week 2 of initiating antimicrobial therapy. Given the low incidence of embolic event after initiation of antibiotic therapy, routine screening for emboli in patients with IE is not recommended. However, patients with persistent fever or bacteremia or localizing symptoms of possible infarction should undergo computed tomographic imaging with radiographic contrast for the diagnosis of embolic complications.

    Embolic events have been found to be an independent predictor of in-hospital death in IE. In patients who experience recurrent embolic events, particularly if they occur after initiation of antibiotic therapy, surgical treatment is indicated. For the prevention of embolic events, surgery may be considered for patients with IE who have residual large (>10 mm), mobile vegetations involving mitral or aortic valve. A recent, small, randomized trial of early surgery for native, left-sided IE has found significant reduction in embolic events in patients treated with earlier surgery.

    Surgical intervention for IE may be performed either in the acute or active phase of infection or after the eradication of infection. The optimal timing of surgery in the setting of active IE has not been well evaluated. In patients with serious, life-threatening complications of IE, surgery should be performed emergently. A number of case series have shown that surgery in the active phase of IE can be performed with acceptable risk and without an obvious risk of infecting a prosthetic valve. Surgery during the active phase is generally considered for patients in whom the likelihood of cure of infection with antibiotic therapy alone is low or in whom severe complications have or will likely occur. In contemporary series, surgery is performed in 40% to 50% of patients with IE during the index hospitalization.

    Surgery after eradication of infection is predominantly performed for adverse hemodynamic effects of valvular regurgitation that results from valve damage.

    Indications for surgery in IE are shown in Box 4. A majority of patients with left-sided IE will have an indication for surgery, but may be poor candidates for surgery due to hemodynamic instability or other comorbid conditions. Heart failure is the most common indication for urgent surgical intervention, yet even without overt heart failure symptoms, hemodynamic evidence of severe regurgitation (such as premature closure of the mitral valve in severe aortic regurgitation or pulmonary hypertension in severe mitral regurgitation) should also prompt surgical intervention because valvular regurgitation—or rarely, stenosis—is a mechanical complication of IE that will not improve with antimicrobial therapy alone. For mitral valve regurgitation, surgical repair of the native valve without replacing the valve with a prosthesis has been reported in a number of case series. However, the role of repair versus replacement has not been evaluated in controlled studies, and its feasibility will be limited by the extent of infection and valvular damage as well as the experience of the surgeon. Surgery for IE may be performed with an acceptable operative mortality, although urgent or emergent surgery is associated with higher mortality.

    Box 4
    Indications for Surgical Intervention in Infective Endocarditis
    Class I Indications

    • Valve dysfunction with heart failure symptoms

    • Left sided IE due to S. aureus, fungal, or other highly resistant organism

    • IE complicated by heart block, annular or aortic abscess, or destructive penetrating lesions

    • Persistent bacteremia or fevers lasting longer than 5 to 7 days after onset of appropriate antimicrobial therapy

    •   Prosthetic valve endocarditis with relapsing infection

    • Complete removal of pacemaker or defibrillator system when evidence of device infection

    Class IIa Indications

    • Recurrent embolic and persistent vegetation despite appropriate antibiotic therapy

    • Complete removal of pacemaker or defibrillator system in patients with IE due to S. aureus or fungal organism, or when undergoing valvular surgery for valvular IE

    Class IIb Indications

    •   Native IE with vegetation >10 mm in length, with or without emboli Definitions: Class I = benefit >>> risk, surgery should be performed; class IIa = benefit >> risk, reasonable to perform surgery; class IIb: benefit ≥ risk, surgery may be considered, additional studies are needed.

    Adapted from Nishimura RA, et al. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation. 2014; 129(23):2440–2492.

    Because embolic complications often involve the central nervous system and can worsen neurologic function after cardiopulmonary bypass, the timing of surgery after a cerebral embolic infarct is controversial. A high percentage of patients with left-sided IE may develop asymptomatic brain embolic events if MRI is performed.

    Studies found that neurologic deterioration did not occur among patients with IE who experienced transient ischemic attacks or asymptomatic emboli, even if surgery was performed acutely.

    However, patients with recent hemorrhagic strokes may be at risk for extension and deterioration after cardiac surgery. In patients with ischemic stroke with major neurologic deficit or intracranial hemorrhage, it is recommended to delay valve surgery for at least 4 weeks.

    Regarding persistent bacteremia as an indication for surgery, it is important to recognize that certain microorganisms, particularly S. aureus, may be associated with prolonged bacteremia (up to 10 days) after initiation of antibiotic therapy. Because of possible difficulty in eradicating infection from prosthetic materials, all cases of prosthetic valve IE should receive surgical consultation. With valve conservation and improved surgical techniques, the surgical mortality rates have declined over time, with recent reported rates in the range of 7% to 14%. In comparison to therapy alone, surgery appears to confer a survival benefit for those patients with major complications of IE, such as heart failure or intracardiac abscess.

    Despite the high rate of surgical intervention in IE, the in-hospital mortality rate for native valve IE in the contemporary era remains high at approximately 15% to 20%, and nearly 25% for prosthetic valve IE. Among host factors, older age, female sex, diabetes mellitus, acute physiology (APACHE II) score, elevated white blood cell count, serum creatinine level greater than 2 mg/dL, and lower serum albumin have been associated with worse outcome. Congestive heart failure, paravalvular complication (e.g., abscess formation), infection with virulent organisms (particularly S. aureus), prosthetic valve infection, and absence of surgical intervention are also factors related to higher mortality in IE.

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  10. 10

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    Circulation. 2015;132:1435–1486.

    Chu V.H., Cabell C.H., Benjamin Jr. D.K., et al. Early predictors of in-hospital death in infective endocarditis. Circulation.


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    Habib G., Lancellotti P., Antunes M.J., et al. 2015 ESC Guidelines for the management of infective endocarditis: The Task Force for the Management of Infective Endocarditis of the European Society of Cardiology (ESC). Endorsed by: European Association for Cardio-Thoracic Surgery (EACTS), the European Association of Nuclear Medicine (EANM). Eur

    Heart J. 2015;36(44):3075–3128.

    Hasbun R., Vikram H.R., Barakat L.A., et al. Complicated left- sided native valve endocarditis in adults: Risk classification for mortality. JAMA. 2003;289(15):1933–1940.

    Hoen B., Alla F., Selton-Suty C., et al. Changing profile of infective endocarditis: Results of a 1-year survey in France. JAMA. 2002;288(1):75–81.

    Kang D.H., Kim Y.J., Kim S.H., et al. Early surgery versus conventional treatment for infective endocarditis. N Engl J Med. 2012;366:2466–2473.

    Kiefer T., Park L., Tribouilloy C., et al. Association between valvular surgery and mortality among patients with infective endocarditis complicated by heart failure. JAMA.


    Li J.S., Sexton D.J., Nettles R., et al. Proposed modifications to the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis. 2000;30(4):633–638.

    Moreillon P., Que Y.A. Infective endocarditis. Lancet.


    Nishimura R.A., Otto C.M., Bonow R.O., et al. 2014 AHA/ ACC guideline for the management of patients with valvular heart disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;63:e57–185.

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About Genomic Medicine UK

Genomic Medicine UK is the home of comprehensive genomic testing in London. Our consultant medical doctors work tirelessly to provide the highest standards of medical laboratory testing for personalised medical treatments, genomic risk assessments for common diseases and genomic risk assessment for cancers at an affordable cost for everybody. We use state-of-the-art modern technologies of next-generation sequencing and DNA chip microarray to provide all of our patients and partner doctors with a reliable, evidence-based, thorough and valuable medical service.