Infective endocarditis

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Infective endocarditis is an inflammation of the endocardium, caused by an infection by a microorganism, and generally localized on cardiac valves.

The aims of echocardiography in infective include:

  1. diagnosis of endocarditis and its complications
  2. prognosis of infective endocarditis, including prediction of the embolic risk
  3. help the physician for determining the indication and optimal timing for surgery
  4. follow patients with infective endocarditis, during and after surgery

Echocardiography for diagnosis of infective endocarditis

The major echographic criteria for IE are vegetation and abscess[1]. Other echocardiographic findings are only suggestive.

Anatomic definitions – echocardiographic correlations (table 1)

Table 1: Anatomic and echocardiographic definitions

Surgery / necropsy Echocardiography
Vegetation Infected mass attached to an endocardial structure, or on implanted intracardiac material Oscillating or non oscillating intracardiac mass on valve or other endocardial structures, or on implanted intracardiac material
Abscess Perivalvular cavity with necrosis and purulent material not communicating with the cardiovascular lumen Thickened, non-homogeneous perivalvular area with echodense or echolucent appearance
Pseudoaneurysm Perivalvular cavity communicating with the cardiovascular lumen Pulsatile perivalvular echo-free space, with colour-Doppler flow detected
Perforation Interruption of endocardial tissue continuity Interruption of endocardial tissue continuity traversed by colour-Doppler flow
Fistula Communication between 2 neighbouring cavities through a perforation Colour-Doppler communication between 2 neighboring cavities through a perforation
Valve aneurysm Saccular outpouching of valvular tissue Saccular bulging of valvular tissue
Dehiscence of a prosthetic valve Dehiscence of the prosthesis Paravalvular regurgitation identified by TTE / TEE, with or without rocking motion of the prosthesis

Anatomically, IE is characterized by a combination of vegetations and destructive lesions[2].

  1. Vegetations are typically attached on the low pressure side of the valve structure, but may be located anywhere on the components of the valvular and subvalvular apparatus, as well as on the mural endocardium of the cardiac chambers or the ascending aorta. When large and mobile, vegetations are prone to embolism and less frequently to valve or prosthetic obstruction.
  2. Destructive lesions are very frequently associated with vegetations or may be observed alone. The consequences of this destructive process may include valve aneurysm, perforation or prolapse, and chordae or less frequently papillary muscle rupture. The main consequences of these lesions are severe valve regurgitation and heart failure.
  3. The third main anatomic feature of IE is abscess formation. Abscesses are more frequent in aortic and prosthetic valve IE and may be complicated by pseudoaneurysm or fistulisation.

These three anatomic features are frequently present together and must be meticulously described by the echocardiographic examination.

Duke “echocardiographic” criteria[1]

The major echographic criteria for IE are vegetation, abscess and new dehiscence of a prosthetic valve. (table 2 below)

Modified Duke criteria for the diagnosis of IE (Adapted from Li & al)

Blood culture positive for IE
  • Typical microorganims consistent with IE from 2 separate blood cultures:

Viridans streptococcus, Streptococcus bovis, HACEK group, Staphylococcus aureus or community acquired enterococci in the absence of a primry focus.

  • Microorganisms consistent with IE from 2 persistely positive blood cultures:

At least 2 positive blood cultures of blood samples drawn > 12h apart or all of 3 or a majority of ≥ 4 separate cultures of blood with first & last sample drawn at least 1h apart.

  • Single positive blood culture for Coxiela burneti or phase I lgC antibody titer > 1:800.
Evidence of endocardial involvement
  • Echocardiogram positive for IE. (Vegetation, Abscess, New partial dehiscence of prosthetic valve).
  • New valvular regurgitation.
  • Predisposition: Predisposing heart condition, injection drug use.
  • Fever: temperature > 38°C.
  • Vascular phenomena: major arterial amboli, septic pulmonary infarcts, mycotic aneurysms.
  • Intracranial haemorrhages, conjunctival haemorrhages, Janeway lesions.
  • Immunologic phenomena: glomerulonephritis Osler's node, Roth's spot, rheumatoid factor.
  • Microbiological evidence: positive blood culture but does not meet a major criterion or serological evidence of active infective with organism consistent with IE.


Echocardiography is the reference method for the diagnosis of vegetation. Typically, vegetation presents as an oscillating mass attached on a valvular structure, with a motion independent to that of this valve (fig 1, movie 1). Vegetations are usually localized on the atrial side of the atrioventricular valves, and on the ventricular side of the aortic and pulmonary valves. The sensitivity of TTE may be reduced in case of low echogenicity, very small vegetations, and in IE affecting intracardiac devices. TEE is mandatory in case of doubtful transthoracic examination, in prosthetic and pacemaker IE, and when an abscess is suspected. TEE enhances the sensitivity of TTE to about 85 to 90 % for the diagnosis of vegetations.

Figure 1 and movie 1: Large vegetation on the anterior mitral leaflet with chordae rupture (arrow) (TEE) LA: Left atrium, LV: left ventricle, Ao: aorta

Abscess formation[3]

The second major echocardiographic criterion for endocarditis is the presence of perivalvular abscesses. They are more frequently observed in aortic valve IE and in prosthetic valve IE. Abscess typically presents as a perivalvular zone of reduced echo density, without colour flow detected inside. The diagnosis is easy in the presence of a clear free-space in the aortic root, but may be much more difficult at the early stage of the disease when only a thickening of the aortic root is evidenced. The sensitivity of TTE is about 50 %, that of TEE 90%.

Three types of perivalvular lesions exist[3]:

  • Abscess is a non communicating zone of necrosis with purulent material. Echographic appearance is a non circulating perivalvular zone of reduced echo density (figure 2)
  • Pseudoaneurysm is characterized by the presence of a pulsatile perivalvular echo free-space with color doppler flow inside. The echographic appearance of partial systolic collapse proves that the abscess communicates with the cardiovascular lumen (movie 2).
  • Fistula may be a complication of both abscesses and pseudoaneurysm. They are defined anatomically by a communication between 2 neighbouring cavities and echographically by a color doppler communication between 2 adjacent cavities (figure 3).
Movie 2: pseudo aneurysm of the aortic annulus (TEE) Figure 2: TEE showing an echodense thickening around the annulus of a bioprosthetic valve corresponding to a periannular abscess (arrow).
Figure 3. Severe native valve IE with commissural abscess and perforation
a: Vegetation and pseudoaneurysm (thick arrow) of the posterointernal commissure of the mitral valve, associated with a small vegetation (thin arrow)
b: Fistulisation of the pseudoaneurysm into the left atrium causing massive mitral regurgitation (arrow)

New dehiscence of a prosthetic valve

It represents the third main diagnostic criterion for IE. IE must be suspected in the presence of a new perivalvular regurgitation, even in the absence of vegetation or abscess. TOE has a better sensitivity than TTE for this diagnosis, especially in mitral prosthetic valve infective endocarditis.

Other echocardiographic findings in IE

Other echocardiographic features are not main criteria for IE but may be suggestive of the diagnosis. They include valve destruction and prolapse, aneurysm and / or perforation of a valve. The most frequent is anterior mitral valve perforation which is usually a complication of aortic valve IE. Perforation of the mitral valve may be the consequence of an infected aortic regurgitant jet and is best visualized by TOE and 3D echocardiography (movies 3 and 4).

Movies 3 and 4: TEE (120° view and color Doppler) showing a mitro-aortic endocarditis with an aortic and mitral perforation.

Indications of different echocardiographic modalities in IE[2][4]

TTE must be performed first in all cases, because it is a non invasive technique giving useful information both for the diagnosis and the assessment of severity of IE. TEE must also be performed in the majority of patients with suspected IE, because of its better image quality and better sensitivity, except in case of good quality negative TTE associated with a low level of clinical suspicion. Respective indications of TTE and TEE are summarized in table 3 below. Endocarditis-fig-4.jpg

Echocardiography for prediction of embolic risk

Embolic events are a frequent and life-threatening complication of IE, with a total risk of embolism of 20 to 50%, and a risk of new EE (i.e. occurring after initiation of antibiotic therapy) of 6 to 21%[5][6][7]. Cerebral embolism is the most frequent and severe localization of embolism. Conversely, embolic events may be totally silent in about 20 % of patients with IE, especially in case of splenic or cerebral embolisms, and must be diagnosed by systematic non invasive imaging. Echocardiography plays a major role in the assessment of embolic risk, although this prediction remains difficult in the individual patient[6]. Several factors have been associated with an increased risk of embolism, including the size and mobility of vegetations, the localization of the vegetation on the mitral valve, the increasing or decreasing size of the vegetation under antibiotic therapy, the type of microorganism, previous embolism, multivalvular endocarditis, and biological markers. The size and mobility of the vegetations are the most potent independent predictors of new embolic event in patients with IE. Patients with left-sided IE and very large (> 15 mm) and mobile vegetations must be considered as at high risk of embolism and need specific management[2].

Echocardiography and decision-making

Echocardiography plays a crucial role both for the decision to operate or not and for the choice of the optimal timing of surgery[4]. Indications for surgery in IE may be subdivided in 3 categories – haemodynamic, infectious and embolic indications[2]. In each category of indication for surgery, echocardiography plays a major role. Main indications for surgery are summarized in table 4 below.

Table 4: Indications and timing of surgery in native and prosthetic valve infective endocarditis[2]

Indication for surgery Timing Class Level of evidence
Aortic or mitral IE or PVE with severe acute regurgitation, obstruction or fistula causing refractory pulmonary oedema or cardiogenic shock Emergency I B
Aortic or mitral IE with severe acute regurgitation or obstruction and persisting heart failure or echocardiographic signs of poor hemodynamic tolerance (early mitral closure or pulmonary hypertension) Urgent I B
Aortic or mitral IE or PVE with severe regurgitation and no HF Elective IIa B
Right HF secondary to severe tricuspid regurgitation with poor response to diuretic therapy Urgent/Elective IIa C
Locally uncontrolled infection (abscess, false aneurysm, fistula, enlarging vegetation) Urgent I B
Persisting fever and positive blood cultures >7-10 days Urgent I B
Infection caused by fungi or multiresistant organisms Urgent/elective I B
PVE caused by staphylococci or gram negative bacteria Urgent/Elective IIa C
Aortic or mitral IE or PVE with large vegetations (> 10 mm) following one or more embolic episodes despite appropriate antibiotic therapy Urgent I B
Aortic or mitral IE or PVE with large vegetations (> 10 mm) and other predictors of complicated course (heart failure, persistent infection, abscess) Urgent I C
Aortic or mitral IE or PVE with isolated very large vegetations (>15 mm)* Urgent IIb C
Persistent tricuspid valve vegetations > 20 mm after recurrent pulmonary emboli Urgent/Elective IIa C

IE=infective endocarditis; PVE=prosthetic valve endocarditis
*Surgery may be preferred if procedure preserving the native valve is feasible


  1. 1.0 1.1 Li JS, Sexton DJ, Mick N, et al. Proposed modifications of the Duke criteria for the diagnosis of infective endocarditis. Clin Infect Dis 2000 ; 30 : 633-8.
  2. 2.0 2.1 2.2 2.3 2.4 Habib G, Hoen B, Tornos P, et al. 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). European Heart Journal (2009) 30, 2369–2413
  3. 3.0 3.1 Karalis DG, Bansal RC, Hauck AJ, Ross JJ, Jr., Applegate PM, Jutzy KR, Mintz GS, Chandrasekaran K. Transesophageal echocardiographic recognition of subaortic complications in aortic valve endocarditis. Clinical and surgical implications. Circulation 1992;86:353-362
  4. 4.0 4.1 Habib G, Badano L, Tribouilloy C, Vilacosta I, Zamorano JL, Galderisi M, Voigt JU, Sicari R, Cosyns B, Fox K, Aakhus S. Recommendations for the practice of echocardiography in infective endocarditis. Eur J Echocardiography 2011
  5. Thuny F, Di Salvo G, Belliard O, Avierinos JF, Pergola V, Rosenberg V, Casalta JP, Gouvernet J, Derumeaux G, Iarussi D, Ambrosi P, Calabro R, Riberi A, Collart F, Metras D, Lepidi H, Raoult D, Harle JR, Weiller PJ, Cohen A, Habib G. Risk of embolism and death in infective endocarditis: prognostic value of echocardiography: a prospective multicenter study. Circulation 2005;112:69-75
  6. 6.0 6.1 Habib G. Embolic risk in subacute bacterial endocarditis. Role of transesophageal echocardiography. Curr Cardiol Rep 2003;5:129–36.
  7. Steckelberg JM, Murphy JG, Ballard D, Bailey K, Tajik AJ, Taliercio CP, Giuliani ER, Wilson WR. Emboli in infective endocarditis: the prognostic value of echocardiography. Ann Intern Med 1991;114:635-640

Further reading list

  1. Durack DT, Lukes AS, Bright DK. New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. Am J Med 1994;96:200-209.
  2. Sochowski RA, Chan KL. Implication of negative results on a monoplane transesophageal echocardiographic study in patients with suspected infective endocarditis. J Am Coll Cardiol 1993 ; 21 : 216-21
  3. San Roman JA, Lopez J, Vilacosta I, Luaces M, Sarria C, Revilla A, Ronderos R, Stoermann W, Gomez I, Fernandez-Aviles F. Prognostic stratification of patients with left-sided endocarditis determined at admission. Am J Med 2007;120:369 e361-367
  4. Hasbun R, Vikram HR, Barakat LA, Buenconsejo J, Quagliarello VJ. Complicated left-sided native valve endocarditis in adults: risk classification for mortality. JAMA 2003;289(15):1933-40
  5. Vilacosta I, San Roman JA, Sarria C, Iturralde E, Graupner C, Batlle E, Peral V, Aragoncillo P, Stoermann W. Clinical, anatomic, and echocardiographic characteristics of aneurysms of the mitral valve. Am J Cardiol 1999;84:110-113, A119.
  6. Vikram HR, Buenconsejo J, Hasbun R, Quagliarello VJ. Impact of valve surgery on 6-month mortality in adults with complicated, left-sided native valve endocarditis. A propensity analysis. JAMA 2003; 290: 3207-3214.
  7. Hill EE, Herijgers P, Claus P, Vanderschueren S, Herregods MC, Peetermans WE. Infective endocarditis: changing epidemiology and predictors of 6-month mortality: a prospective cohort study. Eur Heart J 2007; 28: 196-203
  8. Shapira Y, Weisenberg DE, Vaturi M, Sharoni E, Raanani E, Sahar G, Vidne BA, Battler A, Sagie A. The impact of intraoperative transesophageal echocardiography in infective endocarditis. Isr Med Assoc J 2007;9:299-302.

See also

Echogenic mass

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