Echocardiography is an essential imaging modality for the diagnosis and management of infective endocarditis. It is often the first imaging study ordered when endocarditis is suspected, and serial echocardiographic exams are commonly performed to follow course of illness and inform clinical decision-making. Early use of echocardiography is universally recommended when infectious endocarditis (IE) is suspected, and echocardiographic manifestations of IE are a cornerstone of establishing diagnosis. The presence of vegetation is one of the major modified Duke criteria for diagnosis of IE, and numerous articles and guideline publications utilize echocardiographic assessment of IE to establish diagnosis and guide therapy [ ]. The morbidity and mortality associated with diagnosis of IE is often directly related to complications of infection which are readily assessable by echocardiography, for example, valvular regurgitation due to infectious destruction, vegetation embolic potential based on size and anatomic location, as well as paravalvular extension of infection.
The 2011 ASE Appropriate use guidelines state that transthoracic echocardiography (TTE) is appropriate in patients with suspected IE and positive blood cultures or a new cardiac murmur. Additionally, TTE or TEE would also be appropriate for evaluation of cardiac source of emboli, as this is also a clinical scenario in which IE may present [ ]. Transesophageal echocardiography (TEE) is appropriate and the preferred diagnostic study in certain circumstances ( Figs. 4.1 and 4.2 ). TEE may be considered as the initial diagnostic imaging test when there is felt to be high probability for nondiagnostic TTE due to patient characteristics or in cases of moderate or high pretest probability, for example, prosthetic heart valve or presence of intracardiac device, staph bacteremia, or fungemia. TTE or TEE would also be appropriate for reevaluation of: (1) definite IE with high risk for progression or complication and (2) possible endocarditis with a change in clinical status or cardiac exam. TTE is not considered appropriate for evaluation of transient bacteremia with a pathogen not typically associated with IE or in the case of documented nonendovascular source of infection, however [ ].
Echocardiographic manifestations of IE
The classic lesion of endocarditis is the vegetation. Consisting of a fibrin matrix with associated platelets, leukocytes, and bacteria, the vegetation is the macroscopic manifestation of what begins as a microscopic process, requiring multiple cofactors. Typically, there is a nidus of endothelial disruption or injury to which platelets and fibrin adhere. This may be a site of endothelial injury due to:
mechanical trauma from central venous catheter or pacemaker lead or excoriation of endothelial surface through repetitive injection of particulate matter via IV drug use [ ];
inflammatory endothelial injury associated with acquired, autoimmune disease, or prior IE;
high turbulence flow as in VSD or aortic insufficiency.
Prosthetic endovascular material may also be a nidus for fibrin and platelet adhesion. A microbial pathogen in the bloodstream can then adhere to the fibrin-platelet matrix, establishing a beachhead for infection. Vegetation growth then occurs through interaction between pathogen and platelets. Staphylococcus aureus , for example, has several molecular pathways to adhere to and interact with platelets, causing platelet activation and aggregation, which become key mechanisms of vegetation formation [ , ].
Vegetation, as defined in echocardiography, is an independently oscillating echogenic mass attached to valve leaflet or supporting structures, endothelial tissue, or prosthetic endovascular material [ ]. Fig. 4.3 shows typical vegetation of mitral valve, as seen on TEE. Fig. 4.4 shows tricuspid valve vegetation by TTE, associated with moderate tricuspid valve regurgitation.
Independent oscillation refers to motion separate from or in addition to valve leaflet motion, or, especially in the case of prosthetic valve endocarditis (PVE) or cardiac device infection, motion independent of the expected translation of an intracardiac structure during the cardiac cycle. For example, myxomatous valve changes may appear bulky and vegetation-like, but will move synchronously with the valve leaflet. Similarly, ultrasound artifact from pacemaker lead(s) or prosthetic valve annulus may appear mass-like, but will not exhibit motion independent of the cardiac structure with which they are associated ( Fig. 4.5 ).
In native-valve endocarditis, vegetations are generally found on the “upstream” surface of the valve leaflet, for example, left atrial side of the mitral valve or left ventricular outflow tract side or aortic valve. Vegetations may also be seen attached to chordae, pacemaker leads, prosthetic valves, or intracardiac devices [ , ]. Due to predilection for vegetation to form on valve leaflet, path of regurgitant jet, or intracardiac prosthetic material, echocardiographic assessment should include thorough evaluation of these surfaces. For example, aortic valve endocarditis associated with aortic regurgitation can lead to seeding and infection of the mitral subvalvular apparatus and mitral chordae, so particular attention should be paid to these structures (doubly so in preoperative echocardiography).
The vegetation is the fundamental macroscopic lesion of IE; over the natural history of infection, other pathologic and echocardiographic features of invasive or complicated infection can develop, discussed further below.
Echocardiographic Duke criteria
The modified Duke criteria list the following echocardiographic findings as major criteria for establishing diagnosis of IE [ ]:
Intracardiac or paravalvular abscess
Dehiscence of prosthetic valve
New valvular regurgitation
The last category is the most problematic, as degenerative valve disease is commonly encountered in older patients and may be responsible for noninfectious valvular abnormality and regurgitation, leading to false-positive study.
The presence of vegetation on valve leaflets or inflammatory host defenses may result in malcoaptation of valve leaflet and regurgitation ( Fig. 4.4B ). Valve leaflet destruction or perforation may develop as a complication of IE, resulting in hemodynamically significant regurgitation. Quantitative and semiquantitative echocardiographic techniques should be utilized to assess severity of valvular regurgitation in these cases according to established ASE standards [ ]. Fig. 4.6 depicts holodiastolic flow reversal in the thoracic aorta as detected by TEE, a sign of severe aortic valve regurgitation as a result of native aortic valve infection. The presence of large vegetations in native-valve endocarditis and especially prosthetic valve vegetation(s) in PVE can also result in stenotic valve dysfunction, in which continuous-wave valve gradients should be reported. Fig. 4.7 depicts elevated mitral valve inflow gradient as a result of obstructive mitral valve vegetation.