Introduction and Echocardiographic Features of Infective Endocarditis
- Moses Mathur, MD, MSc
- Susan Wiegers, MD
Infective endocarditis (IE) is a microbial infection of the endocardium or associated implanted intracardiac materials. Chamber walls, conduits, prosthetic implants, pacing electrodes, and indwelling catheters may also be infected. Classically, IE manifests as a mobile vegetation associated with valve leaflets. In general, left-sided lesions are more common than right-sided lesions. However, the latter are more common in the setting of intravenous drug use (IVDU) and congenital abnormalities. ,
Despite advances in antimicrobial therapy, IE remains clinically challenging and carries potential for high morbidity and mortality. One reason for this is the difficulty clinicians often face in establishing an accurate diagnosis in the early stages of infection, where timely detection and treatment could prove essential to preventing a complicated clinical course.
With the advent of M-mode, Doppler, two-dimensional, and three-dimensional echocardiography, it is now increasingly feasible to inspect cardiac structures by direct visualization and hemodynamic assessment. Unlike conventional radiologic modalities, echocardiography requires no radiation exposure, may be safely repeated for serial assessment, and can be performed at bedside, even in the most seriously ill patients. The importance of echocardiography led to the inclusion of echocardiographic findings in the diagnostic Duke criteria in 1994. These were later revised in 2000 as the modified Duke criteria ( Boxes 133.1 and 133.2 ). Compared with the previously used von Reyn criteria, the Duke criteria are more sensitive (80% for Duke criteria; 51% for von Reyn criteria) in pathologically confirmed IE. Today, echocardiography plays a central role not only in the diagnosis but also in the detection of infection complications, serial evaluations following treatment, and assessment of embolic risk from detected vegetations.
Definite Infective Endocarditis
Pathologic Criteria OR Clinical Criteria
- 1.
Microorganisms demonstrated by culture or histologic examination of a vegetation, a vegetation that has embolized, or an intracardiac abscess specimen
OR
- 2.
Pathologic lesions (vegetation or intracardiac abscess) confirmed by histologic examination showing active endocarditis
- 1.
Two major criteria
OR
- 2.
One major criterion and three minor criteria
OR
- 3.
Five minor criteria
Possible Infective Endocarditis
- 1.
One major criterion and one minor criterion
OR
- 2.
Three minor criteria
Rejected
- 1.
Firm alternate diagnosis explaining evidence of infective endocarditis
OR
- 2.
Resolution of infective endocarditis syndrome with antibiotic therapy for ≤ 4 days
OR
- 3.
No pathologic evidence of infective endocarditis at surgery or autopsy, with antibiotic therapy for ≤ 4 days
OR
- 4.
Does not meet criteria for possible infective endocarditis, as stated previously
Definition of Terms
Major Criteria
- 1.
Blood culture positive for IE
- a.
Typical microorganisms consistent with IE from 2 separate blood cultures: viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus; or community-acquired enterococci, in the absence of a primary focus; or
- b.
Microorganisms consistent with IE from persistently positive blood cultures, defined as follows: ≥ 2 positive cultures of blood samples drawn > 12 hr apart; or all of 3 or a majority of ≥ 4 separate cultures of blood (with first and last sample drawn at least 1 hr apart)
- c.
Single positive blood culture for Coxiella burnetii or antiphase I IgG antibody titer > 1:800
- a.
- 2.
Evidence of endocardial involvement
- a.
Echocardiogram positive for IE (TEE recommended in patients with prosthetic valves, rated at least “possible IE” by clinical criteria, or complicated IE [paravalvular abscess]; TTE as first test in other patients), defined as follows: (i) oscillating intracardiac mass on valve or supporting structures, in the path of regurgitant jets, or on implanted material in the absence of an alternative anatomic explanation; (ii) abscess; or (iii) new partial dehiscence of prosthetic valve
- b.
New valvular regurgitation (worsening or changing of preexisting murmur not sufficient)
- a.
Minor Criteria
- 1.
Predisposition, predisposing heart condition, or injection drug use
- 2.
Fever, temperature > 38° C
- 3.
Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway lesions
- 4.
Immunologic phenomena: glomerulonephritis, Osler nodes, Roth spots, and rheumatoid factor
- 5.
Microbiological evidence: positive blood culture, but does not meet a major criterion as noted previously; or serologic evidence of active infection with organism consistent with IE
HACEK , Haemophilus species (Haemophilus parainfluenzae, Haemophilus aphrophilus, Haemophilus paraphrophilus) , Actinobacillus actinomycetemcomitans , Cardiobacterium hominis , Eikenella corrodens , and Kingella species; IE , infective endocarditis; IgG , immunoglobulin G; TEE , transesophageal echocardiogram; TTE , transthoracic echocardiogram.
Vegetations
Vegetations are the hallmark of IE on echocardiography. Their formation is thought to be a function of endothelial disruption caused by high-velocity jets that accompany congenital defects, valvular dysfunction, prosthetic valves, and intracardiac shunts. This nidus of microbes attaches to the damaged endothelium along with platelets and fibrin, and it gradually begins to develop into infected vegetation.
Classically, vegetations are irregularly shaped, low-reflectance structures that may be sessile or pedunculated. They are often described as having a “shaggy” appearance, which may help distinguish them from more organized intramasses, such as thrombi, or cardiac tumors. Because of their association with high-velocity flow jets, vegetations are often mobile, exhibiting a high-frequency chaotic oscillating motion that is usually independent of valve leaflet motion. This mobility can increase the risk for embolism, especially with vegetations larger than 10 mm. The incidence of embolization is higher in the 2 weeks following initiation of antimicrobial treatment. The disappearance of a vegetation on serial echocardiography may either represent regression of disease or peripheral embolization, depending on the clinical scenario. Vegetations are typically on the side of valves exposed to high velocity regurgitant jets (e.g., on the left ventricular side of the aortic valve, or the left atrial side of the mitral valve). They may also associate with chordal structures or valve cusps. Disruption of valve integrity may lead to flail leaflets and regurgitation, and can result in hemodynamic changes and decompensated heart failure.
Other features
Classic clinical situations that are suspicious for IE include new onset heart failure, new regurgitant murmur, persistent fevers, bacteremia, fungemia, peripheral embolic phenomena (e.g., Janeway lesions), and immunologic vascular phenomena (e.g., glomerulonephritis, Osler nodes, and Roth spots). Common risk factors for IE include IVDU, immunosuppressive states, congenital heart disease, and cardiac prostheses.
In these typical scenarios, clear echocardiographic evidence of valvular vegetation may provide a straightforward diagnosis of IE. However, on many occasions the presentation of IE may be subtle, with nonspecific echocardiographic features. This may be due to technical limitations (inadequate windows, poor image quality, or the presence of artifact), or insufficient resolution to detect vegetations in the early stages of IE, particularly by transthoracic echo. Additionally, the presence of other cardiac structures, such as thrombi, calcifications, prosthetic sutures, cardiac tumors, Chiari network, or Lambl excrescence, may obscure the clear identification of a true vegetation.
In the absence of vegetations, other findings can strongly suggest IE. These include abscesses, fistulae, pericardial effusion, destructive valve lesions (perforation, aneurysm, prolapse), changes in prosthetic valve hemodynamics, valve dehiscence, or paravalvular leaks. When present, abscesses are usually nonhomogeneous enclosed areas that can appear echolucent or echodense. Abscesses can form tracts leading to neighboring structures, resulting in fistulae, shunts, or conduction disturbances. Abscesses may also rupture, resulting in pseudoaneurysms, which are usually echo-free outpouchings that exhibit color flow Doppler signal.
Ultimately, clinical judgment should guide the course of action in a case of suspected IE, especially in the context of an indeterminate echocardiogram.
Infective Endocarditis: Role of Transthoracic versus Transesophageal Echocardiography
- Maria C. Todaro, MD
- Concetta Zito, MD, PhD
- Scipione Carerj, MD
- Bijoy K. Khandheria, MD
- Concetta Zito, MD, PhD
Epidemiology of infective endocarditis
Infective endocarditis is one of the most severe infectious diseases, partially because delays in diagnosis result in late initiation of appropriate therapy. Despite major advances in diagnosis and treatment options, infective endocarditis is still considered a disease with poor prognosis and high mortality rates and is associated with prolonged hospitalization and high risk of surgery. The incidence of infective endocarditis ranges among countries from 3 to 10 episodes per 100,000 person-years and increases dramatically with age, reaching a peak incidence of 14.5 episodes per 100,000 person-years in patients aged 70 to 80 years. In all epidemiological studies of infective endocarditis, the male-to-female ratio is greater than 2:1. This higher proportion of men is probably due to the fact that women undergo valve surgery less frequently than men.
Since its first description in 1885, the epidemiology of the disease has greatly changed. In the most developed countries, the increasing and widespread incidences of diabetes, chronic kidney failure requiring hemodialysis, and intravascular devices associated with progress in cardiac valve repair/replacement techniques have generated a new microbiological profile of infective endocarditis, with a prevalence of infections due to staphylococci, enterococci, fungi, and other resistant health-care related agents typically involving older patients with prosthetic valves or degenerative valve disease.
In contrast, developing countries are characterized by a prevalence of streptococcal infections and culture-negative infective endocarditis affecting patients of younger age at presentation and higher incidence of structural cardiac predisposing risk factors such as rheumatic disease and untreated congenital heart disease. , Prognosis is worse in developing countries because of the difficulty in reaching facilities equipped for early surgical intervention that, if performed early by experienced operators, prove to significantly ameliorate patient outcomes.
Types of infective endocarditis
According to the most recent European guidelines for infective endocarditis, this condition includes a cluster of different clinical entities that can be classified according to the site of infection and the presence of intracardiac materials in the following: left-sided native valve infective endocarditis, left-sided prosthetic valve infective endocarditis, right-sided infective endocarditis, and device-related infective endocarditis (on pacemaker or defibrillator wires with or without associated valve involvement).
With regard to acquisition, the following situations can be identified , : (1) community-acquired infective endocarditis (when symptoms start < 48 hours from admission in patients not fulfilling the criteria for health-care associated infective endocarditis; (2) health-care associated infective endocarditis (nosocomial in patients hospitalized > 48 hours before the onset of signs and symptoms of infective endocarditis and non-nosocomial when symptoms start < 48 hours from admission in patients already hospitalized in acute care facilities within 90 days before the onset of symptoms or residents in long-term care facilities and nursing homes); and (3) infective endocarditis in intravenous drug abusers.
According to microbiological findings, the following categories are proposed : (1) infective endocarditis with positive blood cultures (> 85% of all infective endocarditis), with causative microorganisms most often represented by staphylococci, streptococci, and enterococci; (2) infective endocarditis with negative blood cultures because of prior antibiotic treatment; (3) infective endocarditis frequently associated with negative blood cultures provoked by gram-negative bacilli of the HACEK group ( Haemophilus parainfluenzae, H. aphrophilus, H. paraphrophilus, H. influenzae, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae , and K. denitrificans ), Brucella , and fungi; and (4) infective endocarditis associated with constantly negative blood cultures (5% of all infective endocarditis), which is caused by intracellular bacteria such as Coxiella burnetii, Bartonella, Chlamydia , and, as recently demonstrated, Tropheryma whipplei , the agent of Whipple disease.
Pathophysiology
A combination of conditions—such as transient bacteremia, local endocardial inflammation and/or tissue disruption, and immunological predisposition—is responsible for infective endocarditis initiation. Long and persistent bacteremia, especially by pathogens with special tropism for endocardial tissue, play a key role in the pathophysiology of infective endocarditis; however, normal and healthy endocardial tissue with good immunological defense generally prevents establishment of the disease. Local damage with endocardial discontinuation is generally required, with consequent extracellular protein exposition, tissue factor activation, and fibrin and platelet aggregation leading to formation of noninfective thrombus, the ideal substrate for transient pathogen adhesion and infection. Alternatively, local endocardial inflammation without tissue disruption can promote the expression of integrins, transmembrane proteins that connect extracellular determinants to the cellular cytoskeleton. Integrins bind circulating fibronectin to the endothelial surface; S. aureus and other infective endocarditis pathogens carry fibronectin-binding proteins on their surfaces, thus creating a bridge for their internalization into endocardial cells.
Diagnosis
The diagnosis of infective endocarditis is based on the clinical picture, echocardiographic findings, and microbiological diagnosis. The Duke criteria and the modified Duke criteria provide high sensitivity and specificity for diagnosis ( Table 134.1 ). , Infective endocarditis can present acutely with septic changes and rapidly progressive infection, but also as a subacute or chronic disease with low-grade fever and nonspecific symptoms, which may delay diagnosis especially when occurring in patients with no previous history of valve disease. A range of other conditions, including rheumatic disease, chronic infection, malignancy, and autoimmune disease, can be suspected before the diagnosis of infective endocarditis is established.
| Major Criteria |
|---|
| B lood C ultures P ositive for IE |
|
| E vidence of E ndocardial I nvolvement |
|
| Minor Criteria | |
|---|---|
| |
| |
| |
| |
| |
| Diagnosis of IE is definite in the presence of: 2 major criteria; or 1 major and 3 minor criteria; or 5 minor criteria | Diagnosis of IE is possible in the presence of: 1 major and 1 minor criteria; or 3 minor criteria |
In infective endocarditis caused by virulent organisms such as S. aureus , the diagnosis can be missed when extracardiac signs of infection predominate and the clinical signs of valve disease are initially absent or difficult to evaluate (Videos 134.1 and 134.2). It is necessary to consider the diagnosis of infective endocarditis in all cases of sepsis, particularly in all patients presenting with fever of unclear origin and an embolic episode, even if there is no previous history of cardiac disease.
Types of echocardiography: indications and diagnosis
Whenever infective endocarditis is suspected, transthoracic echocardiography (TTE) must be rapidly performed as the first imaging evaluation. Although it is negative or inconclusive in almost 30% of cases, especially in the presence of prosthetic valves or intracardiac electronic devices, TTE’s role is pivotal for detection of complications and risk stratification of patients. Pretest probability of the disease should always be taken into account to avoid overuse of echocardiography. The reason TTE is performed first is because it is a noninvasive technique that provides useful information for both the diagnosis and assessment of infective endocarditis severity. Moreover, TTE is better than transesophageal echocardiography (TEE) for detecting anterior cardiac abscesses and for hemodynamic assessment of valvular dysfunction.
Because of its better image quality and higher sensitivity (88% to 100% compared with 30% to 65% for TTE), TEE must be performed in the majority of patients with suspected infective endocarditis, particularly in patients with high clinical suspicion and poor quality or negative TTE. In cases of positive TTE, TEE should still be performed to evaluate perivalvular involvement and in every patient with prosthetic valves and/or intracardiac devices. In preliminary studies, three-dimensional TEE provided incremental value over two-dimensional TEE in its ability to accurately identify and localize vegetations and to identify complications such as abscesses, perforations, and ruptured chordae.
The only situation in which TTE may be considered sufficient is when a good-quality negative TTE is obtained in a patient associated with a low level of clinical suspicion. Even when the first imaging is negative, TTE/TEE should be repeated within 7 to 10 days whenever clinical suspicion for infective endocarditis is high, as vegetations can be missed when echocardiography is performed either after embolization of the vegetative mass or very early in the clinical course when vegetation size may be very small. , A false-negative TTE finding may also be the result of imaging artifacts such as prosthetic valve shadowing, poor acoustic windows, or a spatial resolution that precludes detection of minute vegetations. On the other hand, even the characteristic finding of a mobile mass attached to a valve surface may instead reflect prior infective endocarditis, noninfectious endocarditis, torn or redundant chordae, Lambl excrescences (filamentous extensions primarily of left-sided valves), fibroelastomas or other benign tumors, and so on. For this reason, even typical echocardiographic findings in patients with low clinical likelihood for native valve infective endocarditis may represent false positives. Three echocardiographic findings represent major criteria in the diagnosis of infective endocarditis: vegetation, abscess, and new dehiscence of a prosthetic valve ( Figs. 134.1 and 134.2 ). ,
Echocardiography: detection of complications
Although concordance between TTE and TEE is high, immediate TEE should be performed in patients with a moderate or high likelihood of infectious endocarditis, especially in those at high risk for complications such as those with prolonged symptoms, hemodynamic instability, new onset of congestive heart failure, or new conduction abnormalities. ,
A high incidence (30% to 50%) of embolic events is reported during infective endocarditis, more so in cerebral circulation, and the role of echocardiography is pivotal for the evaluation of embolic risk through vegetation size and mobility. In particular, vegetation length is a strong predictor of embolism, and the protective effect of surgical management within 48 hours is demonstrated in patients with a vegetation larger than 10 mm associated with severe regurgitation.
Extravalvular extension of infection occurs most commonly in prosthetic valve–related infective endocarditis in the form of periannular abscesses, often resulting in dehiscence of the prosthetic valve or paravalvular fistulae. Abscess formation in the context of native-valve infective endocarditis is usually a complication of aortic valve infection, often involving the aortic annulus, mitral-aortic intervalvular fibrosa, the aortoseptal junction, or atrioventricular conduction pathways, and possibly leading to heart block. TEE has become the gold standard for detection of abscesses in patients who have advanced and persistent fever or bacteremia despite appropriate therapy, or in high-risk patients with prosthetic valves or staphylococcal infections. Recent data have highlighted the diagnostic value of other imaging modalities such as cardiac computed tomography (CT) for the detection of periannular complications (abscess, pseudoaneurysm), and fluorodeoxyglucose positron emission tomography ( 18 F-FDG PET) and radiolabeled leukocyte single-photon emission computed tomography (SPECT) for earlier diagnosis of prosthetic valve/pacemaker/defibrillator endocarditis and for guidance during material extraction.
Development of new or worsening congestive heart failure can be due to intracardiac or paravalvular shunts resulting from fistula formation or valvular incompetence (impairment of valvular coaptation by large vegetations, valve perforation, or rupture of infected chordae). Early or immediate surgical intervention should be considered when New York Heart Association Class III or IV symptoms develop. In this setting, echocardiography is useful for differentiating these complications from other potential etiologies of heart failure, assessing ventricular function, and planning appropriate surgical repair.
Intraoperative TEE is mandatory in patients receiving surgery for infective endocarditis; it provides the surgeon with a final anatomical evaluation of valvular and perivalvular damage and is particularly useful for assessing immediate results of valve repair/replacement. Finally, detailed clinical and echocardiographic follow-up of patients should be performed at 1, 3, 6, and 12 months of the first year after antibiotic treatment ends and/or after surgery. ,
Therapy
Univocal data on the rates of surgical approaches and the benefit of early surgery for prognosis are not available in the literature, mostly because of the heterogeneity of populations, subtle clinical manifestation of the disease, and relative paucity of randomized clinical trials published on the role and exact timing of surgical management. Basing indications for surgery on imaging remains controversial; the most recent European guidelines recommending surgery in cases of heart failure (or high risk of heart failure), high embolic risk, and uncontrolled infection are mostly based on the results of observational series and expert opinion. , Although a meta-analysis on available clinical studies showed the relevant benefit of early surgery for survival, especially for complicated infective endocarditis, in-hospital mortality rates are still high, ranging from 16% to 25%.
Only a multidisciplinary team that includes a cardiologist, infectologist, microbiologist, and surgeon can improve mortality by enhancing the chances of an early diagnosis followed by correct risk stratification and prompt institution of the correct antibiotic treatment as well as appropriate and timely surgical intervention.
Acknowledgment
The authors gratefully acknowledge Joe Grundle and Katie Klein for their editorial assistance and Brian Miller and Brian Schurrer for their help with the figures.
Echocardiography for Prediction of Cardioembolic Risk
- Ferande Peters, MD
- Bijoy K. Khandheria, MD
Introduction
Echocardiography has emerged as an important diagnostic tool used in the workup of patients with cardioembolism. Identification of predisposing factors to cardioembolism often results in the use of appropriate medical, surgical, or interventional therapy to manage these patients. These various therapies may not only prevent recurrent cardioembolism but, in certain instances, may alter prognosis.
Spectrum of cardioembolism
The heart and aorta are the source of cardioembolism to any organ. Major clinical presentations involve either acute neurological dysfunction—transient ischemic attack (TIA) or stroke—or peripheral vascular disease (i.e., acute limb ischemia). From a practical point of view, all cardioembolic causes of TIA/stroke also will cause acute limb ischemia, with additional thromboembolic sources being thrombus/atheroma of the descending and abdominal aorta. Thus, transthoracic echocardiography (TTE) and, in a considerable proportion of cases, transesophageal echocardiography (TEE) are required to exclude these possibilities.
Stroke
Stroke is the third leading cause of death in first-world countries. , The most common type of stroke is ischemic, which accounts for approximately 85% of all strokes. The most common causes of ischemic stroke relate to in situ atherosclerosis and its complications. The TOAST criteria are a useful epidemiological tool to classify stroke, and echocardiography has a role in Category 2, cardioembolic and cryptogenic stroke ( Table 135.1 ). Cardioembolic stroke accounts for 15% to 30% of ischemic strokes. Currently, most patients with stroke are referred for an echocardiogram (echo). This may be because cardioembolism is a possibility or the patient has comorbid atherosclerotic risks for stroke and heart disease such as hypertension. Thus, patients with TIA/stroke frequently have significant cardiac comorbidity, which consequently may be a competing risk for the mechanism of stroke that, more importantly, often places the patient with TIA/stroke at high risk for future cardiovascular morbidity and mortality. The latter is important because the major mode of death is cardiac-related the first 6 months after a stroke or in a patient with TIA. Furthermore, the outcome of cardioembolic stroke is poor, with a 3-year mortality rate of almost 50% in some instances. Thus, the use of TTE to complement a cardiac evaluation in every patient with either a TIA or stroke may be justified, and a detailed systematic echo must be obtained to uncover conditions that predispose to cardioembolism ( Box 135.1 ). However, it is prudent that the use of TTE and, in many instances, TEE be applied in conjunction with an insightful cardiac and neurological evaluation when considering the possibility of cardioembolic stroke rather than a blanket approach of routine TTE and TEE applied to every referral.
| Category | Echocardiographic Features |
|---|---|
| 1 | Large artery atherosclerosis (artery-to-artery embolism/large artery superimposed in situ thrombosis) |
| 2 | Cardiac embolism |
| 3 | Small artery occlusion |
| 4 | Stroke of rare nonatherosclerotic etiologies |
| 5 | Stroke of unknown etiology |
Presence of older previous infarcts
Multiple infarcts, especially in different arterial territories
Hemorrhagic infarcts
Infarct shows cortical extension
Large lenticulostriate infarct
Classic embolic sites
Stem occlusion of middle cerebral artery
Bilateral sylvian fissure infarcts
Cardioembolic Stroke: Clinical Caveats
A complete medical history provides important clues to the possibility of cardioembolism. The abrupt onset of neurological dysfunction with maximum deficit at the onset and the absence of a stuttering course and a severe headache are important clues that suggest cardioembolism. Seizures that accompany such a presentation also may suggest cardioembolism. These clinical features are not always diagnostic because emboli fragment and reocclusion presents in a nonabrupt manner in some instances. Brain imaging, either computed tomography or magnetic resonance imaging, provides useful clues to the presence of a possible embolic presentation (see Box 135.1 ). Additional clues include a history of palpitations or documented atrial fibrillation (AF) or other signs of systemic embolism involving other organs. Some studies have suggested that the most specific features for cardioembolism are infarcts in multiple territories and concurrent systemic embolism. , In the absence of other competing mechanisms of stroke, clinical and brain imaging data must be combined to identify the potential cardioembolic pathology. Thus, finding concomitant low-risk pathology, such as fibrin strands or uncomplicated mitral valve prolapse, cannot be used to infer causality. An important part of the evaluation is to identify the presence of increased intracranial pressure, as this may be a relative contraindication against the use of early TEE in low-risk patients or patients with a normal TTE. Inappropriate agitation/straining during the procedure may worsen increased intracranial pressure.
Cryptogenic Stroke
Stroke presumed to be cryptogenic may have an embolic component that may not be considered based on clinical assessment but may become more obvious after TTE. The link with patent foramen ovale (PFO) is well established in this population, especially in those 55 and younger. However, causality is more difficult to prove, and the outcome of intervention (closure of PFO) in the absence of recurrent neurological events is questionable.
Echocardiographic evaluation
Transthoracic echocardiography is the first-line imaging modality for evaluating cardioembolism because it is widely available, portable, cost-effective, and, with the use of harmonic imaging and contrast, enables most predisposing factors to cardioembolism to be evaluated. Transthoracic echocardiography should be geared toward identifying three major pathophysiological predispositions. First, a careful, systematic, anatomical evaluation should occur to identify masses, such as thrombus, tumors, and vegetations within the heart, and atheroma and its complications within the aorta. Conditions that predispose to thrombus formation, such as old myocardial infarcts, severe left ventricular (LV) dysfunction, and valvular disease (e.g., mitral stenosis) should be explored. Last, a systematic evaluation to exclude conditions that serve as conduits for possible paradoxical embolism, such as PFO and atrial septal defect, should be performed. Transesophageal echocardiography is superior to TTE in identifying thrombus within the left atrial appendage (LAA) and smaller vegetations, and in the evaluation of prosthetic valves for thrombus or endocarditis. Contrast or agitated saline contrast to identify shunts may be used to enhance clinical decision making. Transesophageal echocardiography also may be required to evaluate patients for conduits that may predispose to paradoxical embolism, such as PFO and small atrial septal defects, and is useful in identifying thoracic aortic problems, such as thrombus, atherosclerotic plaques, and aortic dissection. A normal transthoracic echo may warrant further investigation by TEE if the suspicion/clinical presentation of cardioembolism is high, as many of the aforementioned pathologies may be better identified using TEE.
Specific cardioembolic clinical situations
Atrial Fibrillation
Atrial fibrillation is the most common predisposition to cardioembolism. Echocardiography is crucial in differentiating whether AF is valvular or nonvalvular. This distinction is important because the risk of stroke is much higher with valvular AF and therapy may differ, such as in the use of novel anticoagulants, which currently are indicated only in nonvalvular AF. Furthermore, when assessing patients with nonvalvular AF for the use of anticoagulation using the CHA2DS2 VASc Score, identifying LV hypertrophy and a low ejection fraction is important and may influence clinical decision making. The most common site of thrombus formation is the LAA, although thrombus may be found anywhere within the left atrium.
Thrombus
Thrombus is a discrete echo-dense mass with defined margins that are distinct from the underlying wall. Ideally, thrombus should be seen in two different views. Thrombus may be found in the left ventricle, left atrium, or LAA. Transthoracic echocardiography is best to visualize thrombus within the left ventricle, as TEE is often inadequate at assessing the LV apex, which is often foreshortened and in the far field.
Left ventricular thrombus usually occurs when the underlying walls are abnormal (i.e., either hypokinetic or akinetic) or in aneurysms. In a postinfarction aneurysm, LV thrombus may be found in up to 50% of cases. If the thrombus is found on an underlying normal wall, it may represent a manifestation of a hypercoagulable state or, far less commonly, thrombus in transit from another site. Attention to detailed global and regional wall assessment of the left ventricle is required to identify not only wall abnormalities but also the overlying thrombus. This may require off-axis two-dimensional (2D) TTE, xPlane/biplane TTE imaging, or three-dimensional (3D) TTE. When the apex/walls cannot be adequately visualized, the use of contrast is mandatory to improve thrombus detection and function assessment. , Left ventricular thrombi must be distinguished from false tendons, trabeculae, and artifact. The exclusion of tumors can occasionally be challenging, as a tumor may develop over the thrombus. Cardioembolism is not an uncommon complication in isolated LV noncompaction, but vigilance in identifying the thrombus and distinguishing it from trabeculation is required ( Fig. 135.1 ). After LV thrombus identification, evaluation of whether it is layered, calcified, pedunculated, mobile or has central lucency will help determine the age of the thrombus. A central lucency may be associated with a more recently formed thrombus and have a greater potential for cardioembolism ( Fig. 135.2 ). It is also important to note that the mechanism of thrombus may not just relate to the underlying anatomical abnormality, but if there is concomitant stasis, as in low ejection fraction, or a possible accompanying hypercoagulable state (e.g., peripartum cardiomyopathy), LV thrombus is more likely to occur ( Fig. 135.3 ).
Stay updated, free articles. Join our Telegram channel
Full access? Get Clinical Tree
