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ARTICLE 10.1177/8756479305274930 JOURNAL OF DIAGNOSTIC MEDICAL SONOGRAPHY May/June 2005 INFECTIVE ENDOCARDITIS / Peters JDMS 21:192204 JDMS 21:192204 May/June 2005 May/June 2005 VOL. 21, NO. 3

Infective Endocarditis
PRISCILLA J. PETERS, BA, RDCS, FASE
Infective endocarditis is a life-threatening illness associated with significant morbidity and mortality. Previously a uniformly fatal disease, antibiotic therapy has reduced the mortality of native valve endocarditis to less than 20%. The incidence of infective endocarditis has not decreased, however, and 20,000 new cases are reported each year. Continued improvement in the prognosis of endocarditis is largely dependent on early and accurate diagnosis of the disease and its complications. Echocardiography has assumed an important role in the evaluation of infective endocarditis, both for the detection of vegetations and in the assessment of complications of the infectious process. Key words: endocarditis, cardiac abscess, vegetation, antibiotic therapy, microorganism Infective endocarditis (IE) is a life-threatening illness associated with significant morbidity and mortality. Previously a uniformly fatal disease, antibiotic therapy has reduced the mortality of native valve endocarditis to less than 20%. The incidence of IE has not decreased, however, and 20,000 new cases are reported each year.1 Risk factors have evolved: sclerotic disease in the elderly, prosthetic valve disease, mitral valve prolapse, nosocomial disease, hemodialysis, and intravenous drug abuse have replaced rheumatic heart disease as the principal risks for development of the disease.2,3 In addition, new organisms have emerged, and others have become drug resistant. Continued improvement in the prognosis of IE is largely dependent on early and accurate diagnosis of the disease and its complications. Since the first echocardiographic description of vegetations by Dillon et al. in 1973, echocardiography has assumed an important role in the evaluation of IE, both for the detection of vegetations and in the assessment of complications of the infectious process.4-6

In accordance with ACCME Standards, authors are required to disclose any commercial affiliations or financial interests that might be perceived as a real or apparent conflict of interest related to the content of their JDMS CME article. The author, Priscilla J. Peters, BA, RDCS, FASE, did not disclose any real or apparent conflict(s) of interest.

From Cooper University Hospital, Division of Cardiology, Echocardiography Laboratory, Camden, NJ. Correspondence: Priscilla J. Peters, Cooper University Hospital, Division of Cardiology, Echocardiography Laboratory, One Cooper Plaza, Camden, NJ 08103-1489. E-mail: peters-priscilla@ cooperhealth.edu. DOI: 10.1177/8756479305274930

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Introduction
Endocarditis is an infection of the endocardial surface of the heart caused by microorganisms. Vegetations are most likely to occur when there is damage to the endocardial surface. Heart valves are most commonly affected, but bacterial seeding may occur on mural endocardium in the setting of shunt lesions such as ventricular septal defect (VSD) and patent ductus arteriosus. Between 60% and 80% of patients with native valve endocarditis have predisposing cardiac lesions: mitral valve prolapse and congenital malformations are the most common structural abnormalities.7 Degenerative acquired sclerotic and calcific valve changes are the common underlying abnormality in older patients.2 Patients with a history of endocarditis are at risk for recurrence. Organisms that account for native valve endocarditis in the non-drug-abusing population are Streptococci (50%-70%) and Staphylococci (25%). Staphylococcus aureus (S. aureus) is an extremely aggressive organism (especially methicillin-resistant staph aureus, or MRSA), and the vegetations grow very quickly.8 Organisms that are abundant in the mouth, such as Streptococcus viridans, are common pathogens identified in younger patients. Streptococcus bovis is a common organism identified in the elderly; approximately 70% of those patients have colonic malignancies.9 In patients with nosocomial infections, less than 50% have predisposing risk factors. In the intravenous drug abuse (IVDA) population, most patients are males (3:1), and the mean age is 30 years. In IVDA patients, the tricuspid valve is the most common site of infection (54%), followed by the aortic valve (25%) and the mitral valve (20%). Most infected valves (> 60%) in the IVDA cohort are structurally normal, the organism is S. aureus, and the skin is the most common source of the bacteremia.10 Patients with prosthetic valves in place are at particularly high risk for infection; prosthetic valve endocarditis accounts for up to 20% of all cases of IE.11 Fungal endocarditis is uncommon and typically has a more indolent course than bacterial infections. Fungal endocarditis is difficult to treat medically. The mean age of patients with IE has changed from < 30 years in the 1920s to > 50 years in the 1980s; now, approximately 26% of patients with

IE are < 30 years, and 21% are > 60 years. Endocarditis is uncommon in children. Men are more commonly affected than women. Heart failure in infective endocarditis, almost always a result of valve dysfunction, is the leading indication for surgery and the principal cause of death. 12-14

Pathogenesis and Morphology

Certain pathogenetic mechanisms are typically operant in the development of infective endocarditis. Narrow high-pressure/low-pressure pathways, which result from incompetent valves and shunts such as restrictive VSDs, are associated with substantial gradients and a high degree of turbulence. This turbulence traumatizes the endothelium and results in the deposition of platelets and fibrin on the abnormal surface, leading to the formation of nonbacterial thrombotic endocarditis (NBTE). These sterile thrombi are generally the precursor to infected lesions. When bacteremia occurs (poor dentition, urinary tract infections, skin contaminants),* circulating microorganisms infiltrate the thrombus and proliferate. Once colonization of the thrombus occurs, the vegetation enlarges by further deposition of fibrin and platelets and further bacterial proliferation. This bacterial proliferation eventually leads to destruction of underlying cardiac tissue, with progression to leaflet perforation, severe incompetence, and abscess and aneurysm formation. Abscesses can be associated with life-threatening conduction abnormalities; severe valvular regurgitation may initiate the onset of heart failure.15 Large pedunculated vegetations may embolize with resultant neurologic, pulmonary, or vascular deficits. The events that result in endocarditis involving normal cardiac structures are probably different from those that occur with abnormal anatomy and are less well understood. The presence of NBTE is probably not necessary for endocarditis to occur in this setting. The organisms responsible for endocarditis on normal valves are typically very aggressive, especially resistant S. aureus.16 When bacterial seeding occurs

*Most cases of infective endocarditis are not preceded by procedures. Infective endocarditis can result from routine activities such as tooth brushing and chewing.

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FIG. 1. (A) Parasternal long axis view of mitral leaflet perforation (arrow). LA, left atrium. (B) Same patient demonstrating color flow through perforation.

on normal valves, bacteremia usually originates in the skin or the lungs. As visualized by echocardiography, vegetations appear as discrete, irregularly shaped, shaggy echogenic masses contiguous with valve leaflets, with acoustic properties different from the underlying cardiac structure. Vegetations may be pedunculated and dramatically mobile, or sessile, with only slight oscillation. The typical attachment is the atrial surface of the mitral and tricuspid valves, as well as the ventricular surface of the aortic and pulmonary valves. Because of their slow growth, fungal vegetations tend to be larger than bacterial masses at the time of diagnosis and are more likely to occlude the valve orifice. Vegetations can vary in size from a millimeter to several centimeters and may appear different in serial echocardiographic studies, as persistent infection, healing, or embolization may be operant. As vegetations commonly form on valves already diseased, reliable detection will be affected by underlying valve pathology (e.g., ruptured mitral chordae or dense annular calcification can make the secure diagnosis of vegetations precarious). Although not all vegetations change in appearance during the course, or at the termination of, antibiotic therapy, old healed or healing vegetations are usually smaller and more consolidated than their active

counterparts, appearing denser, consistent with the pathologic evolution of fibrosis and calcification.17 The distinction between active and healed vegetations can be problematic in patients with a previous history of endocarditis.

Valvular Heart Disease

Mitral vegetations are most likely to form on the atrial surface of a prolapsing leaflet. Vegetations may attach to one or both leaflets and generally do not interfere with leaflet motion, as might be expected with fibrotic or calcific infiltrates. Some data suggest that vegetations > 1 cm attached to the anterior leaflet pose a substantial risk for embolization.5,18 Careful interrogation of both leaflets in multiple scan planes is important to reliably assess the true size, mobility, and location of the vegetation. Some degree of valvular incompetence is almost always present, and the mechanism can vary from incomplete leaflet coaptation to leaflet perforation (Fig. 1). Pseudoaneurysms of the mitral valve may further result from leaflet perforation and will demonstrate marked systolic expansion due to communication with the left ventricular outflow tract; perforation of the aneurysm itself may occur. Pseudoaneurysms of the anterior mitral leaflet commonly result from extension of aortic

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FIG. 2. Large aortic valve vegetation (arrow).

endocarditis. If the infectious process extends through the supporting apparatus of the mitral valve, chordal rupture may result in a flail leaflet. Endocarditis of the aortic valve may involve congenitally malformed valves or those that have been compromised by rheumatic fever. In the elderly, vegetations can be found in areas of turbulence caused by acquired sclerotic or calcific disease.2,3 The lesions typically involve the ventricular surface of the leaflets and are focal, smudgyappearing clumps, usually with some degree of oscillation (Fig. 2). As aortic vegetations increase in size, they can prolapse into the outflow tract in diastole and through the aorta in systole. Aortic leaflet perforation and disruption, with attendant severe regurgitation and hemodynamic deterioration, can occur. Aortic endocarditis necessitates surgical intervention more frequently than isolated infection of the mitral valve.14,19 Normal variants of the aorta and aortic valve, such as Lambls excrescences and prominent nodules of Arantius, can be confused with vegetations. Involvement of the adjacent structures is a frequent complication in patients with aortic endocarditis. Root abscesses are found in up to 52% of patients at the time of aortic valve replace-

ment.15 A root abscess is purulent material contained within the fibrous capsule of the aorta without intraluminal communication (Fig. 3). Depending on the stage of the infection, abscesses usually appear as walled-off echolucent regions within the aortic annulus, initially without systolic expansion. Early in the course of the infection, the abscess may appear denser. Patients with aortic root abscesses may have significant electrocardiographic (ECG) conduction abnormalities. The abscess may eventually contain rupture of the infected segment of aorta, in which case pseudoaneurysm formation is marked by localized systolic expansion and diastolic collapse (Fig. 4). In addition to root abscess formation, infection can extend into the subaortic structures, both from direct extension of vegetative material and from surface destruction by the septic aortic regurgitant jet. The mitral-aortic intervalvular fibrosa (MAIVF) and the ventricular surface of the anterior mitral leaflet are particularly at risk. The MAIVF is the fibrous tissue between the anterior mitral leaflet and the posterior/left aortic cusps and aortic root. The MAIVF is relatively avascular and has little resistance to infection. Abscesses and aneurysms of the MAIVF are not uncommon in patients with aortic infection; the aneurysm can per-

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FIG. 3. Same patient as in Figure 2, demonstrating posterior aortic root abscess (arrow).

FIG. 4. Transesophageal echocardiogram image of complicated aortic root abscess (arrows) with large vegetation (*). AO, aorta. LV, left ventricle.

forate into the left atrium with significant systolic shunting (usually manifest as an eccentric jet of mitral regurgitation from the apical long axis view) (Fig. 5) or rupture into the pericardium, re-

sulting in pericardial tamponade. As noted in the study by Karalis et al.,20 which was among the first to provide a comprehensive description of these complications and their typical echocardiographic

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FIG. 5. Perforation of the mitral-aortic intervalvular fibrosa with left atrial extension of infected material (arrow).

appearance, early and reliable recognition of these subaortic complications is crucial to patient management for several reasons: (1) involvement of the MAIVF and the anterior mitral leaflet may produce severe mitral regurgitation in a patient already ill, (2) severe mitral valve involvement may present with clinical features suggestive of primary mitral valve disease, and (3) these complications can be overlooked at the time of aortic surgery when mitral surgery is indicated as well.20,21 Rarely, aortic vegetations can cause acute occlusion of coronary vessels with subsequent ischemia. Other uncommon complications of aortic endocarditis include extension of the infection into the interventricular septum (IVS), with resulting septal abscess formation and/or VSD (Figs. 6, 7), or perforation of the aorta/IVS (occurring below the level of the valve) into the right atrium, with extension of vegetative material and subsequent shunt flow (Fig. 8). This left ventricularright atrial communication represents an acquired Gerbode-type defect and demonstrates flow that can easily be confused with tricuspid regurgitation on echo (Fig. 9). In addition, aortic infection can extend antegrade into the sinuses of Valsalva, occasionally resulting in

rupture of a sinus. Rupture of the aorta at this level is always associated with continuous flow (and almost always associated with a continuous murmur) because the pressure in the central aorta is higher than that in the left ventricle (LV) in both systole and diastole. Tricuspid endocarditis should be suspected when an intravenous drug abuser presents with a fever and evidence of septic pulmonary emboli. Vegetations on the tricuspid valve tend to be larger than those seen on other valves and almost always attach to normal tricuspid leaflets. Vegetations usually attach to the atrial surface of the leaflets, but the supporting apparatus and ventricular surface can be involved as well. By the time an echocardiogram is performed in patients with IE of the tricuspid valve, most vegetations are quite large (> 1 cm), quite mobile, and not particularly subtle, in part because these patients commonly present much later in the course of their disease and because the offending organism is usually S. aureus.8 Patients with tricuspid endocarditis who are not IVDA have underlying congenital heart disease (typically small, high VSDs) or have a history of right-heart instrumentation, with or without in-

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FIG. 6. Large aortic vegetation (arrowhead) with interventricular septal abscess (arrow).

FIG. 7. Short axis of the left ventricle in the same patient as Figure 6, demonstrating interventricular septal abscess (arrow).

dwelling catheters. Right-heart failure can occur in tricuspid endocarditis. Dilatation of the right-heart chambers occurs relative to the time course of the disease, the degree of valve destruction and tricuspid regurgitation, and persistent septic pul-

monary emboli. Depending on right-heart pressure, the murmur of tricuspid regurgitation may be soft or absent entirely. As an isolated finding, pulmonary valve endocarditis is uncommon. It is most likely to oc-

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FIG. 8. Apical four-chamber view of same patient as Figure 6, demonstrating aortic lesion (arrow) and right atrium (RA) extension through perforation of the interventricular septum (arrowhead).

cur in the setting of underlying congenital abnormalities, especially subpulmonary ventricular septal defects, tetralogy of Fallot, patent ductus arteriosus (which may cause seeding of the pulmonary artery, not the valve leaflets directly), and valvular pulmonary stenosis. Hemodynamic monitoring lines can occasionally become infected and cause pulmonary leaflet destruction and vegetative seeding. Pulmonary valve endocarditis also occurs in the setting of IVDA, both as an isolated finding and in association with tricuspid infections. Surgery for right-sided endocarditis is less commonly undertaken than for left-sided lesions. Although not performed with much frequency now, an early surgical technique for both tricuspid and pulmonary endocarditis was a valvulectomy, which involved removing the infected valve without replacement. Transesophageal imaging should always be performed when prosthetic valves are in place, as acoustic shadowing and other artifacts can severely limit the transthoracic evaluation of mechanical prostheses.22-24 Vegetations begin on the sewing ring of mechanical valves and on the leaflets of biological valves. All aspects of the prosthesis must be

carefully interrogated for vegetations and disruption, with attendant prosthetic rocking. Thrombus and pannus ingrowth on mechanical prosthesis, as well as acquired degenerative changes of bioprosthetic leaflets, can be difficult to distinguish from vegetations, so definitive echocardiographic diagnosis, even with high-quality data, may not be possible. Torn sewing rings and mobile filamentous fibrin strands are common findings on the transesophageal evaluation of noninfected prosthetic valves and can easily be confused with vegetations. As it can occasionally be quite difficult to distinguish vegetations from other normal or noninfectious pathological processes, the thoughtful integration of all clinical and laboratory findings becomes extremely important when the echocardiographic findings are equivocal.

Discussion
Improvement in the prognosis of infective endocarditis rests on early and accurate diagnosis of the disease and its complications. Reduction in adverse outcomes is the leading clinical imperative in the modern management of IE.25 Given this man-

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FIG. 9. Color flow through interventricular septal perforation into the RA (right atrium) in the same patient as Figure 6.

date to expeditious and comprehensive diagnosis, it is unsettling that the accurate diagnosis of IE is frequently difficult to establish with certainty. The clinical manifestations of IE are numerous, can involve multiple organ systems, and are often nonspecific, so IE is included with many other disorders in the differential diagnosis of febrile illness. In 1981, Von Reyn and colleagues26 from the Beth Israel Hospital of Boston established definite, probable, possible, and rejected categories for the diagnosis of IE, based on strict

clinical case definitions. These criteria were immediately accepted in the community; they preceded widespread use of echocardiography and did not include application of echocardiographic findings. Because of difficulties in making the diagnosis based on Von Reyn parameters, the Duke Endocarditis Service recently proposed new diagnostic criteria (see Appendix A).27,28 Echocardiographic visualization of vegetations, when combined with other diagnostic criteria, now establishes the diagnosis of infective endocarditis.

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Although there is no question that the technology is still operator/interpreter dependent, the high detection rate of vegetations makes echo an extremely useful diagnostic tool. Transesophageal imaging is more sensitive than transthoracic imaging for the detection and characterization of vegetations and is especially useful to evaluate the complications of endocarditis such as abscesses and involvement of the intervalvular fibrosa; defining complications may alter the management course. Transesophageal imaging is indicated when the transthoracic study is negative but suspicion of IE is high, as in persistent unexplained bacteremia; as previously noted, transesophageal imaging should always be performed in patients with prosthetic valves.5,15,18-20,22-24 Serial echocardiography is performed to follow vegetation size and morphology, valvular regurgitation, and LV systolic function. There is still some debate regarding the correlation between the size, shape, and location of vegetations and eventual clinical outcome, although most series now confirm that complications (emboli, heart failure, and need for surgery) increase directly with vegetation size.29-31 Up to 50% of patients with IE have embolic events; central nervous system emboli have the highest mortality rates. In one early study, anterior mitral leaflet vegetations > 1 cm were associated with a higher incidence of embolic events than were vegetations on the aortic valve.5 A more recent study by Durante Mangoni et al.31 identified five risk factors for embolization in hospitalized patients: age, vegetation size, prothrombin activity, serum albumin levels, and C-reactive protein (CRP) levels. There was no relation between embolic events and gender, site of infection, or the microorganism. Although vegetation size alone did not identify a cohort of patients at high embolic risk, those patients who did embolize while in the hospital were younger, had larger vegetations, and had elevated CRP and lower serum albumin levels. Other studies have noted that although larger, more mobile vegetations had a higher incidence of embolization, vegetation size was not significantly different in patients with and without heart failure or in patients surviving or dying during the acute phase of the disease.29 The presence of vegetations, however, is a significant predictor for heart failure and the need for surgical intervention. Among patients with IE

requiring surgery for heart failure, aortic valve infection is more prevalent than mitral infection and is more often associated with extensive complications, including abscess formation.12 Because platelet aggregation plays an important role in the development of vegetations, there has been some interest in the role of aspirin in the treatment of active IE. One small study (nine patients) demonstrated a decrease in active vegetation size with aspirin. However, platelet anti-aggregants will simultaneously decrease platelet-induced bacterial killing.32* In addition, anti-aggregants may increase the risk of secondary bleeding. In a recent prospective, randomized study of aspirin in active endocarditis, Chan et al.33 concluded that the addition of aspirin did not reduce the risk of embolic events and increased the risk of bleeding. They and other authors agree that aspirin is not indicated in the early management of IE.

Conclusion
The diagnosis of infective endocarditis is often difficult to establish on the basis of clinical parameters alone. Echocardiography now plays an extremely important role in the evaluation of endocarditis by enabling the confident detection of vegetations and the reliable assessment of the anatomic extent of the disease and its related hemodynamic complications, as well as by providing follow-up evaluation during and after treatment. This crucial role that echocardiography now plays in the evaluation of infective endocarditis defines a significant and exciting responsibility for cardiac sonographers. As the technology improves, the diagnostic sensitivity increases, and an increased number of smaller vegetations can be detected earlier in the course of the disease. Because reduction in adverse outcomes is the leading clinical imperative of the modern management of endocarditis, technically thorough, comprehensive, and accurate, expeditious evaluation with echocardiography is essential.

*The paradoxical role of platelets in both the proliferation and destruction of bacteria is complex and beyond the scope of this review. The reader is referred to the extensive body of work by Yeaman and Bayer from UCLA for additional information on this intricate pathophysiologic process.

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Appendix A New Duke Criteria for Diagnosis of Infective Endocarditis (IE)

Definite
Pathologic evidence of vegetations or abscess at surgery or autopsy, or two of the following: 1. 2. Multiple positive blood cultures with no known extracardiac source Echocardiographic (transthoracic echocardiography or transesophageal echocardiogram) evidence of vegetation, abscess, or new prosthetic valve dehiscence At least two of the following: Fever New or changing murmur Microvascular phenomena such as Oslers nodes or Janeway lesions

Appendix B Glossary
Albumin One of a group of simple proteins widely distributed in plant and animal tissues. In the blood, albumin acts as a carrier molecule and helps to maintain blood volume and blood pressure. In humans, the principal function of albumin is to prevent plasma loss from the capillaries. Bacteremia Bacteria in the blood. Organisms that enter the body through skin, genitourinary, gastrointestinal, or respiratory tracts damage local cells and stimulate both the inflammatory and cell-mediated immune responses, resulting in the release of cytokines, which enhance immune defenses. When the organism overwhelms local defenses and enters the bloodstream, the resulting condition is septicemia. Depending on the organism involved, septicemia may be referred to as bacteremia, fungemia, or viremia. C-reactive protein (CRP) A globulin that precipitates the C-substance of pneumoccal cells (C-substance is a carbohydrate in the cell wall of pneumoccal cells). CRP is an abnormal protein detectable in blood only during the active phase of certain illnesses, especially rheumatic fever. Infective endocarditis Inflammation of the endocardial surface of the heart when microbes colonize the endocardium. The organism is usually a common bacterium, the site affected is usually a heart valve, and the characteristic lesion is a vegetation. Janeway lesion A small, painless, red-blue macular lesion found on the palms and soles in acute bacterial endocarditis, named after Edward Janeway, a U.S. physician. (Uncommon in the antibiotic era) Nosocomial infection Infection acquired in a hospital. Osler nodes Small, tender, cutaneous nodes, usually present in the fingers and toes, that may be seen in subacute endocarditis. The nodes are due to infected emboli from the

3.

Possible
Findings consistent with IE but not fulfilling above criteria

Rejected
1. 2. 3. Firm alternate diagnosis or Resolution of illness or No pathologic evidence of disease after antibiotic therapy for maximum of three days
6 28

Modified from Yvorchuk and Chan and Durack et al.

A positive echocardiogram (categorized in the Duke criteria as evidence of endocardial involvement) demonstrated (1) an oscillating intracardiac mass on the valve or supporting structures, in the path of regurgitant jets, or on implanted material, in the absence of an alternative anatomic explanation; (2) an abscess; or (3) new partial dehiscence of a prosthetic valve. Persistently positive blood cultures are defined as (1) recovery of a microorganism consistent with infective endocarditis from blood cultures drawn more than 12 hours apart or (2) all of three or a majority of four or more separate blood cultures, with first and last drawn at least one hour apart.*

*The bacteremia of infective endocarditis is continuous. Positive blood cultures from blood draws at least one hour apart are necessary to establish continuous bacteremia. Blood cultures are positive in 95% of cases of infective endocarditis.

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heart, named after Sir William Osler. (Uncommon in the antibiotic era) Platelet aggregation A clustering or coming together of substances. Platelets play an important role in blood coagulation, hemostasis, and blood thrombus formation. When a surface is injured, platelets adhere to each other and to the edges of the injury and form a plug that covers the area.

12.

13.

14.

15.

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OTHER 10.1177/8756479305277574 JOURNAL OF DIAGNOSTIC MEDICAL SONOGRAPHY May/June 2005 JDMS 21:000000 May/June 2005 JDMS 21:205206 JDMS 21:205206 May/June 2005 May/June 2005 VOL. 21, NO. 3

SDMS-JDMS CME TEST

Article: Infective Endocarditis Author: Priscilla J. Peters, BA, RDCS, FASE Category: Adult Echocardiography (AE) Credit: 1.0 Objectives: After studying the article titled Infective Endocarditis, you will be able to 1. Describe risk factors associated with infective endocarditis and characteristics of the disease in specific risk groups. 2. Analyze aspects of morbidity and mortality in infective endocarditis. 3. Sequence the events that lead to infective cardiac vegetations in patients with structural anomalies. 4. Describe characteristics of mitral, aortic, and pulmonic endocarditis. 5. Specify the instrumentation and technique required to evaluate prosthetic valves. 6. Specify factors associated with embolic events in patients with infective endocarditis. 1. Which of the following is not a risk factor for infective endocarditis? a. rheumatic fever b. mitral valve prolapse c. childhood asthma d. nosocomial infection 2. In intravenous drug users, the valve most commonly affected with endocarditis is the _____________ valve. a. aortic b. mitral c. pulmonic d. tricuspid 3. The principal cause of death from infective endocarditis is a. heart failure from valve dysfunction b. impaired left ventricular relaxation c. toxic shock d. embolic cerebral stroke 4. The initial event predisposing patients with structural anomalies to infective endocarditis is a. nonbacterial thrombotic endocarditis b. turbulence causing endothelial damage c. bacterial colonization of existing thrombi d. abscess formation 5. Which of the following statements is true regarding mitral vegetations? Mitral vegetations a. are typically found on the atrial surface of the valve b. may be difficult to differentiate from mitral valve prolapse c. often interfere with leaflet motion d. rarely embolize 6. Aortic endocarditis may involve adjacent structures and lead to additional pathology. Which of the following is not associated with aortic endocarditis? a. root abscesses b. mitral regurgitation c. occlusion of coronary vessels d. dilation of the right ventricle 7. Which of the following risk factors is not associated with pulmonic endocarditis? a. congenital abnormalities b. prosthetic valves c. intravenous drug use d. hemodynamic monitoring lines 8. When imaging prosthetic heart valves, it is essential to use a. transthoracic echocardiography b. transesophageal echocardiography c. intravascular ultrasound d. motion mode (M-mode) echocardiography 9. Which infectious valvular lesion is most likely to result in surgery? a. aortic b. mitral c. pulmonic d. tricuspid 10. In a study of risk factors associated with embolic events in patients hospitalized with infective endocarditis, there was no relationship between embolic events and a. vegetation size b. age c. gender d. prothrombin activity