Infective Endocarditis

10.1177/8756479305274930ARTICLE

JOURNAL OF DIAGNOSTIC MEDICAL SONOGRAPHY May/June 2005 VOL. 21, NO. 3

INFECTIVE ENDOCARDITIS / Peters

JDMS 21:192–204 May/June 2005

JDMS 21:192–204 May/June 2005

InfectiveEndocarditisPRISCILLA J. PETERS, BA, RDCS, FASE

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

Infective endocarditis is a life-threatening illnessassociated with significant morbidity and mor-tality. Previously a uniformly fatal disease, anti-biotic therapy has reduced the mortality ofnative valve endocarditis to less than 20%. Theincidence of infective endocarditis has not de-creased, however, and 20,000 new cases are re-ported each year. Continued improvement in theprognosis of endocarditis is largely dependenton early and accurate diagnosis of the diseaseand its complications. Echocardiography has as-sumed an important role in the evaluation of in-fective endocarditis, both for the detection ofvegetations and in the assessment of complicat-ions of the infectious process.

Key words: endocarditis, cardiac abscess, vege-tation, antibiotic therapy, microorganism

Infective endocarditis (IE) is a life-threateningillness associated with significant morbidity andmortality. Previously a uniformly fatal disease, an-tibiotic therapy has reduced the mortality of nativevalve endocarditis to less than 20%. The incidenceof IE has not decreased, however, and 20,000 newcases are reported each year.1 Risk factors haveevolved: sclerotic disease in the elderly, prostheticvalve disease, mitral valve prolapse, nosocomialdisease, hemodialysis, and intravenous drug abusehave replaced rheumatic heart disease as the princi-pal risks for development of the disease.2,3 In addi-tion, new organisms have emerged, and othershave become drug resistant. Continued improve-ment in the prognosis of IE is largely dependent onearly and accurate diagnosis of the disease and itscomplications. Since the first echocardiographicdescription of vegetations by Dillon et al. in 1973,echocardiography has assumed an important rolein the evaluation of IE, both for the detection ofvegetations and in the assessment of complicationsof the infectious process.4-6

192 JDMS 21:192–204 May/June 2005

From Cooper University Hospital, Division of Cardiology,Echocardiography Laboratory, Camden, NJ.

Correspondence: Priscilla J. Peters, Cooper University Hospital,Division of Cardiology, Echocardiography Laboratory, One CooperPlaza, Camden, NJ 08103-1489. E-mail: [email protected].

DOI: 10.1177/8756479305274930

INFECTIVE ENDOCARDITIS / Peters 193

Introduction

Endocarditis is an infection of the endocardialsurface of the heart caused by microorganisms.Vegetations are most likely to occur when there isdamage to the endocardial surface. Heart valves aremost commonly affected, but bacterial seedingmay occur on mural endocardium in the setting ofshunt lesions such as ventricular septal defect(VSD) and patent ductus arteriosus. Between 60%and 80% of patients with native valve endocarditishave predisposing cardiac lesions: mitral valveprolapse and congenital malformations are themost common structural abnormalities.7 Degenera-tive acquired sclerotic and calcific valve changesare the common underlying abnormality in olderpatients.2 Patients with a history of endocarditis areat risk for recurrence. Organisms that account fornative valve endocarditis in the non-drug-abusingpopulation are Streptococci (50%-70%) and Staph-ylococci (25%). Staphylococcus aureus (S. aureus)is an extremely aggressive organism (especiallymethicillin-resistant staph aureus, or MRSA), andthe vegetations grow very quickly.8 Organisms thatare abundant in the mouth, such as Streptococcusviridans, are common pathogens identified inyounger patients. Streptococcus bovis is a commonorganism identified in the elderly; approximately70% of those patients have colonic malignancies.9

In patients with nosocomial infections, less than50% have predisposing risk factors. In the intrave-nous drug abuse (IVDA) population, most patientsare males (3:1), and the mean age is 30 years. InIVDA patients, the tricuspid valve is the most com-mon site of infection (54%), followed by the aorticvalve (25%) and the mitral valve (20%). Most in-fected valves (> 60%) in the IVDA cohort arestructurally normal, the organism is S. aureus, andthe skin is the most common source of thebacteremia.10 Patients with prosthetic valves inplace are at particularly high risk for infection;prosthetic valve endocarditis accounts for up to20% of all cases of IE.11 Fungal endocarditis isuncommon and typically has a more indolentcourse than bacterial infections. Fungal endo-carditis is difficult to treat medically.

The mean age of patients with IE has changedfrom < 30 years in the 1920s to > 50 years in the1980s; now, approximately 26% of patients with

IE are < 30 years, and 21% are > 60 years. Endo-carditis is uncommon in children. Men are morecommonly affected than women. Heart failure ininfective endocarditis, almost always a result ofvalve dysfunction, is the leading indication for sur-gery and the principal cause of death.12-14

Pathogenesis and Morphology

Certain pathogenetic mechanisms are typicallyoperant in the development of infective endo-carditis. Narrow high-pressure/low-pressure path-ways, which result from incompetent valves andshunts such as restrictive VSDs, are associatedwith substantial gradients and a high degree of tur-bulence. This turbulence traumatizes the endothe-lium and results in the deposition of platelets andfibrin on the abnormal surface, leading to the for-mation of nonbacterial thrombotic endocarditis(NBTE). These sterile thrombi are generally theprecursor to infected lesions. When bacteremia oc-curs (poor dentition, urinary tract infections, skincontaminants),* circulating microorganisms infil-trate the thrombus and proliferate. Once coloniza-tion of the thrombus occurs, the vegetationenlarges by further deposition of fibrin and plate-lets and further bacterial proliferation. This bacte-rial proliferation eventually leads to destruction ofunderlying cardiac tissue, with progression to leaf-let perforation, severe incompetence, and abscessand aneurysm formation. Abscesses can be associ-ated with life-threatening conduction abnormali-ties; severe valvular regurgitation may initiate theonset of heart failure.15 Large pedunculatedvegetations may embolize with resultant neuro-logic, pulmonary, or vascular deficits. The eventsthat result in endocarditis involving normal cardiacstructures are probably different from those thatoccur with abnormal anatomy and are less well un-derstood. The presence of NBTE is probably notnecessary for endocarditis to occur in this setting.The organisms responsible for endocarditis on nor-mal valves are typically very aggressive, especiallyresistant S. aureus.16 When bacterial seeding occurs

*Most cases of infective endocarditis are not preceded byprocedures. Infective endocarditis can result from routine activitiessuch as tooth brushing and chewing.

on normal valves, bacteremia usually originates inthe skin or the lungs.

As visualized by echocardiography, vegetationsappear as discrete, irregularly shaped, shaggyechogenic masses contiguous with valve leaflets,with acoustic properties different from the underly-ing cardiac structure. Vegetations may be pedunc-ulated and dramatically mobile, or sessile, withonly slight oscillation. The typical attachment isthe atrial surface of the mitral and tricuspid valves,as well as the ventricular surface of the aortic andpulmonary valves. Because of their slow growth,fungal vegetations tend to be larger than bacterialmasses at the time of diagnosis and are more likelyto occlude the valve orifice. Vegetations can varyin size from a millimeter to several centimeters andmay appear different in serial echocardiographicstudies, as persistent infection, healing, orembolization may be operant. As vegetations com-monly form on valves already diseased, reliable de-tection will be affected by underlying valvepathology (e.g., ruptured mitral chordae or denseannular calcification can make the secure diagnosisof vegetations precarious). Although not allvegetations change in appearance during thecourse, or at the termination of, antibiotic therapy,old healed or healing vegetations are usuallysmaller and more consolidated than their active

counterparts, appearing denser, consistent with thepathologic evolution of fibrosis and calcification.17

The distinction between active and healedvegetations can be problematic in patients with aprevious history of endocarditis.

Valvular Heart Disease

Mitral vegetations are most likely to form on theatrial surface of a prolapsing leaflet. Vegetationsmay attach to one or both leaflets and generally donot interfere with leaflet motion, as might be ex-pected with fibrotic or calcific infiltrates. Somedata suggest that vegetations > 1 cm attached to theanterior leaflet pose a substantial risk forembolization.5,18 Careful interrogation of both leaf-lets in multiple scan planes is important to reliablyassess the true size, mobility, and location of thevegetation. Some degree of valvular incompetenceis almost always present, and the mechanism canvary from incomplete leaflet coaptation to leafletperforation (Fig. 1). Pseudoaneurysms of the mitralvalve may further result from leaflet perforationand will demonstrate marked systolic expansiondue to communication with the left ventricular out-flow tract; perforation of the aneurysm itself mayoccur. Pseudoaneurysms of the anterior mitral leaf-let commonly result from extension of aortic

194 JOURNAL OF DIAGNOSTIC MEDICAL SONOGRAPHY May/June 2005 VOL. 21, NO. 3

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


endocarditis. If the infectious process extendsthrough the supporting apparatus of the mitralvalve, chordal rupture may result in a flail leaflet.

Endocarditis of the aortic valve may involvecongenitally malformed valves or those that havebeen compromised by rheumatic fever. In the el-derly, vegetations can be found in areas of turbu-lence caused by acquired sclerotic or calcificdisease.2,3 The lesions typically involve the ventric-ular surface of the leaflets and are focal, “smudgy”-appearing clumps, usually with some degree of os-cillation (Fig. 2). As aortic vegetations increase insize, they can prolapse into the outflow tract in di-astole and through the aorta in systole. Aortic leaf-let perforation and disruption, with attendantsevere regurgitation and hemodynamic deteriora-tion, can occur. Aortic endocarditis necessitatessurgical intervention more frequently than isolatedinfection of the mitral valve.14,19 Normal variants ofthe aorta and aortic valve, such as Lambl’s excres-cences and prominent nodules of Arantius, can beconfused with vegetations.

Involvement of the adjacent structures is a fre-quent complication in patients with aorticendocarditis. Root abscesses are found in up to52% of patients at the time of aortic valve replace-

ment.15 A root abscess is purulent material con-tained within the fibrous capsule of the aorta with-out intraluminal communication (Fig. 3). Depend-ing on the stage of the infection, abscesses usuallyappear as “walled-off” echolucent regions withinthe aortic annulus, initially without systolic expan-sion. Early in the course of the infection, the ab-scess may appear denser. Patients with aortic rootabscesses may have significant electrocardiographic(ECG) conduction abnormalities. The abscess mayeventually contain rupture of the infected segmentof aorta, in which case pseudoaneurysm formationis marked by localized systolic expansion and dia-stolic collapse (Fig. 4). In addition to root abscessformation, infection can extend into the subaorticstructures, both from direct extension of vegetativematerial and from surface destruction by the septicaortic regurgitant jet. The mitral-aortic intervalvu-lar fibrosa (MAIVF) and the ventricular surface ofthe anterior mitral leaflet are particularly at risk.The MAIVF is the fibrous tissue between the ante-rior mitral leaflet and the posterior/left aortic cuspsand aortic root. The MAIVF is relatively avascularand has little resistance to infection. Abscesses andaneurysms of the MAIVF are not uncommon in pa-tients with aortic infection; the aneurysm can per-

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

forate into the left atrium with significant systolicshunting (usually manifest as an eccentric jet of“mitral regurgitation” from the apical long axisview) (Fig. 5) or rupture into the pericardium, re-

sulting in pericardial tamponade. As noted in thestudy by Karalis et al.,20 which was among the firstto provide a comprehensive description of thesecomplications and their typical echocardiographic


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.


appearance, early and reliable recognition of thesesubaortic complications is crucial to patient man-agement for several reasons: (1) involvement of theMAIVF and the anterior mitral leaflet may producesevere mitral regurgitation in a patient already ill,(2) severe mitral valve involvement may presentwith clinical features suggestive of primary mitralvalve disease, and (3) these complications can beoverlooked at the time of aortic surgery when mi-tral surgery is indicated as well.20,21

Rarely, aortic vegetations can cause acute occlu-sion of coronary vessels with subsequent ischemia.Other uncommon complications of aortic endo-carditis include extension of the infection into theinterventricular septum (IVS), with resulting septalabscess formation and/or VSD (Figs. 6, 7), or per-foration of the aorta/IVS (occurring below the levelof the valve) into the right atrium, with extension ofvegetative material and subsequent shunt flow(Fig. 8). This left ventricular–right atrial communi-cation represents an acquired Gerbode-type defectand demonstrates flow that can easily be confusedwith tricuspid regurgitation on echo (Fig. 9). In ad-dition, aortic infection can extend antegrade intothe sinuses of Valsalva, occasionally resulting in

rupture of a sinus. Rupture of the aorta at this levelis always associated with continuous flow (and al-most always associated with a continuous murmur)because the pressure in the central aorta is higherthan that in the left ventricle (LV) in both systoleand diastole.

Tricuspid endocarditis should be suspectedwhen an intravenous drug abuser presents with afever and evidence of septic pulmonary emboli.Vegetations on the tricuspid valve tend to be largerthan those seen on other valves and almost alwaysattach to normal tricuspid leaflets. Vegetationsusually attach to the atrial surface of the leaflets,but the supporting apparatus and ventricular sur-face can be involved as well. By the time anechocardiogram is performed in patients with IE ofthe tricuspid valve, most vegetations are quite large(> 1 cm), quite mobile, and not particularly subtle,in part because these patients commonly presentmuch later in the course of their disease and be-cause the offending organism is usually S. aureus.8

Patients with tricuspid endocarditis who are notIVDA have underlying congenital heart disease(typically small, high VSDs) or have a history ofright-heart instrumentation, with or without in-

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

dwelling catheters. Right-heart failure can occur intricuspid endocarditis. Dilatation of the right-heartchambers occurs relative to the time course of thedisease, the degree of valve destruction andtricuspid regurgitation, and persistent septic pul-

monary emboli. Depending on right-heartpressure, the murmur of tricuspid regurgitationmay be soft or absent entirely.

As an isolated finding, pulmonary valveendocarditis is uncommon. It is most likely to oc-


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).


cur in the setting of underlying congenital abnor-malities, especially subpulmonary ventricularseptal defects, tetralogy of Fallot, patent ductusarteriosus (which may cause seeding of the pulmo-nary artery, not the valve leaflets directly), and val-vular pulmonary stenosis. Hemodynamic monitor-ing lines can occasionally become infected andcause pulmonary leaflet destruction and vegetativeseeding. Pulmonary valve endocarditis also occursin the setting of IVDA, both as an isolated findingand in association with tricuspid infections. Sur-gery for right-sided endocarditis is less commonlyundertaken than for left-sided lesions. Althoughnot performed with much frequency now, an earlysurgical technique for both tricuspid and pulmo-nary endocarditis was a valvulectomy, which in-volved removing the infected valve withoutreplacement.

Transesophageal imaging should always be per-formed when prosthetic valves are in place, asacoustic shadowing and other artifacts can severelylimit the transthoracic evaluation of mechanicalprostheses.22-24 Vegetations begin on the sewingring of mechanical valves and on the leaflets of bio-logical valves. All aspects of the prosthesis must be

carefully interrogated for vegetations and disrup-tion, with attendant prosthetic rocking. Thrombusand pannus ingrowth on mechanical prosthesis, aswell as acquired degenerative changes ofbioprosthetic leaflets, can be difficult to distinguishfrom vegetations, so definitive echocardiographicdiagnosis, even with high-quality data, may not bepossible. Torn sewing rings and mobile filamen-tous fibrin strands are common findings on thetransesophageal evaluation of noninfected pros-thetic valves and can easily be confused withvegetations. As it can occasionally be quite diffi-cult to distinguish vegetations from other normal ornoninfectious pathological processes, the thought-ful integration of all clinical and laboratoryfindings becomes extremely important when theechocardiographic findings are equivocal.

Discussion

Improvement in the prognosis of infectiveendocarditis rests on early and accurate diagnosisof the disease and its complications. Reduction inadverse outcomes is the leading clinical imperativein the modern management of IE.25 Given this man-

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

date to expeditious and comprehensive diagnosis,it is unsettling that the accurate diagnosis of IE isfrequently difficult to establish with certainty. Theclinical manifestations of IE are numerous, can in-volve multiple organ systems, and are often non-specific, so IE is included with many otherdisorders in the differential diagnosis of febrile ill-ness. In 1981, Von Reyn and colleagues26 from theBeth Israel Hospital of Boston established “defi-nite,” “probable,” “possible,” and “rejected” cate-gories for the diagnosis of IE, based on strict

clinical case definitions. These criteria were imme-diately accepted in the community; they precededwidespread use of echocardiography and did notinclude application of echocardiographic findings.Because of difficulties in making the diagnosisbased on Von Reyn parameters, the Duke Endo-carditis Service recently proposed new diagnosticcriteria (see Appendix A).27,28

Echocardiographic visualization of vegetations,when combined with other diagnostic criteria, nowestablishes the diagnosis of infective endocarditis.


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


Although there is no question that the technology isstill operator/interpreter dependent, the high detec-tion rate of vegetations makes echo an extremelyuseful diagnostic tool. Transesophageal imaging ismore sensitive than transthoracic imaging for thedetection and characterization of vegetations and isespecially useful to evaluate the complications ofendocarditis such as abscesses and involvement ofthe intervalvular fibrosa; defining complicationsmay alter the management course. Transesophagealimaging is indicated when the transthoracic studyis negative but suspicion of IE is high, as in persis-tent unexplained bacteremia; as previously noted,transesophageal imaging should always be per-formed in patients with prosthetic valves.5,15,18-20,22-24

Serial echocardiography is performed to followvegetation size and morphology, valvular regurgi-tation, and LV systolic function.

There is still some debate regarding the correla-tion between the size, shape, and location ofvegetations and eventual clinical outcome, al-though most series now confirm that complications(emboli, heart failure, and need for surgery) in-crease directly with vegetation size.29-31 Up to 50%of patients with IE have embolic events; centralnervous system emboli have the highest mortalityrates. In one early study, anterior mitral leafletvegetations > 1 cm were associated with a higherincidence of embolic events than were vegetationson the aortic valve.5 A more recent study by Du-rante Mangoni et al.31 identified five risk factors forembolization in hospitalized patients: age, vegeta-tion size, prothrombin activity, serum albumin lev-els, and C-reactive protein (CRP) levels. There wasno relation between embolic events and gender,site of infection, or the microorganism. Althoughvegetation size alone did not identify a cohort ofpatients at high embolic risk, those patients whodid embolize while in the hospital were younger,had larger vegetations, and had elevated CRP andlower serum albumin levels. Other studies havenoted that although larger, more mobile vegeta-tions had a higher incidence of embolization, vege-tation size was not significantly different in pa-tients with and without heart failure or in patientssurviving or dying during the acute phase of thedisease.29 The presence of vegetations, however, isa significant predictor for heart failure and the needfor surgical intervention. Among patients with IE

requiring surgery for heart failure, aortic valve in-fection is more prevalent than mitral infection andis more often associated with extensive complica-tions, including abscess formation.12

Because platelet aggregation plays an importantrole in the development of vegetations, there hasbeen some interest in the role of aspirin in the treat-ment of active IE. One small study (nine patients)demonstrated a decrease in active vegetation sizewith aspirin. However, platelet anti-aggregantswill simultaneously decrease platelet-induced bac-terial killing.32* In addition, anti-aggregants mayincrease the risk of secondary bleeding. In a recentprospective, randomized study of aspirin in activeendocarditis, Chan et al.33 concluded that the addi-tion of aspirin did not reduce the risk of embolicevents and increased the risk of bleeding. They andother authors agree that aspirin is not indicated inthe early management of IE.

Conclusion

The diagnosis of infective endocarditis is oftendifficult to establish on the basis of clinical param-eters alone. Echocardiography now plays an ex-tremely important role in the evaluation ofendocarditis by enabling the confident detection ofvegetations and the reliable assessment of the ana-tomic extent of the disease and its relatedhemodynamic complications, as well as by provid-ing follow-up evaluation during and after treat-ment. This crucial role that echocardiography nowplays in the evaluation of infective endocarditis de-fines a significant and exciting responsibility forcardiac sonographers. As the technology improves,the diagnostic sensitivity increases, and an in-creased number of smaller vegetations can be de-tected earlier in the course of the disease. Becausereduction in adverse outcomes is the leading clini-cal imperative of the modern management of endo-carditis, technically thorough, comprehensive, andaccurate, expeditious evaluation with echocardi-ography is essential.

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

Appendix ANew Duke Criteria for Diagnosis of Infective

Endocarditis (IE)

DefinitePathologic evidence of vegetations or abscess at

surgery or autopsy, or two of the following:

1. Multiple positive blood cultures with no knownextracardiac source

2. Echocardiographic (transthoracic echocardi-ography or transesophageal echocardiogram)evidence of vegetation, abscess, or new pros-thetic valve dehiscence

3. At least two of the following:FeverNew or changing murmurMicrovascular phenomena such as Osler’s nodesor Janeway lesions

PossibleFindings consistent with IE but not fulfilling above

criteria

Rejected

1. Firm alternate diagnosis or2. Resolution of illness or3. No pathologic evidence of disease after

antibiotic therapy for maximum of three days

Modified from Yvorchuk and Chan6

and Durack et al.28

A positive echocardiogram (categorized in the Dukecriteria as evidence of endocardial involvement)demonstrated (1) an oscillating intracardiac mass on thevalve or supporting structures, in the path of regurgitantjets, or on implanted material, in the absence of analternative 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 infectiveendocarditis from blood cultures drawn more than 12hours apart or (2) all of three or a majority of four ormore separate blood cultures, with first and last drawn atleast one hour apart.*

Appendix BGlossary

Albumin One of a group of simple proteinswidely distributed in plant and animal tissues.In the blood, albumin acts as a carrier mole-cule and helps to maintain blood volume andblood pressure. In humans, the principalfunction of albumin is to prevent plasma lossfrom the capillaries.

Bacteremia Bacteria in the blood. Organismsthat enter the body through skin, genito-urinary, gastrointestinal, or respiratory tractsdamage local cells and stimulate both theinflammatory and cell-mediated immuneresponses, resulting in the release ofcytokines, which enhance immune defenses.When the organism overwhelms localdefenses and enters the bloodstream, theresulting condition is septicemia. Dependingon the organism involved, septicemia may bereferred to as bacteremia, fungemia, orviremia.

C-reactive protein (CRP) A globulin thatprecipitates the C-substance of pneumoccalcells (C-substance is a carbohydrate in thecell wall of pneumoccal cells). CRP is anabnormal protein detectable in blood onlyduring the active phase of certain illnesses,especially rheumatic fever.

Infective endocarditis Inflammation of theendocardial surface of the heart whenmicrobes colonize the endocardium. Theorganism is usually a common bacterium, thesite affected is usually a heart valve, and thecharacteristic lesion is a vegetation.

Janeway lesion A small, painless, red-bluemacular lesion found on the palms and solesin acute bacterial endocarditis, named afterEdward Janeway, a U.S. physician.(Uncommon in the antibiotic era)

Nosocomial infection Infection acquired in ahospital.

Osler nodes Small, tender, cutaneous nodes,usually present in the fingers and toes, thatmay be seen in subacute endocarditis. Thenodes are due to infected emboli from the


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


heart, named after Sir William Osler.(Uncommon in the antibiotic era)

Platelet aggregation A clustering or comingtogether of substances. Platelets play animportant role in blood coagulation,hemostasis, and blood thrombus formation.When a surface is injured, platelets adhere toeach other and to the edges of the injury andform a plug that covers the area.

References

1. Horstkotte D, Follath F, Gutschik E, et al, and the TaskForce on Infective Endocarditis of the European Societyof Cardiology: Guidelines on prevention, diagnosis andtreatment of infective endocarditis. Eur Heart J2004;25(3):267–276.

2. Di Salvo G, Thuny F, Rosenberg V, et al: Endocarditis inthe elderly: clinical, echocardiographic and prognosticfeatures. Eur Heart J 2003;24(17):1576–1583.

3. Spies C, Madison JR, Schatz IJ: Infective endocarditis inpatients with end-stage renal disease: clinical presenta-tion and outcome. Arch Intern Med 2004;164(1):71–75.

4. Dillon LC, Feigenbaum H, Konecke LL, Davis RH,Chang S: Echocardiographic manifestations of valvularvegetations. Am Heart J 1973;86:698–704.

5. Mugge A, Daniel WG, Frank G, Lichtlen PR:Echocardiography in infective endocarditis: reassess-ment of prognostic implications of vegetation size deter-mined by the transthoracic and transesophagealapproach. J Am Coll Cardiol 1989;14:631–638.

6. Yvorchuk KJ, Chan K: Applications of transthoracic andtransesophageal echocardiography in the diagnosis andmanagement of infective endocarditis. J Am SocEchocardiogr 1994;14:294–308.

7. Bright DK, Durack DT, Foster-Smith K, et al: Infectiveendocarditis. Infect Dis Clin North Am 1993;7:1–167.

8. Chang FY, MacDonald BB, Peacock JE Jr, et al: Prospec-tive multicenter study of Staphylococcus aureusbacteremia: incidence of infective endocarditis, risk fac-tors for mortality, and clinical impact of methicillin resis-tance. Med (Balt) 2003;82(5):322–332.

9. Gonzalez-Juanatey C, Gonzalez-Gay MA, Llorca J, et al:Infective endocarditis due to Streptococcus bovis in a se-ries of non-addict patients: clinical and morphologiccharacteristics of 20 cases and review of the literature.Can J Cardiol 2003;19(10):1139–1145.

10. Chang FY, Peacock JE Jr, Musher DM, et al: Staphylo-coccus aureus bacteremia: recurrence and the impact ofantibiotic treatment in a prospective multicenter study.Med (Balt) 2003;82(5):333–339.

11. Chu VH, Cabell CH, Benjamin DK Jr, et al: Early predic-tors of in-hospital death in infective endocarditis. Circu-lation 2004;109(14):1745–1749.

12. Delahaye F, Celard M, Roth O, de Gevigney G: Indica-tions and optimal timing for surgery in infectiveendocarditis. Heart 2004;90(6):618–620.

13. Larbalestier RI, Kinchla NM, Aranki SF, et al: Acute bac-terial endocarditis: optimizing surgical results. Circula-tion 1992;86(Suppl II):II68–II74.

14. Olaison L, Pettersson G: Current best practices andguidelines: indications for surgical intervention in infec-tive endocarditis. Cardiol Clin 2003;21(2):235–251.

15. Daniel WG, Mugge A, Martin RP, et al: Improvement inthe diagnosis of abscesses associated with endocarditisby transesophageal echocardiography. N Engl J Med1991;324:795–800.

16. Petti CA, Fowler VG Jr: Staphylococcus aureusbacteremia and endocarditis. Cardiol Clin 2003;21(2):219–233.

17. Vuille C, Nidorf M, Weyman A, Picard M: Natural his-tory of vegetations during successful treatment ofendocarditis. Am Heart J 1994;128:1200–1209.

18. Rohmann S, Erbel R, Gorge G, et al: Clinical relevance ofvegetation localization by transesophageal echocardi-ography in infective endocarditis. Eur Heart J 1992;12:446–452.

19. Sanfilippo AJ, Picard MH, Newell JB, et al: Echo-cardiographic assessment of patients with infectiveendocarditis: prediction of risk for complications. J AmColl Cardiol 1991;18:1191–1199.

20. Karalis DG, Bansal RC, Hauck AJ, et al: Trans- esopha-geal echocardiographic recognition of subaortic compli-cations in aortic valve endocarditis: clinical and surgicalimplications. Circulation 1992;86:353–362.

21. Sexton DJ, Spelman D: Current best practices and guide-lines: assessment and management of complications ininfective endocarditis. Cardiol Clin 2003;21(2):273–282.

22. Erbel R, Rohmann S, Drexler M, et al: Improved diagnos-tic value of echocardiography in patients with infectiveendocarditis by transesophageal approach: a prospectivestudy. Eur Heart J 1988;9:43–53.

23. Khanderia BK: Suspected bacterial endocarditis: to TEEor not to TEE. J Am Coll Cardiol 1993;21:222–224.

24. Shively BK, Gurule FT, Roldan CA, et al: Diagnosticvalue of transesophageal echocardiography comparedwith transthoracic echocardiography in infectiveendocarditis. J Am Coll Cardiol 1991;18:391–397.

25. Moreillon P, Que YA: Infective endocarditis. Lancet2004;363(9403):139–149.

26. Von Reyn CF, Levy BS, Arbeit RD, et al: Infectiveendocarditis: an analysis based on strict case definitions.Ann Int Med 1981;94(I):505–518.

27. Andres E, Bandoux C, Noel E, Goichot B, Schlienger JL,Blickle JF: Value of Von Reyn and Duke diagnostic crite-ria for infective endocarditis in internal medicine prac-tice: study of 38 cases. Eur J Intern Med 2003;14(7):411–414.

28. Durack DT, Lukes AS, Bright DK, and the DukeEndocarditis Service: New criteria for diagnosis of infec-tive endocarditis: utilization of specific echocardi-ographic findings. Am J Med 1994;96:200–209.


29. Anderson DJ, Goldstein LB, Wilkinson WE, et al: Strokelocation, characterization, severity, and outcomes in mi-tral vs. aortic endocarditis. Neurology 2003;61(10):1341–1346.

30. Deprele C, Berthelot P, Lemetayer F, et al: Risk factorsfor systemic emboli in infective endocarditis. ClinMicrobiol Infect 2004;10(1):46–53.

31. Durante Mangoni E, Adinolfi LE, Tripodi MF, et al: Riskfactors for “major” embolic events in hospitalized pa-

tients with infective endocarditis. Am Heart J2003;146(2):311–316.

32. Yeaman MR: Platelets in antimicrobial disease. Clin In-fect Dis 1997;25:951.

33. Chan KL, Dumesnil JG, Cujec B, et al, and the Investiga-tors of the Multicenter Aspirin Study in InfectiveEndocarditis: A randomized trial of aspirin on the risk ofembolic events in patients with infective endocarditis. JAm Coll Cardiol 2003;42(5):775–780.

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SDMS-JDMS CME TESTArticle: Infective EndocarditisAuthor: Priscilla J. Peters, BA, RDCS, FASECategory: Adult Echocardiography (AE)Credit: 1.0

Objectives: After studying the article titled “InfectiveEndocarditis,” you will be able to

1. Describe risk factors associated with infectiveendocarditis and characteristics of the disease in specificrisk groups.

2. Analyze aspects of morbidity and mortality in infectiveendocarditis.

3. Sequence the events that lead to infective cardiacvegetations in patients with structural anomalies.

4. Describe characteristics of mitral, aortic, and pulmonicendocarditis.

5. Specify the instrumentation and technique required toevaluate prosthetic valves.

6. Specify factors associated with embolic events in patientswith infective endocarditis.

1. Which of the following is not a risk factor for infectiveendocarditis?a. rheumatic feverb. mitral valve prolapsec. childhood asthmad. nosocomial infection

2. In intravenous drug users, the valve most commonlyaffected with endocarditis is the _____________ valve.a. aorticb. mitralc. pulmonicd. tricuspid

3. The principal cause of death from infective endocarditis isa. heart failure from valve dysfunctionb. impaired left ventricular relaxationc. toxic shockd. embolic cerebral stroke

4. The initial event predisposing patients with structuralanomalies to infective endocarditis isa. nonbacterial thrombotic endocarditisb. turbulence causing endothelial damagec. bacterial colonization of existing thrombid. abscess formation

5. Which of the following statements is true regarding mitralvegetations? Mitral vegetationsa. are typically found on the atrial surface of the valveb. may be difficult to differentiate from mitral valve pro-

lapsec. often interfere with leaflet motiond. rarely embolize

6. Aortic endocarditis may involve adjacent structures andlead to additional pathology. Which of the following is notassociated with aortic endocarditis?a. root abscessesb. mitral regurgitationc. occlusion of coronary vesselsd. dilation of the right ventricle

7. Which of the following risk factors is not associated withpulmonic endocarditis?a. congenital abnormalitiesb. prosthetic valvesc. intravenous drug used. hemodynamic monitoring lines

8. When imaging prosthetic heart valves, it is essential to usea. transthoracic echocardiographyb. transesophageal echocardiographyc. intravascular ultrasoundd. motion mode (M-mode) echocardiography

9. Which infectious valvular lesion is most likely to result insurgery?a. aorticb. mitralc. pulmonicd. tricuspid

10. In a study of risk factors associated with embolic events inpatients hospitalized with infective endocarditis, therewas no relationship between embolic events anda. vegetation sizeb. agec. genderd. prothrombin activity

Infective Endocarditis

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