9 Infective Endocarditis

Goals of Echocardiography in Infective Endocarditis

To contribute to the diagnosis of infective endocarditis (IE). The diagnosis of endocarditis is never based solely on imaging findings; imaging findings, although critical, must be part of a larger clinical picture.

To identify the location, number, size and mobility of vegetations

To determine whether complications of endocarditis have occurred

• Functional complications include insufficiency, fistulae, and stenosis/obstruction.

• Structural complications include abscesses, dehiscences, and false aneurysms.

Scanning Issues

Required Parameters to Obtain from Scanning

Scanning must investigate each valve in detail for vegetations and insufficiency. The aortic root and mitral annulus also must be investigated in detail for abscess and fistulae.

The diagnosis of IE is based on the following findings:

Bacteriologic—plausible blood cultures, with positive results

Any of the following signs on echocardiography

• Vegetations

• Abscesses of the aortic root

• Prosthetic valve dehiscence

• Fistulization

The new Duke criteria for the diagnosis of IE classify cases into “definite,” “possible,” and “rejected” categories on basis of two major and eight minor criteria. The new/modified criteria substantially increase the number of definite cases, as proven in a study that compared the new versus the old criteria and pathology correlation.¹ The criteria of the categories are presented in Boxes 9-1 and 9-2.

Reporting Issues

Unlike the assessment of aortic stenosis, where echocardiography alone can make the diagnosis, echocardiography alone cannot make a final diagnosis of endocarditis. The clinical aspects of the case need to be understood to establish the other entities that offer diagnostic contribution, and, as importantly, to establish a pretest (pre-echo) probability of endocarditis. Ideally, the case should be discussed with the referring physician to understand the background and the clinical grounds for suspicion.

Full consideration of the usual shortcomings of transthoracic echocardiography (TTE) for the diagnosis of IE must be recalled:

The inability to reliably image smaller (<5 mm vegetations)

The inability to reliably depict lesser involvement of the aortic annulus/root in detail, or determine the full extent of complex annular disruption.

The inability to image the atrial side of a mitral prosthesis, especially a mechanical prosthesis for vegetations

The inability to image the posterior half of an aortic valve prosthesis

Consideration also must be given to the shortcomings of transesophageal echocardiography (TEE) for the diagnosis of IE:

Difficulty imaging the aortic valve in the case of a mechanical mitral valve replacement, as it shadows imaging

Difficulty/impossibility of imaging the anterior aortic root in the presence of an aortic valve prosthesis

Difficulty/impossibility imaging the pulmonic valve in the case of an aortic valve replacement due to shadowing

Occasional false negatives/imperfect negative predictive values

Possible false positives—distinguish vegetations from

• Myxomatous disease of the mitral or aortic valves

• Lambl’s excrescences of the aortic valve

• Prosthetic valve strands or sutures

• Sclerosis or fibrocalcific degeneration

• Valve tumors

• Thrombi

Some cases will simply remain of intermediate or indeterminate probability of endocarditis.

Notes on Infective Endocarditis

IE is a necrotizing infection that eventually will destroy the valves or other cardiac structures it involves. Thus, valvular insufficiency and prosthesis dehiscence are expected findings and constitute important echocardiographic findings in favor of the diagnosis of IE. The echocardiographic hallmarks are as follows:

Evidence of tissue destruction

• Valve flail elements

• Valve insufficiency

• Fistula formation

• Valve perforations

• Abscess formation

• Dehiscence

Evidence of an infected mass (vegetation, abscess)

IE remains a clinical diagnosis, based on

• Clinical suspicion

• Presence of a systemic, usually febrile, illness

• Positive blood cultures establishing that the illness is an infection

• Imaging that establishes that the infection is within the heart

Echocardiographic Criteria of Infective Endocarditis²

Major criteria

• Oscillating intracardiac mass, with hazy/shaggy borders, without plausible alternate explanation

• Dehiscence of a valve prosthesis

• Abscess formation

• The development of new and significant valve insufficiency

Minor criterion

• Appearance of a lesion compatible with, but not highly specific for, a vegetation

Complications of Infective Endocarditis

Cardiac Complications

Congestive heart failure (CHF) and intractable CHF most commonly are due to the following:

Valvular destruction

• Perforation of a valve leaflet or cusp^*

• Flail or torn leaflet or cusp^*

• Aneurysm of a leaflet, cusp, sinus, or artery^*

Deep tissue destruction:

• Aortic annular or root abscess^*

• Myocardial (or septal) abscess, usually an extension of an aortic root abscess^*

• Fistulae (usually from the aortic root) to the left atrium, right atrium, and right ventricle^*

• Perforation of the interventricular septum causing a ventricular septal defect (VSD)^*

Other cardiac complications include the following:

Myocardial infarction due to coronary artery embolus (may be large or micro)^*

Papillary muscle rupture due to extension of infection from mitral valve IE, or from seeding of the papillary muscle from the jet of aortic insufficiency of aortic valve IE^*

Pericardial extension via:

Ring abscess

Mycotic aneurysm of the aorta into the pericardial sleeve

Septic coronary artery embolus

Myocardial abscess extending outward through the epicardium^*

Pericardio-mediastinal fistula

Valve prostheses

• Paravalvular insufficiency

• Dehiscence (i.e., rocking of the prosthesis and insufficiency)

• Thrombosis of the prosthesis^*

• Infection of intracardiac patches^*

Vascular, Noncardiac Complications of Infective Endocarditis

Metastatic Infection

Mycotic aneurysms, ruptured mycotic aneurysm, ruptured aorta

Ruptured aneurysm of a sinus of Valsalva^*

Neurologic Complications

Embolic cerebral infarctions

Meningitis

Mycotic aneurysms of cerebral arteries

Cerebral abscesses

Spinal cord infarction

Renal Complications

Renal infarction from emboli

Micro-emboli: “flea bitten” kidney

Macro-emboli

• Renal infarction

• Renal abscesses from septic emboli

Glomerulonephritis (focal and diffuse)

Terminology

Relapse: redevelopment of IE within 3 months of therapy

Recurrence: redevelopment of IE 3 months after therapy

“Early”: occurring <60 days after insertion of the prosthesis. Usually a Staphylococcus epidermidis or aureus infection acquired through incisions. Dominant (>50%) mortality.

“Late”: occurring >60 days after insertion of the prosthesis. Bacteriologic spectrum constitutes the usual for IE (e.g., Streptococcus viridans).

Dehiscence: tearing away of the sewing ring of a valve replacement from the annulus, resulting in excessive rocking of the prosthesis and usually ≥3+ insufficiency, and occasionally of hemolytic anemia

The risk of embolism and death in IE is nearly double when vegetation length is >15 mm.³

Cardiac Complications of Infective Endocarditis That May Be Apparent on Echocardiography

Valvular Insufficiency

Valvular insufficiency is the hallmark disturbance of IE. It is due to necrotizing destruction of valvular, annular, or sewing ring integrity; to impaired coaptation; or to an underlying abnormality. Valvular insufficiency is noted in 90% of patients.⁴

Heart Failure

Eighty percent of patients with IE and CHF have regurgitant valve lesions. Aortic insufficiency from acute aortic valve IE is the most common cause of death from IE, and commonly requires surgery.⁵

Abscesses

Abscesses may be echo-opaque (commonly) or echo-lucent (uncommonly), and usually are thick-walled. Many abscesses will, as the result of progressive necrotizing infection, erode into an adjacent cardiac cavity or the aorta, producing a false aneurysm or fistulous communication between chambers. If the abscess has not ruptured and contains pus, it is less apparent than if it has ruptured, and contains lucent blood. The septal abscess is the most difficult to evaluate, unless it has ruptured/emptied. Communication of the lumen of the abscess with a cardiac chamber cavity or the aorta is suggested by systolic bulging of the abscess, and is confirmed by color or pulsed-wave Doppler flow mapping. Most abscesses are located within or extending from the aortic root. Mitral annular abscesses are much less common.

Myocardial Abscesses

Myocardial abscesses are found in 20% of patients who die of IE. They may be apparent on echocardiography as single or multiple focal abnormalities, or as a generalized depression of myocardium, but it must be emphasized that echocardiography is not a sensitive test to depict myocardial abscesses. They occur most often in S. aureus and enterococcal infections, and rarely in S. viridans infections, and are most common in aortic valve IE. Septal abscesses may rupture and produce VSDs. Abscesses of the lower interventricular septum are classically to be suspected when the aortic valve conduction time increases and a left bundle branch block develops. The septal abscess is the most difficult to evaluate, unless it has ruptured/emptied.

Fistulae

Fistulae form by perforation of an abscess into another chamber or cavity. The Gerbode defect results in communication between the left ventricular outflow tract and the right atrium via the ventriculoatrial portion of the membranous septum, and may be congenital or result from aortic valve IE and fistula formation.

Pericardial Effusions

Pericardial effusions may result from either hematogenous dissemination or direct spread of the infective process of IE. The pericarditis of acute IE is usually purulent.

Myocardial Infarction

Myocardial infarction from coronary embolization may be manifest by wall motion abnormalities. It is most likely to occur with aortic valve endocarditis, given the proximity of aortic valve vegetations to the coronary ostia.

Myocarditis

Myocarditis develops from immune reaction or septic staining. It may be manifest as global myocardial dysfunction.

Native Valve Infective Endocarditis

Rheumatic heart disease underlies 40% to 50% of cases of IE. Underlying mitral insufficiency causes infection more often than does mitral stenosis.

As the incidence of rheumatic heart disease recedes, mitral valve prolapse underlies relatively more cases of IE—as many as 25% of some series.

Congenital heart disease underlies some cases of IE, particularly that which has shunt lesions (e.g., VSD, patent ductus arteriosus, mitral regurgitation, complex lesions, such as tetralogy of Fallot, and complex repairs). However, purely obstructive congenital lesions (e.g., pulmonary stenosis, aortic stenosis, coarctation) also may infect, as may bicuspid aortic valves.

Prosthetic Valve Infective Endocarditis

Echocardiographic Findings

Two-Dimensional and Real Time

Dehiscence of the valve ring, seen as rocking, excessive motion, or reduced prosthesis motion

“Fuzzy” appearance of the prosthesis image due to overlying vegetations or valve ring abscesses

M-Mode

Is the best means to depict the rocking motion of the prosthesis (e.g., mitral valve replacement)

Mitral valve replacement moves toward the left atrium in systole, not apically.

Doppler

For pressure gradients (which will increase in sepsis and with prosthesis insufficiency)

For presence and amount of prosthesis insufficiency

• Paravalvar insufficiency is the hallmark of mechanical prosthesis infection.

• Bioprostheses may develop paravalvar insufficiency when the sewing ring has allowed infection into the annulus, or transvalvar insufficiency when the infection has destroyed tissue leaflets

For evidence and location of fistulization

Recall that TEE is almost invariably needed to adequately evaluate MVRs comprehensively for all the sites of infection, insufficiency, and dehiscence.

Notes

Perivalvular/valve ring abscesses are a major pathologic finding. They have no consistent echocardiographic findings but may be evident by the following features:

An area of increased or complex echo-density

An area of lucency (if the pus has drained into the bloodstream)

Prosthetic valve rocking

Sinus of Valsalva aneurysm

Independent motion of the leaflet and the annulus due to devitalization of the integrity of the tissue of the annulus

Anterior aortic wall thickness >10 mm

Posterior aortic wall thickness >10 mm

Perivalvular density >14 mm⁶

If present, note systolic expansion of the abscess, or check for flow into and out of it—these findings indicate contiguity with a vascular channel. Valve ring abscesses may lead to paravalvular leak and dehiscence, occasionally to a VSD and/or other fistulous communication, such as aortic root to right ventricle or right atrial fistula. TTE lacks sensitivity for the detection of infective abscesses (about 15%).

“Early” prosthetic valve IE is the term usually applied to infection occurring within the first 60 days postoperatively. Staphylococci are the most common organisms (47.5%), and S. epidermidis is the most common subset (27% overall). The incidence of “early” prosthetic valve IE peaks at 15 days following the operation. The fatality rate is very high (about 75%).

“Late” prosthetic valve IE is the term usually applied to infection occurring later than the first 60 days postoperatively. The usual native valve organisms are seen (streptococci predominate, at about 42%). The case fatality rate is considerably less; about 10%.

Right-Heart Infective Endocarditis

Right-sided IE accounts for 5% to 10% of cases of most IE series, and is of rising incidence in many North American cities. The tricuspid valve is involved more often than is the pulmonic valve, at a ratio of 10 to 20 to 1. But both right-sided valves may be simultaneously infected. Frequently, pulmonic valve IE is associated with underlying congenital heart disease.

Right-sided IE may feature as part of a more complex disease process, for example, VSD with left-to-right flow, infected septal leaflet of the tricuspid valve (impact site of the VSD jet). Extracardiac manifestations predominate: 60% to 100% have either a “pulmonary emboli”-like or “pneumonia-like” picture, with little systemic arterial disease activity. Most are of “acute” clinical course.

S. aureus accounts for half of cases; Streptococcus pneumoniae, Neisseria gonorrhoeae, Streptococcus fecalis, S. viridans, and mixed flora account for most of the remainder.

Predisposing factors include skin infections, respiratory infections (S. pneumoniae), dental sepsis, septic abortion, pelvic infection, IV drug abuse, ethanol abuse, and immune compromise.

Pulmonary complications include pulmonary infarctions, septic pulmonary arteritis, pneumonia, cavitation, pleural infarction/effusion

The typical clinical course of right-sided IE is that of recurrent “pneumonia,” followed by hepatomegaly, jaundice, and, finally, renal failure in persistently febrile patients. How the course evolves depends largely on the virulence of the embolized organism: viridans rarely causes septic complications. Blood cultures often are negative initially and become positive after established pulmonary sepsis occurs. Pulmonary artery blood cultures may help. Right-sided IE caused by Pseudomonas species, fungi, or gram-negative bacteria may have a better prognosis with partial or complete (usually) tricuspid valve excision. If the pulmonary artery pressures are normal, the hemodynamic tolerance of tricuspid valve excision is fair.

Notes on Vegetations

Vegetations may be bacterial, fungal, noninfective (marantic), or rheumatic in origin. The differential diagnosis of a vegetation includes the following:

Tumor, especially papillary fibroelastoma

Wear-and-tear lesions (e.g., Lambl’s excrescences)

Valve strands

Flail valve elements

Artifact

Paravalvular structures

Myxomatous changes

Noninfective calcific degeneration

Vegetations generally take multiple weeks to form. S. aureus may produce large vegetations. Fungal vegetations often are the largest and may present as obstructive embolus to a large artery. Some cases of endocarditis occur without well-defined vegetations, the so-called “nonvegetant” endocarditis.

Marantic Vegetations

Noninfective (marantic) vegetations usually are not very large, and may be seen on both sides of leaflets. They may be seen in a number of scenarios, including systemic lupus erythematosus, anti-cardiolipin antibodies, and malignancy (especially pancreatic adenocarcinoma and lymphoma).

Localization of Vegetations

Vegetations characteristically occur on the low pressure side of valves (original model described by Rodbard in 1964)⁷ or at the impact site of a regurgitant jet.

In aortic insufficiency, jets may appear in a number of locations:

The underside of aortic valve leaflets

The anterior mitral leaflet, ventricular side

The anterior mitral leaflet chordae

In MR, they appear in the following locations:

The atrial side of mitral valve leaflets

The left atrial wall

Characteristic imaging features of vegetation are as follows:

Mobility

Occurrence on valve leaflets or sites of jet impact

Reflectiveness

Association with insufficiency

Usually have shaggy borders

Serial Assessment of Vegetations

Vegetations have been observed to shrink, remain the same size, or to increase in size with both appropriate and inappropriate antimicrobial therapy. Vegetations can persist after the IE illness. Typically, in appropriately treated infections, bacterial vegetations become smaller and more echoreflective over months after the illness.⁸

Significance of Vegetations and Their Size

Valve destruction, insufficiency, the risk of embolization, and the requirement for surgery are greater in patients in whom vegetations have been documented,^4,9,10

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Related

Related posts:

1. The Aortic Valve
2. Coronary Artery Disease: Ischemia, Infarction, and Complications
3. Pericardial Diseases
4. Mitral Insufficiency

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