Early steps in bacterial valve colonization . (a) Colonization of damaged epithelium: exposed stromal cells and extracellular matrix proteins trigger deposition of fibrin-platelet clots to which Streptococci bind (upper panel); fibrin-adherent Streptococci attract monocytes and induce them to produce tissue-factor activity (TFA) and cytokines (middle panel); these mediators activate coagulation cascade, attract and activate blood platelets, and induce cytokine, integrin, and TFA production from neighboring endothelial cells (lower panel), encouraging vegetation growth. (b) Colonization of inflamed valve tissues: in response to local inflammation, endothelial cells express integrins that bind plasma fibronectin, which microorganisms adhere to via wall-attached fibronectin-binding proteins, resulting in endothelial internalization of bacteria (upper panel); in response to invasion, endothelial cells produce TFA and cytokines, triggering blood clotting and extension of inflammation, and promoting formation of the vegetation (middle panel); internalized bacteria eventually lyse endothelial cells (green cells) by secreting membrane-active proteins—e.g., hemolysins (lower panel). From Philippe Moreillon, Yok-Ai Que. Infective endocarditis. The Lancet. 2004;363(9403):139–49. Reproduced with permission from Elsevier Limited
Vegetations on the mitral valve (arrows) in a patient with infective endocarditis [Image courtesy of Dr. Edwin P. Ewing Jr. and the Centers for Disease Control and Prevention (CDC)]
Organism-related factors include virulence and adherence properties, and obviously procedures predisposing to bacteremia such as invasive dental procedures, colonoscopy, and insertion of indwelling hemodialysis catheters play an important role.
Classification
Traditionally, endocarditis was classified into acute, subacute, and chronic depending on clinical course. Acute native valve endocarditis usually displays a rapidly progressive course with high mortality rates typically caused by virulent organisms such at Staphylococcus aureus or group B Streptococci. The course in subacute/chronic endocarditis is more indolent and associated with more nonspecific symptoms, typically associated with less virulent organisms. Other classifications differentiate between native and prosthetic valve endocarditis, endocarditis associated with intravenous drug use and right- and left-sided endocarditis. Classification is now mainly based on defining the clinical setting, organism, location, and mode of acquisition as these factors are more important in guiding choice of treatment strategy and outcome.
Microbiology of Infective Endocarditis
Microbiologic etiology in 2781 patients with definite infective endocarditis
Microbial etiology | Number (%) of patients | |||
|---|---|---|---|---|
Native valve IE | Intracardiac device IE | |||
Drug abusers (n = 237) | Not drug abusers (n = 1644) | PVIE (n = 463) | Other devicesa (n = 172) | |
Staphylococcus aureus | 160 (68) | 457 (28) | 129 (23) | 60 (35) |
Coagulase-negative staphylococci | 7 (3) | 148 (9) | 95 (17) | 45 (26) |
Viridans group streptococci | 24 (10) | 345 (21) | 70 (12) | 14 (8) |
Streptococcus gallolyticus b | 3 (1) | 119 (7) | 29 (5) | 5 (3) |
Other streptococcic | 5 (2) | 118 (7) | 26 (5) | 7 (4) |
Enterococcus species | 11 (5) | 179 (11) | 70 (12) | 10 (6) |
HACEK groupd | 0 (0) | 30 (2) | 13 (2) | 1 (0.5) |
Othere | 6 (3) | 62 (4) | 38 (7) | 10 (6) |
Fungi/yeast | 3 (1) | 16 (1) | 23 (4) | 2 (1) |
Polymicrobial | 6 (3) | 16 (1) | 5 (0.8) | 0 (0) |
Negative cultures | 12 (5) | 154 (9) | 65 (12) | 18 (11) |
Coagulase-negative staphylococci (CNS) are an infrequent cause of native valve endocarditis. The infection is healthcare associated in one-half of patients, with a large proportion of patients having an indwelling pacemaker or implantable defibrillator. Compared with patients who have S. aureus native valve endocarditis, patients with CNS IE have a much more indolent course and are less likely to have vascular or immunologic evidence of infective endocarditis on physical examination. Heart failure is a frequent complication (>40%) and mortality rates are substantial (25%) [15]. Coagulase-negative staphylococci are a common cause of prosthetic valve endocarditis, with nearly one-half of cases occurring between 60 and 365 days following valve replacement [16]. One-half of patients develop intracardiac abscesses; mortality is approximately 24%.
Viridans streptococci (S. mitis, S. sanguis, S. mitior, S. mutans) are less frequent causes of infective endocarditis with the decreasing prevalence of rheumatic heart disease. These organisms cause a subacute syndrome resulting in symptoms that can last weeks to months. Valvular complications are less common than in IE cases caused by S. aureus. Organisms previously referred to as “nutritionally-deficient streptococci ” include Abiotrophia defectiva and Granulicatella adiacens. Identification of these bacteria is more difficult because of their slow growth and the requirement for addition of pyridoxal hydrochloride to culture media. These organisms have been associated with large vegetations, embolic phenomena, and valvular destruction [17].
Organisms, formerly known as Streptococcus bovis , have undergone taxonomic reclassification, although this reclassification has not been enthusiastically embraced. S. gallolyticus is the newly recognized name for S. bovis biotype I. These organisms, usually categorized as group D streptococci, can occasionally be erroneously identified as viridans streptococci by the laboratory. S. gallolyticus causes disease most commonly in elderly individuals, usually with some underlying chronic illnesses. Up to 60% of patients with infective endocarditis due to S. gallolyticus will ultimately be found to have a concomitant adenoma or carcinoma of the bowel upon thorough investigation. Therefore, any patient with infective endocarditis due to this organism warrants an evaluation for gastrointestinal disorders [18].
Infective endocarditis due to Streptococcus pneumoniae is uncommon, accounting for only 1.4% of cases of endocarditis in one large Spanish cohort [19]. It is accompanied by a substantial mortality rate, in excess of 35%, because the diagnosis of endocarditis is often missed, overshadowed by other manifestations of pneumococcal disease, such as pneumonia and meningitis. Left heart failure is common due to aortic or mitral valvular involvement.
Enterococcal species are now the third most common cause of infective endocarditis with Enterococcus faecalis accounting for 90% of these cases and with E. faecium being less frequently implicated. These organisms tend to affect the elderly and debilitated, frequently patients with underlying cardiac disorders or valvular prostheses. Twenty-five percent of cases are healthcare associated, 30% of which affect prosthetic valves. Recently, trends in North America indicate an increasing number of cases caused by antimicrobial-resistant E. faecium strains. The mortality rate for enterococcal endocarditis has not changed according to recent surveys, ranging between 11 and 18% [20].
HACEK is an acronym assigned to a group of fastidious, gram-negative bacteria that colonize the oropharynx and are responsible for about 1.4% of cases of infective endocarditis. Organisms in this group include Haemophilus parainfluenzae, Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans, A. aphrophilus, A. paraphrophilus, A. snegnis, Cardiobacterium hominis, C. valvarum, Eikenella corrodens, Kingella kingii, and K. denitrificans. HACEK organisms tend to cause disease in younger individuals, and produce a subacute syndrome characterized by a higher prevalence of immunologic and vascular phenomena, including emboli. Patients infected with HACEK organisms suffer from heart failure less frequently than IE caused by other agents. Despite the higher incidence of embolic manifestations, the overall prognosis of endocarditis due to the HACEK group of organisms tends to be excellent with a lower mortality (4%), and good outcomes with either medical or surgical therapies [21].
Non-HACEK gram-negative bacilli are unusual causes of infective endocarditis, and include various members of the Enterobacteriaceae and Pseudomonas spp., most frequently. The portal of entry is also changing. While previously, parenteral drug abusers were more commonly afflicted, recent data indicate that the disease is often nosocomially acquired, and involvement of implanted endovascular devices is frequent. Forty percent of cases occur on native valves, and 60% on prosthetic valves and devices. These patients are more likely to have undergone previous invasive gastrointestinal or genitourinary procedures before diagnosis of IE, with symptoms frequently being present for longer than a month [22, 23].
Fungal causes of endocarditis account for 2–4% of all cases [24]. Several different host risk factors predispose to infection by fungi, including parenteral drug abuse, individuals with indwelling vascular catheters and prosthetic devices, and patients with a compromised immune system. Clinical manifestations of fungal endocarditis are nonspecific, although vascular embolic manifestations are not uncommon. Candida spp. are the most frequently implicated fungi, with C. albicans and non-albicans Candida accounting for equal numbers; however, recent data suggests an increase in the frequency of non-albicans Candida spp. which has significant implications for antifungal therapy. Aspergillus IE most commonly occurs as a prosthetic valve infection, and can be difficult to diagnosis because of the infrequency of positive blood cultures; diagnosis is occasionally made from examination of embolectomy specimens.
Despite improved blood culture systems, the increased utilization of molecular biological techniques and serological methodologies, 5–10% of cases of endocarditis are still unidentified. Culture negative cases can result from previous antibiotic therapy, endocarditis due to fastidious organisms, and true blood culture negative cases that result from organisms that cannot be grown using conventional techniques. The latter group includes such organisms as Coxiella burnetti, Bartonella sp., and Tropheryma whipplei, the causative agent of Whipple’s disease [25].
Diagnosis
Key to the outcome of IE is the rapid identification of patients with highly probable or definite IE and subsequent institution of treatment (antibiotics with and without surgery). Diagnosis is made based on a combination of clinical, microbiologic, and echocardiographic features. Although certain guidelines such as the Duke criteria can assist in diagnosing IE, a comprehensive individual evaluation is critical.
Clinical Features
The clinical manifestations of IE can range from subtle and nonspecific symptoms to fulminant symptoms. The rate of progression depends on the extent of preexisting cardiac disease, virulence of the organism, and age and immunity of the patient. The diagnosis of endocarditis is straightforward in patients who present with the four cardinal Oslerian manifestations of IE: the presence of persistent bacteremia or fungemia, the presence of active valvulitis, the occurrence of large-vessel embolic events, and the presence of immunologic vascular phenomena. In many patients, however, especially patients with right-sided endocarditis, the peripheral stigmata are absent.
Symptoms
Fever is almost universal and is present in 80–90% of the patients. However, fever is less frequent in the elderly and immunocompromised patients, and hence a high index of suspicion and low threshold for investigation to exclude IE are essential in these groups. Patients can present with symptoms of heart failure, neurologic symptoms and demonstrate symptoms from embolic phenomena. Other nonspecific symptoms that are observed include fatigue, weight loss, malaise, chills, night sweats, arthralgias, and myalgias, especially back pain.
Physical Findings
Virtually all organ systems can be affected by IE. Thus, a comprehensive physical exam is critical in recognizing signs that may suggest IE. Cardiovascular exam may demonstrate new or changing murmurs indicative of valve damage, which are more prevalent in acute endocarditis and are frequently harbingers of heart failure. However, murmurs may be absent with right-sided endocarditis or intracardiac device infection. The murmur of acute and fulminant aortic regurgitation or mitral regurgitation may also be particularly difficult to hear. Signs of congestive heart failure may be present, and depending on the acuity of the disease process, patients’ symptoms can range from mild heart failure symptoms to acute decompensated heart failure with hemodynamic compromise.
Neurologic findings are most commonly caused by embolic complications of endocarditis. They include embolic strokes, intracranial hemorrhage secondary to rupture of mycotic aneurysms and less frequently meningitis, brain abscess or encephalopathy.
Various mucocutaneous manifestations of endocarditis are often observed. Petechiae are present in 20–40% of patients presenting with IE and can be found on the conjunctiva, buccal or palatal mucosa and extremities. Splinter hemorrhages are red, linear, flame-shaped streaks seen in the proximal nail bed of fingers or toes. Whereas both petechiae and splinter hemorrhages are nonspecific, Osler’s nodes, Janeway lesions, and Roth spots are more specific for IE. Osler’s nodes are small, tender, violaceous, subcutaneous nodules usually seen in the pulp of the digits. Roth spots are retinal hemorrhages with a pale center. Osler’s nodes and Roth spots are a result of immune complex deposition. Janeway lesions are non-tender, erythematous skin lesions that often appear in crops on the palms or soles and are a result of septic emboli to the skin with formation of microabscesses.
Other organ manifestations include abdominal symptoms due to bowel ischemia secondary to emboli to mesenteric arteries. Splenomegaly can be encountered and is the result of splenic infarcts and/or activation of the immune system. Flank tenderness can be present due to renal infarction as a result of emboli and a splenic friction rub may be present in cases of embolic splenic infarction.
Diagnosis of infective endocarditis based on Duke criteria
Definitive IE Pathological criteria • Microorganisms demonstrated by culture or histological examination of a vegetation, a vegetation that has embolized, or an intracardiac abscess specimen or • Pathological lesions; vegetation or intracardiac abscess confirmed by histological examination showing active endocarditis Clinical criteria (using definitions listed in Table 3.3 ) • Two major criteria or • One major criterion and three minor criteria or • Five minor criteria |
Possible IE • One major criterion and one minor criterion or • Three minor criteria |
Rejected IE • Firm alternative diagnosis explaining evidence of IE or • Resolution of IE syndrome with antibiotic therapy for ≤4 days or • No pathological evidence of IE at surgery or autopsy, with antibiotic therapy for ≤4 days |
Definition of terms used in the modified Duke criteria for the diagnosis of IE
Major criteria Positive blood cultures • Typical microorganisms consistent with IE from two separate blood cultures: Viridans streptococci, Streptococcus bovis, HACEK group, Staphylococcus aureus or community acquired enterococci in the absence of a primary focus or • Microorganisms consistent with IE from persistently positive blood cultures defined: at least two positive cultures of blood samples drawn >12 h apart; or all of three or a majority of four or more separate cultures (with first and last sample drawn at least 1 h apart); or • Single positive blood culture for Coxiella burnetii or anti-phase 1 IgG antibody titer >1:800 Evidence of endocardial involvement • Echocardiogram positive for IE defined as follows: − 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 or − Abscess or − New partial dehiscence of prosthetic valve • New valvular regurgitation (worsening or changing or preexisting murmur not sufficient) |
Minor criteria • Predisposition, predisposing heart condition, or intravenous drug use • Fever, temperature ≥38 °C • Vascular phenomena, major arterial emboli, septic pulmonary infarcts, mycotic aneurysm, intracranial hemorrhage, conjunctival hemorrhages, and Janeway’s lesions • Immunologic phenomena: glomerulonephritis, Osler’s nodes, Roth’s spots, and rheumatoid factor • Microbiological evidence: positive blood culture but does not meet a major criterion as noted above or serological evidence of active infection with organism consistent with IE |
Definite diagnosis of IE requires pathologic evidence (histologic and/or bacteriologic examination of vegetations, intracardiac abscess or emboli demonstrating typical pathology or cultured microorganisms) or clinical evidence that includes two major criteria or one major criterion and three minor criteria or five minor criteria.
Possible cases of IE do not meet the criteria for definite IE but satisfy one major criterion and one minor criterion or three minor criteria.
A rejected diagnosis of IE is present when there is no pathological evidence of IE at autopsy or surgery, rapid resolution of the clinical syndrome with either no treatment or short-term antibiotic therapy or when a firm alternative diagnosis has been found. The usefulness of the Duke criteria is limited in early stages of IE, in the setting of negative blood cultures and in the presence of prosthetic valves and device leads [29].
Microbiologic Diagnosis
Blood cultures remain the cornerstones for the diagnosis of IE and therefore should be obtained prior to initiation of antibiotic therapy. Three separate sets of blood cultures, each from a separate venipuncture site, obtained over 24 h, are recommended to evaluate patients with suspected endocarditis. Each set should include a bottle containing an aerobic and anaerobic medium, and at least 10 mL of blood should be placed in each bottle. Blood cultures may be collected at any time; they do not need to be obtained at the time of fever or chills since patients with IE typically have continuous bacteremia. With this strategy, a microbiological diagnosis can be made in ~90% of patients. However, blood cultures can be negative in up to 30% of cases, often due to prior exposure to antibiotics or infection with intracellular bacteria, fungi, or fastidious organisms [30, 31]. A microbiologic diagnosis in these situations may require special media, longer culture time (due to slower growth of certain organisms), and serologic tests. Serologic tests can be used to make diagnosis of endocarditis caused by Brucella species, Legionella species, Bartonella species, Coxiella brunetti, or Chlamydia species. Special techniques such as polymerase chain reaction (PCR) allow rapid and reliable detection of fastidious and non-culturable microorganisms. Moreover, if patients go to surgery, organisms can be identified in the valve tissue by culturing, immunohistochemical staining, or PCR.
Other abnormal laboratory tests that can be encountered include anemia, which is found in 70–90% of patients but may be absent in acute endocarditis. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) are elevated in most patients with IE. A CRP level that is elevated at baseline and normalizes with therapy is associated with good outcomes [32]. Similarly, the outcome of surgery in patients with increasing preoperative CRP levels has been demonstrated to be poor [33]. Hematuria and proteinuria may be present in patients with renal dysfunction due to immune-mediated glomerulonephritis or septic emboli causing renal infarction.
Imaging
Echocardiography
Echocardiography is central to the diagnosis and management of IE. Not only does echocardiography provide evidence of IE, it also provides important data regarding the hemodynamic consequences of the infection and helps predict short- and long-term prognosis. Furthermore, it helps in identifying patients at high risk for complications, diagnoses those complications, and identifies patients who benefit from surgery.
Echocardiography should be performed as soon as possible after the diagnosis of IE is suspected. Transthoracic echocardiography (TTE) is usually performed first in all cases, because it is a noninvasive technique that provides rapid, useful information for both the diagnosis and the assessment of IE severity. However, image resolution is limited by TTE and lesions <3 mm in size may not be detected. Transesophageal echocardiography (TEE) is performed in the majority of patients with suspected IE, because of its better image quality and sensitivity, particularly for the diagnosis of complications. TEE is indicated in patients with a negative TTE but high clinical suspicion for IE, poor TTE quality and suspected IE of prosthetic valves or device leads. Some centers perform TEE even if TTE shows evidence of IE to better evaluate the vegetation and valve structure and identify complications. The only situation in which TTE may be considered sufficient is the case of good-quality negative TTE associated with a low level of clinical suspicion. Negative echocardiography (TTE and TEE) and high suspicion for IE should prompt repeat studies. Many findings identified by TEE can also be detected on transthoracic views. Thus, concurrent TTE images can serve as a baseline and follow-up for a noninvasive comparison of vegetation size, valvular insufficiency, or change in abscess cavities during the course of the patient’s treatment and in case of clinical deterioration. TTE can be superior to TEE in certain settings. Anterior cardiac structures such as the tricuspid valve and the right ventricular outflow tract may occasionally be better visualized with TTE. Moreover, TTE is superior to TEE in acquiring hemodynamic information such as calculating left ventricular function, quantifying severity of regurgitant lesions, and assessing filling pressures and pulmonary artery pressures. Thus, information acquired by TTE and TEE is complementary.
Transesophageal echocardiogram demonstrating a large vegetation (arrow) on the mitral valve in a patient with infective endocarditis. From Shah T: Endocarditis. In Levine G (ed.): Color Atlas of Cardiovascular Disease. 2015, Jaypee Brothers Medical Publishers, Philadelphia, with permission
Echocardiography can detect structural damage and dysfunction of the valves. Valve leaflet perforation is the result of destruction of valve tissue by the infection and is generally associated with a virulent microorganism or when the infection continues undetected for a substantial amount of time. The endocarditis process can cause significant valvular regurgitation without perforation of the leaflets. Vegetations on the valve leaflets can obstruct coaptation and cause regurgitation. Less frequently, obstruction of the valve orifice by a vegetation can cause valvular stenosis. Moreover, significant regurgitation can be caused by chordal rupture and flail leaflet. Infection of a prosthetic v alve typically affects the valve ring leading to valve dehiscence. Dehiscence occurs through infectious destruction of the sutures and ring leading to partial detachment of the ring from the surrounding tissue. This can result in a rocking motion of the prosthetic valve and perivalvular regurgitation.
Echocardiography is critical for the diagnosis and management of complications of endocarditis and in strategizing the timing of surgery. Heart failure, perivalvular extension of infection, and embolic events represent the three most frequent and severe complications of IE and the three main indications for early surgery [34]. Valve destruction causing acute regurgitation is the most characteristic mechanism leading to HF in native valve IE. Echocardiography provides (1) a detailed assessment of the mechanism (valve perforation, cusp fenestration, torn leaflet, flail leaflet due to ruptured infected chordae, or interference of the vegetation mass with leaflet closure) and (2) a reliable quantification and evaluation of the hemodynamic impact of the regurgitation.
Echocardiography plays a key role in the assessment of perivalvular extension of infection. Transesophageal echocardiography is the technique of choice for the diagnosis of perivalvular extension and its resulting complications. The infectious process can extend into the adjacent structures resulting in the formation of abscesses, pseudoaneurysms and fistulae. A fistulous connection is formed if the infectious process extends through the myocardium and ruptures into a cavity.
TTE and particularly TEE should be performed in the setting of any embolic event. By assessing the size, mobility, and location of vegetations, echocardiography is useful in predicting embolic risk and therefore plays a key role in identifying a subgroup of patients who might benefit from early surgery to avoid embolism. The size and mobility of vegetations are powerful echocardiographic predictors of new embolic events. Vegetations greater than 10 mm are at higher risk of embolism and risk is even higher in patients with very large (>15 mm) and highly mobile vegetations [35]. Embolism occurs more frequently in patients with vegetations located on the mitral valve (in particular on the anterior mitral leaflet) and when increasing or decreasing size of the vegetation is observed under antibiotic therapy.
When surgery is undertaken, intraoperative TEE evaluation includes assessment of the infected, dysfunctional valve, other valves, and contiguous structures. TEE also aids in confirming the adequacy of valve repair or replacement and documents the successful closure of fistulous tracts. Perivalvular leaks should be recognized and documented to avoid later confusion about whether the leaks are new and possibly the result of recurrent infection [36].
Repeat echocardiographic imaging is indicated if the initial exams did not show evidence of endocarditis but clinical suspicion remains high, in the setting of a new complication and as a follow-up in patients on medical therapy. The type and timing of repeat echocardiographic examinations depend on the clinical presentation and the initial echocardiographic findings.
Multi-Slice Computer Tomography
Although echocardiography is the “gold standard” method used to assess the anatomy of the cardiac valves and perivalvular apparatus, its effectiveness may be limited by the patient’s anatomy and by artifacts due to valvular calcifications or prosthetic material [37]. Also echocardiography requires a highly trained operator and results are to a certain degree operator dependent. Multi-slice computer tomography (MSCT) offers another modality for imaging valvular and perivalvular damage, providing high-resolution anatomic information and affording multiplanar reformations. CT scanning offers the possibility to rapidly image the heart and other organs and thus to identify cardiac lesions and extracardiac complications, such as embolic events, infectious aneurysms, hemorrhages, and septic metastases, which can modify the therapeutic strategy. It also provides an anatomical assessment of the coronary bed, which is important in the preoperative evaluation. In a small study of 37 consecutive patients with clinically suspected IE, Feuchtner et al. found good results in detecting valvular and perivalvular damage using MSCT. Although small leaflet perforations were missed, CT provided more accurate anatomical information regarding presence of abscess/pseudoaneurysm than TEE [38]. Fagman et al. recently investigated the role of MSCT in the diagnosis of aortic prosthetic valve IE. The authors showed that MSCT had comparable diagnostic performance to TEE. Moreover, intraoperative findings demonstrated that MSCT detected three additional pseudoaneurysms not found by TEE [39].
MRI may be indicated in some instances in the evaluation of infective endocarditis. Although it is less accurate than TTE and TEE in identifying valvular vegetations, it can be used primarily for the evaluation of complications such as paravalvular and myocardial abscesses and infectious pseudoaneurysms. Moreover, MRI is useful in the identification of embolic complications to the brain and spinal cord and identification of mycotic aneurysms of the aorta and its branches.
PET-CT of a 64-year- old woman with a mass on thickened mitral valve but no pathogen identified by blood cultures or serology. FDG fluorodeoxyglucose. (a) Transaxial CT scan. (b) Transaxial PET-CT fused image showing an increase FDG uptake in the area of the mitral valve (green arrow). The endocarditis diagnosis was confirmed by pathological examination after surgery (recurrent emboli) showing vegetation but no pathogen could be identified. From Thuny F, Grisoli D, Collart F, Habib G, Raoult D. Management of infective endocarditis: challenges and perspectives. Lancet. 2012;379(9819):965–75. Reproduced with permission from Elsevier Limited
Gallium-67, indium-111, or technetium-99m-hexamethylpropyleneamine oxime labelled leukocyte scintigraphy is another option for imaging of infection, with or without incorporation of CT images. Compared to PET/CT, this method is more specific for infection, however is more time-consuming. The sensitivity and the specificity of 99mtechnetium radiolabelled leukocyte scintigraphy in patients with a suspicion of prosthetic valve IE and an inconclusive echocardiogram have been reported as 57% and 78%, respectively [41]. Because of a better specificity in detection of infection, this modality might be better than PET/CT in differentiating early prosthetic valve IE from postoperative inflammation.
IE Complications
Complications of IE
Complications of infective endocarditis |
|---|
Structural • Leaflet perforation • Ruptured chordae/flail leaflet • Perivalvular extension • Abscess • Aneurysm • Fistula • Valve dehiscence • Pericardial effusion |
Hemodynamic—heart failure • Acute valvular or perivalvular regurgitation • Valve obstruction • Intracardiac shunt • Myocarditis • Myocardial infarction |
Extracardiac manifestations • Renal • Infarct (embolic) • Immune-mediated glomerulonephritis • Neurologic • Stroke • Embolic • Mycotic aneurysms • Meningitis • Encephalitis • Pulmonary embolism (right-sided or device-related IE) • Emboli to other abdominal organs • Spleen • Liver • Mesenteric vessels • Spine • Coronary emboli |
Treatment related • Drug toxicity • Secondary bacteremia due to intravenous lines • Thrombosis of vascular lines |
Cardiac Complications
Local, intracardiac extension of the infection can lead to tissue destruction of the valve apparatus and surrounding cardiac tissue resulting in cardiac complications . Cardiac complications include heart failure, perivalvular abscess formation, fistula formation, and pericarditis.
TEE (a) Large vegetation (arrow) on the posterior mitral valve leaflet complicated by formation of aneurysm. (b) Color Doppler imaging demonstrates mitral regurgitation at the leaflet coaptation and regurgitation through the posterior leaflet consistent with leaflet perforation
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