Mitral valve infective endocarditis (IE) is one of the more devastating complications of mitral valve disease, and if left untreated, it is universally fatal, like any other form of IE. In surgical practice, mitral valve endocarditis is usually less common than aortic valve endocarditis, with most infections occurring in native mitral valves. Although the distribution of causes of mitral valve dysfunction has changed in recent years, the overall incidence of IE has increased during the past 3 decades.^1-6 Rheumatic valve disease, which was a frequent predisposing factor to IE in the 1980s, is now rare in industrialized nations.^6-7 Predisposing factors more frequently encountered today, several of which are consequences of advances that characterize modern medicine,^1-7 include degenerative valvular disease, prosthetic valves, other intravascular prostheses and devices, hemodialysis, nosocomial infections, intravenous drug abuse, and immunosuppression. Repaired valves have a low risk of endocarditis compared with prosthetic valves. (To learn more about the epidemiology of IE, see Chapter 31.)

More effective antimicrobial agents have improved the early and long-term outcomes of patients treated for endocarditis. However, endocarditis is still associated with high rates of complications, morbidity, and mortality and frequently requires an operation for cure.^1-13 Increased experience and advances in surgical techniques have improved the success of these challenging operations.

Native Mitral Valve Endocarditis

Native valve endocarditis (NVE) begins with endocardial injury, which allows deposition of fibrin and platelets with subsequent attachment of bacteria.^6,14 Endocardial injury may be secondary to rheumatic valvulitis or other leaflet disease, or valvular or annular calcification. Although vegetations may be seen anywhere on the leaflets or chordae, the usual site at which infective NVE of the mitral valve causes valvular destruction and invasion is the base of the atrial aspect of the mitral valve leaflets. Annular or subanular invasion is more likely to cause atrioventricular (AV) separation when the invasion site is underneath the leaflet and is exposed to high ventricular pressure. Invasion into the AV groove fat with abscess formation is more serious and difficult to radically debride and sterilize (Fig. 38-1).¹⁵ Fortunately, mitral annular invasion more often opens toward the atrium and is therefore shallow in most cases; invasion is generally more common and deeper in aortic valve IE.¹⁶

Destruction of the fibrous trigones and intervalvular fibrosa between the anterior mitral valve leaflet and the aorta is usually a consequence of aortic valve endocarditis with secondary mitral involvement.¹⁷ An infected aortic valve may seed the anterior mitral leaflet or the tensor apparatus of the mitral valve, resulting in double-valve endocarditis; the mechanism may be a large vegetation hitting and directly infecting the anterior mitral leaflet or a jet lesion from aortic regurgitation that becomes infected.¹⁸

Prosthetic Mitral Valve Endocarditis

Prosthetic valve endocarditis (PVE) is on the rise as the number of patients with prosthetic valves continues to increase. PVE is more common in the aortic than the mitral position.¹⁶ This is because a majority of mitral valves are repaired, and repair is associated with a lower risk of endocarditis.

PVE within the first postoperative year is considered early endocarditis, and cases appearing more than 1 year after operation are termed late.^6,19 The risk of early PVE appears to be greatest approximately 5 weeks after valve implantation and declines thereafter.¹⁹ The overall incidence of early PVE is 1%,²⁰ and the incidence of late PVE is 0.5 to 1% per year.^21-23 The type of prosthesis (mechanical vs bioprosthesis) does not influence the risk of PVE.

Early PVE is usually the result of intraoperative infection. Common portals of entry for bacteria that cause PVE are dental procedures, intravascular catheters, and skin infection.^6,24 Nosocomial infections contribute to late PVE, particularly in patients with medical comorbidities that require frequent hospital admissions or instrumentations (eg, hemodialysis) or immunosuppression (eg, organ transplantation).

Early PVE usually affects the sewing ring or the interface of the prosthetic valve and the annulus (often a site of clot formation). Involvement of the sewing ring starts locally but eventually becomes circumferential. Enzymatic degradation of the tissue holding the sutures results in dehiscence of the prosthesis and periprosthetic leak. Progression of the infection and invasion may lead to tissue necrosis, abscess, and pseudoaneurysm formation. Mitral PVE may extend anteriorly to the fibrous trigone or posteriorly, causing AV separation.

Endocarditis of native valves is most often caused by Streptococcus viridans, Staphylococcus aureus or epidermidis, or Enterococci, with proportions varying according to valve (native vs prosthetic), pathology stage (noninvasive vs invasive), source of infection, patient age, and coexisting conditions.^2,3,6,24-26 S. aureus accounts for 25 to 30% of all infections and is also the most common organism in each major risk group, including intravenous drug users and those with intracardiac devices.^4,6,25 In our study, S. aureus was the most common pathogen for NVE (27.6%) and the second most common cause of PVE (22.1%), for which coagulase-negative Staphylococcus was most common (24.1%).⁸ Among the major causative organisms, Staphylococcus species are most likely to be associated with invasive endocarditis (49%) and Streptococcus least likely (11%).¹⁶ (IE microbiology is discussed in more detail in Chapter 31.)

Clinical Presentation

The diverse nature and evolving epidemiologic profile of IE ensure that it remains a diagnostic challenge.⁶ The clinical presentation varies according to causative organism, preexisting cardiac disease, comorbidities, and complications. Mitral IE may present as an acute, rapidly progressive infection or as a subacute or chronic disease. Up to 90% of patients present with fever, often associated with systemic symptoms of chills, poor appetite, and weight loss.⁶ Other findings include a new murmur (85%) or a change in an existing murmur. Embolic phenomena may cause petechiae, Roth spots, Osler nodes, and Janeway lesions. Embolic events occur in 20 to 50% of patients. Neurologic events develop in 20 to 40% of all patients with IE and are mainly the consequence of embolism of vegetation material, while mycotic aneurysm is much less common.⁶ Splenomegaly may be present in both NVE and PVE. A high index of suspicion and low threshold of investigation to exclude IE are essential to diagnose and treat these affected patients early.

Laboratory findings include an elevated white blood cell count, anemia, and hematuria. Blood cultures from separate sites are usually positive in patients with bacterial endocarditis; two positive cultures out of three are considered diagnostic. However, cultures in patients with fastidious organisms or fungi may take more than 3 weeks to become positive, although diagnostic methods have improved. When IE is suspected, ideally three or more blood cultures should be collected before antibiotics are initiated, and at least two should be obtained immediately from different peripheral sites. Additional blood cultures should be obtained a few hours later. Unless the patient is septic, it is appropriate to hold off on starting antibiotics until an adequate number of blood cultures have been collected. Cases of IE in which blood cultures are negative (10%) may reflect either patients treated with antibiotics before the blood culture was drawn or infections caused by fastidious organisms.³ For cases caused by fastidious organisms, serologic testing or valve or blood polymerase chain reaction (PCR) assay can identify the pathogen 60% of the time.^3,6

Echocardiography and Imaging Studies

The present gold-standard diagnostic modality for documenting IE is transesophageal echocardiography (TEE). Specificity for TEE is approximately 90% and sensitivity is 90 to 100%.⁶ In contrast, transthoracic echocardiography (TTE) is more operator dependent, and images may be compromised by surrounding structures; it is only 50% sensitive and 90% specific for IE.⁶ Echocardiography must be performed as soon as IE is suspected.⁶ TTE should be performed first, but often both TEE and TTE need to be performed.⁶ Echocardiographic findings of IE include vegetations, periprosthetic leakage in patients with PVE, intracardiac fistulae, and abscess cavities. The echocardiographic examination is very good at evaluating valve function, but less reliable for assessing the severity and invasiveness of the infection. A negative echocardiogram does not exclude the diagnosis of IE. In situations with strong suspicion of IE, the diagnosis may be pursued by magnetic resonance imaging (MRI). In most patients with IE, MRI will demonstrate abnormal consistency of tissue in the annulus.

Metastatic infection is a possibility, and patients with IE and abdominal symptoms should undergo computed tomography (CT) scanning to rule out splenic or hepatic abscesses. Embolic infection of viscera is typically caused by staphylococcal organisms, and the brain is the most important and frequent site for emboli.^3,6 Any neurologic deficit or abnormality should trigger investigation with CT or MRI of the brain, funduscopic examination, and occasionally cerebrospinal fluid examination. We require a CT or MRI of the brain irrespective of symptoms if the patient is going to undergo operation. Preoperative coronary angiography is indicated in all patients age 40 years or older, particularly if they have a history of coronary artery disease or previous revascularization procedures, or if coronary embolization is suspected. Clinical judgment must be exercised in patients with renal dysfunction.

Diagnostic Criteria and Their Limitations

The Duke (and modified Duke) criteria for IE, based on echocardiographic results along with clinical, microbiologic, and pathologic findings, provide high sensitivity and specificity (~80% overall) for the diagnosis of IE (Table 38-1).²⁷ The Duke criteria, discussed in more detail in Chapter 31, are useful for the classifying IE, but do not replace clinical judgment for diagnosing IE when blood cultures are negative or when infection affects a prosthetic valve or pacemaker lead.

Surgery plays a pivotal role in managing native mitral valve endocarditis. Indications for surgical intervention in patients with NVE and PVE are presented in Table 38-2.

Congestive heart failure is the most common indication for surgery. Our indications for surgery have gradually moved toward earlier intervention to avoid devastating complications.