Epidemiology
Infective endocarditis of a native valve is relatively rare with the incidence reported as roughly 2–10 cases per 100,000 person-years by several sources [ , ]. However, the burden of the disease remains large because of the high morbidity and mortality associated with it; patients with infective endocarditis have an ~20% in-hospital mortality rate and experience a variety of complications including stroke, embolization, and heart failure [ ]. Endocarditis is often broadly divided by whether it affects a native or prosthetic valve. One prospective cohort study that included 2781 endocarditis patients found that 72% of patients had native-valve endocarditis, and more specifically that 41% of patients had mitral valve endocarditis [ ].
Risk factors for endocarditis can be divided into cardiac or noncardiac etiologies. Cardiac-related factors include prosthetic valves, pacemaker leads, congenital heart disease, and acquired valvular damage. Noncardiac risk factors include intravenous drug use and poor dental hygiene [ , , ]. While IV drug use was previously considered the cause in a minority of endocarditis cases, there has been shift due to the recent opioid epidemic. Several studies have shown an increase in both injection drug use and endocarditis related to drug use since 2005 in the United States and Canada [ , ].
Mitral valve–specific risk factors include rheumatic and degenerative mitral disease. One study retrospectively reviewed echocardiography images and found that 60% of patients with mitral valve endocarditis had mitral annular calcification (MAC). The authors concluded that MAC may serve as a nidus for infection [ ].
Pathogenesis
Development of mitral valve endocarditis requires (1) that a sufficient quantity of bacteria enter the bloodstream, and (2) that they find a surface to colonize where they are not easily accessible to host defenses. The mechanism by which bacteria can colonize and replicate has been well described. A valve can become damaged due to disturbances such as turbulent blood flow from a congenital defect or an acquired abnormality, chronic inflammation like degenerative mitral valve disease, or repeated exposure to solid particles via intravenous drug use [ ].
Damage to the valvular endothelium exposes subendothelial collagen causing platelets and fibrin to adhere to the surface. This structure is easily bound to by circulating bacteria which then cause further platelet and fibrin formation. The three-dimensional structure that forms is called a vegetation and is relatively impenetrable by both host defenses and antibiotics because it is a multilayer structure [ , , ].
Diagnosis
The diagnosis of infective endocarditis is made using the modified Duke criteria as described earlier in this book. There are two important considerations specific to mitral valve endocarditis. First, on physical exam a new or worsening murmur in mitral valve endocarditis would present as the holosystolic murmur that is characteristic of mitral regurgitation. Second, since the mitral valve is a left-sided structure, a focused neurologic exam to evaluate for possible cerebral complications is particularly important. Other physical exam findings and laboratory tests are the same as endocarditis in general which have been discussed previously.
Imaging
Echocardiography is the mainstay of imaging in infective endocarditis. Many patients will undergo both transthoracic (TTE) and transesophageal echo (TEE) during workup. In general, all patients with high suspicion for endocarditis should have a TTE. If TTE is nondiagnostic and clinical suspicion for endocarditis remains high then patients should undergo TEE [ , , ]. Findings on echocardiogram vary and include vegetations which are seen in 90% of cases, regurgitation which is seen in 60% of cases, and valvular abscesses which are seen in 20% of cases [ ]. Papers published as early as 1986 report the ability of the transthoracic echocardiogram and color doppler to diagnose complications of endocarditis such as mitral valve perforation [ ]. Additionally, in a more recent paper Yuan et al. showed that there was no difference between TTE findings and surgical observations for 69 patients with infective endocarditis at their institution. TTE was able to successfully identify the size, number, and location of vegetations as well as valve perforation, valve prolapse, and rupture of the chordae tendineae [ ].
Any patient with neurologic symptoms should additionally have a neurology consult and the appropriate brain imaging. Patients with mitral valve endocarditis (or any left-sided lesion) should have brain imaging even in the absence of symptoms [ ]. Cerebral complications are an important consideration for the cardiac surgeon, as their presence can affect the timing of surgery which we will discuss later.
Medical therapy
Medical therapy is essential to effective treatment of endocarditis regardless of whether or not the patient will undergo surgery. Treatment consists of a prolonged course of intravenous antimicrobials at doses sufficient to obtain source control. The choice of therapy is usually made in consultation with an infectious disease team and depends on the offending pathogen. Prior to culture data showing speciation and antibiotic sensitivities, vancomycin and ceftriaxone can be given empirically. After culture data are obtained, the antimicrobials should be tailored appropriately. A common regimen for a variety of pathogens is penicillin G plus gentamicin, but of course there are a variety of options [ ].
Surgical therapy
Surgery is often required in endocarditis. The agreed upon indications for surgery include heart failure, uncontrolled infection, and systemic embolization [ , , , ]. In a patient with mitral valve endocarditis, heart failure symptoms can occur as a result of severe mitral regurgitation from either valve dysfunction or perforation. Uncontrolled infection is usually the result of either abscess or vegetation that cannot be penetrated by antibiotics. Similarly, systemic embolization occurs when pieces of a vegetation break off and enter the bloodstream. When there is a left-sided lesion, there is concern for embolization to the brain as mentioned above.
Within the medical community at large, the timing of surgery remains controversial [ ]. However, the most recent American Association for Thoracic Surgery (AATS) consensus guidelines suggest that surgery should occur as soon as possible once an indication is established [ ]. There are a few studies that lend evidence to this guideline, one such study by Kang et al. (2012) randomized 76 patients to either early surgery or conventional treatment and found that the early surgery reduced risk of both in-hospital death and embolic events at 6 weeks. 60% of these patients had mitral valve endocarditis, implying that mitral valve surgery is safe and maybe even beneficial early in a patient’s course [ ].
Medical and surgical sources agree that the decision about when to proceed with surgery must be made in conjunction with neurology when neurologic complications are present. Current AATS guidelines recommend waiting roughly 1–2 weeks for nonhemorrhagic strokes and 3–4 weeks for hemorrhagic strokes [ ].
The goal of surgery is to obtain source control by removing all infected and necrotic tissue, and to repair any defects caused by the disease [ ]. In mitral valve endocarditis, the most common question a surgeon faces is whether to replace or repair the mitral valve. Data that mitral valve repair (MVr) can be safe in infective endocarditis date back as early as 1992 when Hendren et al. published a study where 22 patients successfully underwent MVr for mitral insufficiency secondary to endocarditis. They described the use of a multiple different techniques including suture or patch closure of a perforation, chordal shortening or transfer, leaflet resection and closure, leaflet resection, and closure, and finally annuloplasty [ ]. The authors point out that repair can be particularly beneficial for young endocarditis patients who may be unlikely to comply with anticoagulation. While this paper [ ] described a small number of patients, it provided proof of concept for the use of MVr in endocarditis.
Since that time, several studies have shown benefits to repair over replacement when possible including improved short- and long-term survival, less recurrent IE, and lower complication rates [ ]. Given the number of studies that have shown benefits of mitral repair, the AATS guidelines do recommend MVr whenever possible [ ]. The only limitation of these data is that we do not know if patients who underwent mitral repair were comparable to those who underwent replacement. It is possible that the patients who underwent replacement had more extensive disease such that repair was not technically feasible. Regardless, there is still consensus that repair is safe and should be attempted before performing replacement.
At our institution we perform repair whenever possible. Here, we present one example of a patient that presented with a new holosystolic murmur and upon workup was found to have mitral valve endocarditis. TTE showed severe mitral insufficiency and vegetations on both leaflets. The patient was taken to the operating room and the mitral valve was approached via minimally invasive right anterior thoracotomy. Both leaflets were extensively debrided (see Figs. 16.1 and 16.2 ) .
