Surgery for native mitral valve endocarditis

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 [ , , ].