Infective Endocarditis  - Surgical and Anticoagulant Therapies


                Replacement of an infected native valve with a valvular prosthesis is indicated in the following situations (Table 7):

                1) CHF secondary to valvular dysfunction. CHF in infective endocarditis indicates a grave prognosis. In those patients with CHF, cardiac valve replacement should not be delayed to allow further antibiotic therapy. Delayed surgery when associated with worsening of CHF increases operative mortality from 6-8% in patients with mild or no CHF to 17-33% with severe CHF. The incidence of reinfection of a newly placed cardiac valvular prosthesis is estimated to be 2-3%, which is far less than the mortality associated with uncontrolled CHF. Although operative mortality and PVE is higher when a prosthetic valve is implanted in the presence rather than absence of active infection, the overall outcome is better if the valve replacement is prompt, before severe CHF or spread of infection into the perivalvular tissues ensues.

               2) Multiple clinically significant emboli, despite antibiotic therapy for two weeks. However the first or second embolic episode may so impair the patient, that prosthetic valve replacement at that point may be futile. Use of a variety of factors to predict significant embolization, such as the large size or continued enlargement of vegetations on medical therapy, location on anterior leaflet of the mitral valve, the pathogen being fungi or S. aureus, as indicators for valve replacement remains unresolved.

               3) Endocarditis due to certain pathogens that rarely respond to medical therapy alone such as fungi, enterococci for which there is no synergistic bactericidal combination (e.g., high-level aminoglycoside-resistant enterococci and beta-lactam or fluoroquinolone resistant gram-negative bacilli.

               4) Uncontrolled bacteremia despite optimal antibiotic therapy. However, it should be remembered that the average duration of S. aureus bacteremia on vancomycin therapy is 8 days, with bacteremia persisting for several weeks in some patients before its ultimate resolution.

               5) Valve ring abscess. Although valve ring abscess, especially if small (<2 cm) and not complicated by fistulous tracts, rarely may heal on antimicrobial therapy alone, surgery is indicated for progressive enlargement of a valve ring abscess on antibiotic therapy when monitored by transesophageal echocardiography. Because of extensive periannular tissue destruction in some patients, human aortic homograft may be required to replace the destroyed valve and supporting tissues. Patients with valve ring abscess must also be monitored closely for the development of conduction abnormalities, which may require placement of a transvenous pacemaker because of the risk of high-grade heart block.

               To avoid the complications of prosthetic valve placement (e.g., PVE, bleeding, thrombo-embolic events, and prosthetic valve deterioration over time), new surgical options for treatment of native valve infective endocarditis have been proposed as an alternative to placement of a prosthetic valve; these options include valve debridement, valvuloplasty, and repair or replacement of the paravalvular structure with pulmonary root autograft. Presence of a prosthetic valve in an intravenous drug users is problematic, because the prosthetic valve places these frequently noncompliant patients at continued high risk of PVE. Alternatively, tricuspid valve resection without placement of a prosthetic valve can be tolerated hemodynamically for extended periods of time in many of these patients.

               The surgical indications for PVE are the same as those outlined for native valve endocarditis above. Some patients with PVE without evidence of infection at the valve annulus may be treated medically.

               Tissue should be removed at surgery for microbiologic evaluation (e.g., gram or other histochemical staining, culture and other studies, such as PCR when indicated. The presence of microorganisms in surgical specimens will determine duration of post-operative antibiotic therapy (see above), and retesting their antimicrobial susceptibility will evaluate the emergence of antibiotic resistance on therapy.

               Intrathoracic, intra-abdominal or peripheral mycotic aneurysms usually require surgical excision or endovascular stenting. Intracranial mycotic aneurysms should be followed closely with serial angiograms or MRI/MRA. Although some small intracranial aneurysms may heal on medical therapy alone, most will usually require prompt surgical clipping or ligation or endovascular stenting as an alternative to surgery if accessible and enlarging or bleeding. Myocardial revascularization should be performed at the time of elective valve surgery if significant coronary artery disease is present. However, patients who require emergency placement of prosthetic valve for hemodynamic decompensation secondary to acute infective endocarditis may not tolerate the radiocontrast load necessary for coronary angiography and the additional bypass surgery.

               Embolization of vegetations may result in bland splenic infarcts or septic infarcts/abscesses. Contrast-enhanced abdominal computerized tomography and MRI usually can distinguish a septic from bland process. Ultrasound may show sonolucent areas when abscesses are present. Septic infarcts and abscesses, which can cause persistent or recurrent fever and bacteremia despite appropriate antimicrobial therapy, will usually require splenectomy, with increasing use of percutaneous drainage as an alternative when feasible in patients who are poor surgical candidates. Pneumococcal vaccination should be done prior to splenectomy, and splenectomy should be planned prior to anticipated prosthetic valve placement to prevent hematogenous microbial seeding of the newly placed prosthetic valve from the splenic abscesses.



                Although anticoagulant therapy may impede further enlargement of vegetations in experimental models of infective endocarditis, anticoagulant therapy is relatively contraindicated in infective endocarditis due to the increased risk of intracranial hemorrhage from either occult mycotic aneurysms, cerebral emboli, or cerebral immune vasculitis. Anticoagulation may be used for an over-riding indication that is separate from infective endocarditis, but for deep vein thrombophlebitis of the lower extremities, an inferior vena caval filter would be preferable to anticoagulation. Anticoagulation is particularly problematic when S. aureus is the pathogen because of the increased risk of cerebral embolism with this organism, and in patients with infective endocarditis who undergo prosthetic valve replacement within 2-4 weeks after a neurologic event. In these later patients, it has been suggested that valve surgery be delayed for a minimum of 2 weeks after either a cerebral embolus or bleed or repair of intracranial mycotic aneurysm and use of a bioprosthesis that will not require post-operative continuation of anticoagulation is preferable to use of a mechanical prosthesis that will require further anticoagulation. Similarly, anticoagulation should be discontinued in patients with S. aureus PVE for at least 2 weeks after a cerebral embolus to prevent acute hemorrhagic transformation of the cerebral infarct.

               Although aspirin has shown a beneficial effect in experimental S. aureus endocarditis, in a randomized trial of aspirin in patients with infective endocarditis, aspirin had no effect on vegetation resolution and valvular dysfunction, did not reduce the risk of embolic events and was likely to be associated with an increased risk of bleeding.

Table 7: Indications for Surgical Intervention with Infective Endocarditis

Clinical Situations

Echocardiography Findings

Refractory CHF secondary to valvular dysfunction

Persistent vegetations after a major systemic embolic episode

>2 serious systemic embolic episode

Large (>1cm diameter) anterior mitral valve vegetation

Uncontrolled infection (persistent bacteremia)

Acute mitral insufficiency

Endocarditis caused by certain pathogens (Candida sp, Fungi, Enterococci with synergistic treatment options, left sided MRSA endocarditis)

Increase in vegetation size 4 weeks after antibiotic therapy

Ineffective antimicrobial therapy

Valve perforation or rupture

Most cases of prosthetic valve IE (if no perivalvular involvement, medical treatment may be considered)

Periannular extension of infection including perivalvular or myocardial abscess

Resection of mycotic aneurysms

Physiologically significant valve dysfunction as demonstrated by echo