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David TE. Surgical Treatment of Aortic Valve Endocarditis.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:857866.

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Chapter 33

Surgical Treatment of Aortic Valve Endocarditis

Tirone E. David

DEFINITION
EPIDEMIOLOGY
PATHOGENESIS AND PATHOLOGY
MICROBIOLOGY
CLINICAL PRESENTATION AND DIAGNOSIS
TREATMENT
SURGICAL TREATMENT
????Clinical Results
REFERENCES

?? DEFINITION
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Infective endocarditis is a disease in which a microorganism colonizes a focus in the heart, producing fever, heart murmur, splenomegaly, embolic manifestations, and bacteremia or fungemia. Early diagnosis of this condition is extremely important because it almost invariably leads to devastating complications and death if not treated properly.


?? EPIDEMIOLOGY
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Predisposing factors for infective endocarditis are cardiac abnormalities that disrupt the endocardium by means of a jet injury as well as the presence of blood-borne microorganism that colonize these abnormal surfaces. Congenitally bicuspid aortic valve is the most common predisposing lesion for endocarditis of the aortic valve.1 Other congenital abnormalities of the aortic valve, degenerative calcific aortic stenosis, aortic insufficiency secondary to connective tissue disorders, and rheumatic aortic valve disease, are also predisposing lesions for infection. Depending on the virulence of the offending microorganism, normal aortic valves can also be affected. Patients with prosthetic heart valves have a constant risk of developing infective endocarditis.

It is difficult to determine the incidence and prevalence of native aortic valve endocarditis in the general population because this disease is continuously changing.2 The annual incidence of infective endocarditis is estimated to range from 1.7 to 6.2 episodes per 100,000 patient-years in North America.34

Patients with prosthetic aortic valves are reported to have an incidence of infective endocarditis of 0.2 to 1.4 episodes per 100 patient-years, which varies with the type of aortic valves.511 Approximately 1.4% of patients undergoing aortic valve replacement develop prosthetic valve endocarditis during the first postoperative year.12

Dental extractions have been demonstrated to produce bacteremia, however, even simple mastication, teeth brushing or cleaning, and oral irrigation can produce transient bacteremia. Endoscopic procedures may also produce bacteremia. Intravenous drug users are particularly susceptible to infective endocarditis, which often occurs in structurally normal heart valves. Infective endocarditis in hemodialysis patients is relatively infrequent but it is associated with high mortality.13


?? PATHOGENESIS AND PATHOLOGY
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In 1928, Grant et al14 theorized that platelet-fibrin thrombi on the heart valve served as a nidus for bacteria adherence. In 1963, Angrist and Oka15 introduced the term "nonbacterial thrombotic endocarditis" to describe sterile vegetations on a heart valve and provided experimental animal evidence supporting the role of these vegetations in the pathogenesis of endocarditis. Experimental inoculation in animals with preexisting "nonbacterial thrombotic endocarditis" produced by mechanical abrasion of the endothelial covering of heart valves causes a prompt leukocytic infiltration of the thrombi.16 As the microorganism multiplies, more leukocytes and thrombotic material accumulate in the area and a verrucous vegetation begins to form.

Depending on the virulence of the microorganism and the resistance of the host, the aortic valve can be destroyed and the infection may spread into the annulus and surrounding structures with abscess formation. The abscess may rupture into the pericardial cavity or into a cardiac cavity.

Infective endocarditis of the aortic valve not only causes destruction of the aortic cusps, paravalvular abscess, and cardiac fistulas, but also can cause coronary and systemic embolization of vegetations.17 Cerebral infarction, either ischemic due to arterial occlusion or hemorrhagic due to rupture of the mycotic aneurysm, is common in these patients.18,19 Mycotic aneurysms, infarcts, and abscesses of other organs such as spleen, liver, kidneys, and limbs are also common.17 Aortic valve endocarditis with a large vegetation that prolapses into the left ventricle and comes in contact to the anterior leaflet of the mitral valve can cause secondary involvement of this valve.20,21

Infection of a mechanical heart valve is usually located in its sewing ring.22,23 Infection of a porcine or pericardial valve may involve the cusps, the sewing ring, or both.24,25 Infection in aortic valve homografts and pulmonary autografts resembles that of native aortic valve: it begins in the aortic cusps and destroys them, causing aortic insufficiency, but it may also extend into surrounding structures.26 Endocarditis after aortic root replacement with mechanical valves frequently causes dehiscence of the valve from the aortic annulus with consequent false aneurysm.27


?? MICROBIOLOGY
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Staphylococcus aureus and Streptococcus viridans are the most common microorganisms responsible for native aortic valve endocarditis.2832 Staphylococcus aureus is extremely virulent and able to cause infection in patients with normal aortic valves. Streptococcus viridans is not as virulent and causes infection that often follows a protracted course. Staphylococcus epidermidis and various other streptococci can also cause endocarditis.

Endocarditis due to gram-negative bacteria is uncommon, but it is often resistant to antibiotic therapy and may cause serious complications. Haemophillus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella (HACEK group) are gram-negative bacilli grouped together for their characteristic fastidiousness requiring prolonged incubation period before growth. Endocarditis by the HACEK group is also uncommon. Fungal endocarditis is rare but extremely serious. Candida albicans and Aspergillus fumigatus are the usual agents.

The microbiology of prosthetic aortic valve endocarditis is different from that of the native valve.23,2833 Prosthetic valve endocarditis has been arbitrarily classified as early when it occurs within the first two months after surgery and late when it occurs after two months.34 However, it is possible that many cases of prosthetic valve endocarditis that occur during the first year after surgery are acquired at the time of implantation of the artificial heart valve. This may be particularly true when the infection is caused by the HACEK group of bacteria. Early prosthetic valve endocarditis is caused by contamination of the valve at the time of implantation of by perioperative bacteremia.12,33 Staphylococcus epidermidis, Staphylococcus aureus, and Enterococcus faecalis are among the more common microorganisms responsible for early prosthetic valve endocarditis.12,2833 The sources of late prosthetic valve endocarditis are more difficult to determine. Bacteremia is probably the principal cause of late endocarditis. Although streptococci and staphylococci are commonly encountered in these patients, a myriad of microorganisms can cause late prosthetic valve endocarditis.23,28,33

In a small proportion of cases of aortic valve endocarditis, no microorganism can be cultured from either the blood or surgical specimens.2833 This is called "culture-negative endocarditis," but it is important to rule out fastidious microorganisms and every effort should be made to identify them.


?? CLINICAL PRESENTATION AND DIAGNOSIS
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It is helpful to classify infective endocarditis as acute and subacute because there are major differences between these two clinical presentations. Subacute endocarditis is often caused by less virulent microorganism such as S. viridans. When this organism affects a diseased aortic valve, the clinical course is protracted and antibiotics alone cure most cases. On the other hand, acute endocarditis is frequently caused by a virulent microorganism such as S. aureus and may affect a normal aortic valve. The clinical course is acute, and antibiotics alone seldom cure the infection.

The onset of subacute endocarditis in most cases is subtle, with low-grade fever and malaise. Patients think they have the "flu" and are often treated with oral antibiotics for a week to 10 days with improvement of symptoms. However, in most cases the symptoms recur a few days after stopping antibiotics. In the majority of cases no predisposing factor is identified. An aortic valve murmur is present in nearly all patients because they have preexisting aortic valve disease. Splenomegaly is common. Clubbing of the fingers and toes may develop in long-standing cases. Skin and mucous membrane signs occur late in this form of endocarditis. Petechiae appear on any part of the body. Small areas of hemorrhage may be seen in the ocular fundi. Hemorrhages in the nail beds usually have a linear distribution near the distal end, hence the name splinter hemorrhages. Osler's nodes are acute, tender, barely palpable nodular lesions in the pulp of the fingers and toes. Bacteria have been cultured from these lesions. Embolization of large vegetation fragments may cause dramatic clinical events such as acute myocardial infarction, stroke, or splenic or hepatic infarcts. Any other organ also may be involved. Destruction of the aortic cusps causes aortic insufficiency and heart failure. The blood picture is not distinctive in subacute endocarditis. Anemia without reticulocytosis develops in patients untreated for more than a few weeks. The leukocyte count is moderately elevated. Blood cultures frequently identify the offending microorganism.

The clinical course of acute endocarditis is often fulminating. A preexisting source of bacteremia may be identified. This form of endocarditis can present all symptoms and signs described under subacute endocarditis, but they are more acute and patients are often sicker with overwhelming signs of sepsis. Early metastatic infections are common. Two physical signs are seen only in acute endocarditis: the Janeway lesion (a painless red-blue hemorrhagic lesion of a few millimeters in diameter found in the palms of the hands and in the soles of the feet) and the Roth spot (an oval pale area near the optic disc surrounded by hemorrhage). Acute endocarditis is common in patients with no preexisting aortic valve disease. Early cardiac decompensation due to aortic insufficiency is common. Paravalvular abscess is also common, and, depending on the location of the abscess, the electrocardiogram may show an increased PR interval or heart block. The blood picture is one of acute sepsis. Blood culture often isolates the infecting agent.

Prosthetic valve endocarditis may present as acute or subacute endocarditis.

Doppler echocardiography is extremely useful in the diagnosis and management of infective endocarditis.3538 Transesophageal echocardiography is usually better than transthoracic echocardiography, and multiplane is better than monoplane for the diagnosis of endocarditis. Echocardiography can detect vegetations as small as 1 or 2 mm in size, but it is more reliable in native than in prosthetic valve endocarditis. It is more useful for tissue than for mechanical valves because of the acoustic shadowing of ball, disc, or leaflet motion of mechanical heart valves. Echocardiography is also extremely sensitive for detecting paravalvular abscess and cardiac fistulas.38,39

Clinical investigators from Duke University proposed certain criteria for confirming or rejecting the diagnosis of infective endocarditis.40 These criteria have been confirmed by other investigators and are now widely used.41,42 Table 33-1 summarizes the Duke University criteria for the diagnosis of infective endocarditis. Heart catheterization and coronary angiography increase the risk of embolization in patients with aortic valve vegetations and should be avoided.


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TABLE 33-1 Duke University criteria for diagnosis of infective endocarditis

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?? TREATMENT
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An appropriate antibiotic is the most important aspect of the management of patients with infective endocarditis.17,28,29 Antibiotic therapy should be started soon after obtaining several blood cultures. The initial choice of antibiotics is based on clinical circumstances and the suspected source of infection. Patients who had recent dental work should receive antibiotics to counteract bacteria from the oral cavity; those who had recent urinary or colonic procedures should be treated with antibiotics that are effective against gram-negative bacteria. Intravenous drug users are usually infected with S. aureus or S. epidermidis, and antibiotics should be chosen accordingly. Once the microorganism is identified by blood cultures and its sensitivity to specific antibiotics is known, antibiotic therapy is adjusted accordingly. A combination of two or three antibiotics that potentiate each other is often needed in the treatment of endocarditis caused by virulent microorganisms. Intravenous antibiotic therapy is continued for 6 weeks.

It is difficult to eradicate infection caused by virulent microorganisms with antibiotics alone because they often destroy the native aortic valve very rapidly and cause aortic insufficiency and congestive heart failure. These infections are usually due to S. aureus, Pseudomonas aeruginosa, Serratia marcescens, or fungi.

Surveillance blood cultures are performed in 48 hours to monitor the efficacy of antibiotic therapy. The patient must be watched closely for signs of congestive heart failure, coronary and systemic embolization, and persistent infection. Daily electrocardiograms and frequent echocardiograms are performed during the first two weeks of treatment. At any evidence of increasing aortic insufficiency, enlarging vegetations, recurrent embolism, paravalvular abscess, or persistent infection, surgery should be immediately performed. It is important to operate on patients before they develop intractable heart failure, cardiogenic or septic shock, or extensive aortic root abscesses. Patients with vegetations larger than 10 mm present a clinical problem because they are more likely to develop serious complications and early surgery is justifiable.3537

Anticoagulation is not effective in preventing embolization of vegetations in native and biological valves and is associated with an increased risk of neurologic complications.43

Early surgical treatment should be considered in patients with signs of congestive heart failure, acute valve dysfunction, paravalvular abscess or cardiac fistulas, recurrent systemic embolization when aortic valve vegetations are present, and persistent sepsis despite adequate antibiotic therapy for more than 4 to 5 days. Prosthetic valve endocarditis is best treated by early surgery, particularly in patients with mechanical valves.23,29,30 Acute endocarditis of the aortic valve due to S. aureus is also best treated with early surgery because of the destructive power of the bacteria.27,28

Patients with neurologic deficits should have computed tomography scan or magnetic resonance imaging to determine if the cerebrovascular accident is ischemic or hemorrhagic. Ischemic damages are far more common than hemorrhagic, but both are associated with increased mortality and morbidity.4446 Mycotic aneurysms should be treated before valve surgery. Aortic valve replacement should be postponed for 2 weeks after an ischemic stroke and 4 weeks after a hemorrhagic stroke if possible.46


?? SURGICAL TREATMENT
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Patients who need surgery are often very sick and may be in congestive heart failure. For this reason and because they often require complex and long operative procedures, myocardial protection is of utmost importance. Another important aspect of surgery for endocarditis is avoidance of contamination of the surgical field, instruments, drapes, and gloves with vegetations and pus. Instruments used to extirpate contaminated areas in the heart should be discarded before reconstruction of the ventricle and aortic root begins. In addition, local drapes, suction equipment, and surgical gloves should all be changed.

When the infection is limited to the cusps of the native aortic valve or a bioprosthetic valve, complete removal of the valve and implantation of a biological or mechanical valve usually resolve the problem. There is no evidence that bioprostheses are better than mechanical valves in patients with active infective endocarditis,32 but aortic valve homograft is believed to be ideal for patients with endocarditis.47 Some surgeons favor the pulmonary autograft, particularly in young patients.48

If the aortic annulus is involved in the infective process, resection of the necrotic or inflamed area is needed before a prosthetic valve can be implanted. The defect created by the resection should be patched before a prosthetic valve is implanted. We prefer to use fresh autologous pericardium to patch small defects (1 or 2 cm wide) in the aortic root and left ventricular outflow tract, and glutaraldehyde-fixed bovine pericardium for larger defects.49,50 Some surgeons also use Dacron fabric to reconstruct the aortic root.4852 Here again, aortic valve homograft is believed to be ideal for reconstruction of the aortic root and left ventricular outflow tract.5355 The mitral valve of the aortic valve homograft can be used to patch defects in the left ventricular outflow tract by correctly orienting the homograft. The pulmonary autograft has also been used in cases of extensive destruction of the aortic root.56 However, an aortic valve homograft or a pulmonary autograft is by no means a substitute for radical resection of all infected tissues, because persistent infection can occur with these biological grafts.57,58

Surgery for aortic root abscess and/or cardiac fistulas is challenging. The most important aspect in the surgical treatment of these patients is radical resection of all infected tissues.23,29,50 We believe that the type of valve implanted is less important than complete extirpation of all infected and edematous tissues.50 These patients frequently require replacement of the entire aortic root and reconstruction of the surrounding structures that are also involved by the abscess. These operations must be individualized because the pathology of aortic root abscess is variable. Extensive resection and reconstruction may be needed.49,50 Thus, patching of the interventricular septum, dome of the left atrium, intervalvular fibrous body, right atrium, and pulmonary artery may be necessary, as well as repair of the left and/or right coronary arteries. The aortic root is often replaced with a valved conduit.

Figure 33-1 illustrates a procedure in which the dome of the left atrium and noncoronary sinus was patched before implanting a mechanical aortic valve.



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FIGURE 33-1 Repair of a localized aortic root abscess. One patch is used to reconstruct the dome of the left atrium and one for the aortic root. (Reproduced from David TE: Aortic valve surgery. Curr Probl Surg 1999; 336:421, with permission from Mosby.)

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Figure 33-2 illustrates an operation in which the entire aortic annulus and dome of the left atrium were reconstructed before a new valved conduit was implanted. An aortic valve homograft is ideal in this circumstance because the patch in the aortic annulus may not be necessary.



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FIGURE 33-2 Repair of aortic annular abscess after aortic root replacement. One patch is used to reconstruct the dome of the left atrium and one to reconstruct the left ventricular outflow tract before a new valved conduit is implanted. (Reproduced from David TE: Aortic valve surgery. Curr Probl Surg 1999;336:421, with permission from Mosby.)

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Aortic root abscess extending into the intervalvular fibrous body or into a prosthetic aortic and mitral valve is particularly difficult to treat.59 In these cases, the resection and reconstruction can be performed through the aortic root and dome of the atrium.59,60 After removing the native or prosthetic aortic valve, the aortotomy is extended into the intervalvular fibrous body and dome of the left atrium as illustrated in Figure 33-3. The abscess is best excised en bloc even if it is necessary to resect an excessive amount of tissue. If the abscess is limited to the intervalvular fibrous body, it may be possible to save the mitral valve. The proximal third of the anterior leaflet of the mitral valve can be safely resected and reconstructed. However, when in doubt, it is safer to remove the entire anterior leaflet than to leave infected tissue behind. If the native or prosthetic mitral valve is removed (Fig. 33-4), the base of the left ventricle becomes widely open without separation between its inflow and outflow tracts. It is necessary to create a new intervalvular fibrous body, and this can be accomplished by suturing two triangular shaped patches of bovine pericardium to the fibrous trigones (Fig. 33-5). A mitral valve prosthesis is secured to the posterior mitral annulus and to the double patch superiorly. The incision in the dome of the left atrium is closed with the outer patch and the aortic root reconstructed with the inner patch (Fig. 33-6). An aortic valve prosthesis is secured to the patch and normal aortic annulus (Fig. 33-7). When an aortic valve homograft is used for this type of reconstruction, the anterior leaflet of the mitral valve of the homograft can be used as patch material for the new fibrous body between the aortic and mitral valves. Actually, aortic and valve homografts in a single bloc of tissue have been used to treat this condition.61



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FIGURE 33-3 Double valve endocarditis with reconstruction of the intervalvular fibrous body. The aortic and mitral valves are excised through the aortic root and dome of the left atrium. (Reproduced from David TE, Kuo J, Armstrong S: Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766, with permission from Mosby.)

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FIGURE 33-4 Both valves are excised along with any infected surrounding tissues. (Reproduced from David TE, Kuo J, Armstrong S: Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766, with permission from Mosby.)

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FIGURE 33-5 The left ventricular inflow and outflow tracts become a single orifice that is divided into mitral and aortic orifices with two triangular shape patches sutured to the lateral and medial fibrous trigones or endocardium of the left ventricle depending on the extensiveness of the resection. (Reproduced from David TE, Kuo J, Armstrong S: Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766, with permission from Mosby.)

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FIGURE 33-6 A prosthetic mitral valve is secured in the mitral annulus posteriorly and patches superiorly. The outer patch is used to close the dome of the left atrium. (Reproduced from David TE, Kuo J, Armstrong S: Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766, with permission from Mosby.)

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FIGURE 33-7 A prosthetic aortic valve is secured to the aortic annulus and medial patch, which is in turn used to close the aortotomy. (Reproduced from David TE, Kuo J, Armstrong S: Aortic and mitral valve replacement with reconstruction of the intervalvular fibrous body. J Thorac Cardiovasc Surg 1997;114:766, with permission from Mosby.)

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Postoperative complications are common after surgery for active infective endocarditis. Septic patients may have severe coagulopathy and may bleed excessively after cardiopulmonary bypass. Antifibrinolytic agents, particularly aprotonin, should be used. Transfusion of platelets, cryoprecipitate, and fresh frozen plasma is often necessary to obtain hemostasis. Radical resection of aortic root abscess may cause heart block, for which a permanent pacemaker will be needed postoperatively. Depending on the patient's clinical condition before surgery, multiorgan failure may develop postoperatively. Neurologic deterioration may occur in patients with preexisting cerebral emboli. Pulmonary, splenic, hepatic, and other metastatic abscesses seldom require surgical treatment. Large metastatic abscesses, may have to be drained, and in the case of the spleen, splenectomy should be performed because of the risk of rupture.62

Clinical Results

The prognosis of aortic valve endocarditis depends largely on when the disease is diagnosed and how promptly it is treated.27 Patients with prosthetic aortic valve endocarditis have a more serious prognosis than patients with native aortic valve endocarditis.28,29 The results of surgery for infective endocarditis have improved significantly during the past three decades.17 The operative mortality for patients with infection limited to the cusps of the aortic valve is as low as for aortic valve replacement without endocarditis28,29; it is higher in patients with prosthetic valve endocarditis23,24,2932 and in those with aortic root abscess.5053 In recent series of surgically treated patients the operative mortality for native valve endocarditis was under 10% and for prosthetic valve endocarditis was 20% to 30%.23,2932

A review of our experience with surgery for active infective endocarditis in 122 patients found a 10-year survival of 61% ? 6%. Patients operated on for active infective endocarditis have a higher risk of developing endocarditis again than do patients with prosthetic valves who never had endocarditis.29,30 In our experience, 8 of 122 patients developed recurrent infection after a mean interval of 47 months; freedom from recurrent endocarditis at 10 years was 79% ? 9%.29 In most of these patients, a different microorganism caused the second episode of endocarditis.


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