Chapter 39

Surgical Treatment of Mitral Valve Endocarditis

Farzan Filsoufi/ David H. Adams

PATHOLOGY
    Isolated Native Mitral Endocarditis
    Secondary Native Mitral Endocarditis
    Prosthetic Mitral Valve Endocarditis
INDICATIONS FOR SURGERY
TIMING OF SURGERY
PREOPERATIVE INVESTIGATION
OPERATIVE TECHNIQUE
    Principles
    Native Mitral Valve Endocarditis
        LEAFLET PERFORATION OR DETACHMENT
        POSTERIOR LEAFLET PROLAPSE
        ANTERIOR LEAFLET PROLAPSE
        COMMISSURAL PROLAPSE
        ANNULOPLASTY
    Prosthetic Mitral Valve Endocarditis
        REDO STERNOTOMY
        RIGHT ANTEROLATERAL THORACOTOMY
        MITRAL VALVE EXPOSURE
        RECONSTRUCTION OF THE MITRAL ANNULUS
RESULTS
REFERENCES

   INTRODUCTION
 
Infective endocarditis is a well-established cause of valvular heart disease and carries a high risk of morbidity and mortality. During the last 50 years, the introduction and wide use of antimicrobial therapy have significantly changed the course of this disease. The majority of patients can be successfully treated medically with total eradication of the disease process. In certain clinical presentations, however, surgical intervention remains an indispensable adjunct to the management of acute and subacute endocarditis.

Despite the use of preventative measures such as antibiotic prophylaxis in patients with valvular heart disease undergoing invasive procedures, the overall incidence of infective endocarditis continues to rise. Infective endocarditis affects primarily the left-sided valves with a higher incidence of aortic versus mitral valve involvement. When the mitral valve is involved, the existence of predisposing conditions such as rheumatic heart disease or degenerative mitral disease is a common finding. Infective endocarditis can also occur in patients with a mitral prosthetic valve. Epidemiologic studies estimate the actuarial cumulative incidence of prosthetic valve endocarditis from 1.4% to 3.1% at 1 year and 3.2% to 5.7% at 5 years.1–3 The risk is greatest during the first 6 months following surgery and declines over time to a lower rate of around 0.2% to 0.35% per year.

Valvular endocarditis is most often due to infection by either streptococcal or staphylococcal bacteria. The principal organisms involved in native valve endocarditis are Streptococcus viridans, Streptococcus bovis, and Staphylococcus aureus.4,5 However, during the last decade, Staphylococcus epidermidis has assumed an increasing role in native mitral valve endocarditis in patients with underlying degenerative mitral valve disease. The microbiology of infective endocarditis is relatively predictable in some patients with additional risk factors. Staphylococcus aureus is the most common cause of infection in patients who abuse intravenous drugs as well as in patients with insulin-dependent diabetes mellitus. Early prosthetic valve endocarditis, defined as endocarditis during the first 2 months following surgery, is frequently due to coagulase-negative staphylococci, primarily Staphylococcus epidermidis.4,5 The microbiology profile of late prosthetic endocarditis is similar to that of native valve endocarditis with the addition of gram-negative bacilli, particularly the HACEK group (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kingella), and fungi (Candida species).4–7


   PATHOLOGY
 
The pathology of mitral valve endocarditis varies with the route of infection.

Isolated Native Mitral Endocarditis

In isolated mitral valve endocarditis, the infectious process begins on and remains localized to the mitral valve. Mitral valve endocarditis can cause several types of lesions including vegetations, chordal rupture, leaflet abscess/perforation, and mitral annulus abscess.

Vegetations are made up bacteria, altered polynuclear cells, and fibrin deposits, and are indicators of the acute nature of the infectious process. They are often localized on the atrial side of mitral leaflets, particularly the anterior leaflet (Fig. 39-1). They may be mobile or adherent with a sessile or pedicled base of insertion. Vegetations can vary in size and rate of growth. Highly virulent organisms such as HACEK, MRSA (methicillin-resistant Staphylococcus aureus), and fungal infections cause particularly large vegetations and are at high risk for embolization. Occasionally, these large vegetations can cause mitral valve obstruction with congestive heart failure. Vegetations may remain on the mitral valve and become organized and calcified despite the eradication of the infectious process.



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  		FIGURE 39-1 Vegetation on the atrial side of the A3 segment of the anterior leaflet (posterior paracommissural area).

 
If the infectious process starts at the free margin of the leaflets, or directly at the level of subvalvular apparatus, chordal rupture with leaflet prolapse can occur. These lesions are usually located at the middle scallop of anterior or posterior leaflets as well as the posterior commissural area.

The valvular abscess consists of a mass of necrotic tissue and active inflammation located underneath the endocardial surface of the valve. It most often involves the anterior leaflet of the mitral valve. Occasionally, leaflet abscess causes a true aneurysm of the body of the anterior leaflet (Fig. 39-2). Locally, leaflet perforation can be the final stage in the evolution of an abscess, although extension into the annulus and/or intervalvular fibrous body may also occur.



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  		FIGURE 39-2 Aneurysm of the body of the anterior leaflet, complicated by leaflet perforation.

 
Two different patterns explain the formation of mitral annular abscess. The most common is extension of infection from the body of the leaflet toward the annulus. The second mechanism is primary infection of calcified annular lesions. In the absence of appropriate surgical treatment, an annular abscess can cause false aneurysm of the left ventricle or the atrioventricular groove.

Secondary Native Mitral Endocarditis

Because of the close anatomic relationship between the aortic and mitral valves, aortic valve endocarditis can lead to concomitant mitral valve endocarditis. The localization of the infectious process to the mitral valve can be explained by two different mechanisms. In the first, an aortic annular abscess can extend to the intervalvular fibrous body and then to the mitral annulus. Subsequent infection can spread to the anterior leaflet of the mitral valve, which may result in its partial/complete detachment from the annulus.

In the second mechanism, the diastolic jet of aortic regurgitation due to the primary aortic endocarditis can produce a secondary lesion on the ventricular surface of the anterior mitral leaflet. This lesion can be a vegetation, leaflet abscess, and/or leaflet perforation. This so-called "kissing lesion" is observed in 10% to 15% of patients with endocarditis.8,9

Prosthetic Mitral Valve Endocarditis

Prosthetic valve endocarditis often produces three types of lesions: vegetation, valve dehiscence with paravalvular leak, and paravalvular abscess.4,6,10,11 Early bioprosthetic endocarditis usually involves the sewing ring and leads to an annular abscess and paravalvular leak. Conversely, late bioprosthetic endocarditis often starts at the level of the leaflets, potentially leading to valve obstruction or regurgitation secondary to a large vegetation or leaflet perforation, respectively. In these late cases, the risk remains for extension of infection to the sewing ring with subsequent annular abscess and valve dehiscence. Mechanical mitral prosthetic endocarditis usually involves the sewing ring with complications similar to those mentioned above.


   INDICATIONS FOR SURGERY
 
Surgical intervention plays an important role in the overall management of native mitral valve endocarditis. Several clinical presentations are currently considered absolute indications for surgical intervention. They are:

  1. Significant mitral regurgitation, with or without symptoms of congestive heart failure
  2. Uncontrolled sepsis despite proper antibiotic therapy
  3. Presence of an antibiotic-resistant organism
  4. Endocarditis caused by fungus, Staphylococcus aureus, or gram-negative bacteria
  5. Evidence of mitral annular abscess, extension of infection to intervalvular fibrous body, or formation of intracardiac fistulas
  6. Onset of a new conduction disturbance
  7. Large vegetations (> 1 cm), particularly those that are mobile and located on the anterior leaflet, and thus at high risk for embolic complications
  8. Multiple emboli after appropriate antibiotic therapy

In these situations, surgical therapy has dramatically improved both morbidity and mortality over medical treatment alone.

Indications for surgical intervention in patients with prosthetic valve endocarditis include those stated above as well as unstable prosthesis with paravalvular leak. It should be emphasized that surgical intervention is rarely avoided in the setting of prosthetic endocarditis because the infection of foreign material cannot be treated effectively with antibiotics alone.


   TIMING OF SURGERY
 
When there is an indication for surgery, the procedure should be performed soon after the diagnosis is made regardless of the duration of antimicrobial therapy. Even in the setting of severe valvular regurgitation with minimal clinical symptoms, early surgical intervention is justified. Surgery should be delayed, however, in patients who present with recent neurologic injury.12,13 There is a significant correlation between the interval of neurologic event and surgery and the exacerbation of cerebral complications.13 Patients who have suffered a recent ischemic or hemorrhagic cerebral injury should not be operated upon for at least 2 or 4 weeks, respectively. Daily neurologic examination, CT scans, and MRI at regular intervals should be performed to determine the appropriate timing of surgery.


   PREOPERATIVE INVESTIGATION
 
Echocardiography (transthoracic or transesophageal), the principal preoperative examination, must be performed in every patient. Echocardiography provides evidence of new valvular regurgitation and/or detects valvular lesions such as vegetations, leaflet or annular abscess, and new partial dehiscence of prosthetic valve (Figs. 39-3 and 39-4).5,14–16 In the presence of sepsis, these findings are strongly suggestive of infective endocarditis.



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  		FIGURE 39-3 Vegetation on the atrial surface of the anterior leaflet seen on transesophageal imaging.

 


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  		FIGURE 39-4 Four-chamber mid-esophageal view showing a true aneurysm of the body of the anterior leaflet.

 
In patients with mitral insufficiency, Carpentier's functional classification can be used to describe the mechanism of regurgitation (Fig. 39-5).17 This functional classification determines valvular dysfunction based on an assessment of the amplitude of anterior and posterior leaflet motion during systole and can be applied to patients with mitral regurgitation secondary to endocarditis. The precise location of valve dysfunction is then established using segmental valve analysis. The mitral valve is composed of two commissures (anterior and posterior) and two leaflets. The presence of two indentations at the free margin of the posterior leaflet divides the leaflets into three segments. P1 and A1 are the anterior paracommissural segments of the posterior and anterior leaflet, respectively. P2 and A2 are middle scallops and P3/A3 are posterior paracommissural segments. During echocardiography, the transgastric view best visualizes these different components of the mitral valve.



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  		FIGURE 39-5 Carpentier's functional classification of mitral regurgitation. Type I: normal leaflet motion. Type II: increased leaflet motion (leaflet prolapse). Type III: restricted leaflet motion; IIIa, restriction in diastole and systole; IIIb, restriction in systole. Types I and II valvular dysfunctions are due to leaflet perforation and chordal rupture, respectively, in the setting of mitral endocarditis.

 
In native mitral endocarditis, lesions are usually extensive. Patients often present with a combination of lesions, which may include perforation of the anterior leaflet (type I valvular dysfunction) in association with posterior leaflet prolapse secondary to ruptured chordae (type II dysfunction). Typically, one or more vegetations may also be present. In patients with preexisting valve pathology (e.g., degenerative or ischemic mitral disease), annular dilatation is a common finding and constitutes a secondary lesion, which is not related directly to the infectious process. Rarely, type IIIa dysfunction is seen in patients with chronic healed mitral endocarditis due to calcified vegetations located on leaflets or subvalvular apparatus. Mitral valve endocarditis does not cause type IIIb valvular dysfunction.

Transthoracic echocardiography (TTE) has an excellent specificity for vegetation. However, TTE cannot exclude several aspects of endocarditis, including prosthetic valve infection, annular abscess, and intracardiac fistula. Patients at risk of perivalvular extension or prosthetic valve endocarditis should undergo transesophageal echocardiography (TEE). TEE has a significantly higher sensitivity (76% to 100%) and specificity (94%) than TTE for perivalvular infection.5 TEE also improves visualization of prosthetic valves, with 86% to 94% sensitivity and 88% to 100% specificity for vegetations. Echocardiography is also used to diagnose the potential concurrent infective endocarditis on aortic and tricuspid valves.

The preoperative examination also consists of a complete sepsis workup (i.e. serial blood cultures, urinalysis, dental exam, etc.) in order to confirm the diagnosis and identify potential sources of infection. Other studies may be necessary to rule out potential complications of endocarditis, such as renal dysfunction, peripheral septic emboli including cerebral embolism, thrombocytopenia, and coagulopathy.


   OPERATIVE TECHNIQUE
 
Principles

Surgery of both native and prosthetic mitral valve endocarditis may be challenging and requires experience with mitral reconstructive and reoperative procedures, respectively. However, regardless of the type of surgery, a systematic approach using the following principles should be applied to optimize surgical results:

  1. Intraoperative transesophageal echocardiography should be performed in every patient. It can be used initially to determine the mechanism of mitral regurgitation and at the completion of the procedure to evaluate the quality of repair or assess prosthetic valve function.
  2. Cardiac manipulation before aortic cross-clamping should be minimized to prevent peripheral embolization of vegetations. This is particularly important in patients with large, mobile, and friable vegetations.
  3. Following valve exposure, an accurate valve analysis should be performed to confirm the echocardiographic data and to assess the extent of lesions (perivalvular abscess, intervalvular fibrous body/ventricular involvement, and presence of intracardiac fistula).
  4. Radical resection of all infected and necrotic tissues is performed with a 1- to 2-mm margin of normal tissue. An infected prosthetic valve should be removed completely. Multiple specimens including vegetation and valvular debris should be sent for further microbiologic analysis. Local application of an antiseptic solution may be used.
  5. Surgical instruments including suction tips should be changed after debridement of infected tissue.
  6. The aortic valve may need to be inspected to rule out the extension of infection to the aortic root and the presence of any secondary lesions on the cusps.

Native Mitral Valve Endocarditis

A full sternotomy is performed. Cardiopulmonary bypass is established after the cannulation of the distal ascending aorta and superior/inferior vena cava with moderate systemic hypothermia. Myocardial protection is achieved with warm and cold blood cardioplegia delivered in an antegrade fashion (caution must be used when placing a retrograde cannula not to dislodge mitral vegetations). The mitral valve is exposed via a left atriotomy through the interatrial groove.

All macroscopically involved tissues are widely excised without any concern about the possibility of repair. Once the debridement is performed, reconstructive surgery using Carpentier's technique should be considered.18 The feasibility of mitral repair depends on the availability of healthy tissue following debridement. In the event of entire leaflet involvement or extensive destruction of the subvalvular apparatus, prosthetic valve replacement is performed using standard techniques. Because multiple studies have failed to identify differences in the recurrence of infection between mechanical and bioprosthetic valves, standard criteria should be applied for valve selection.7,19,20 There have also been reports of mitral homograft replacement in the setting of acute endocarditis, but at this time clinical experience remains limited.21

Mitral valve repair can be performed safely in multiple anatomic presentations provided sufficient tissue remains to allow valvular reconstruction without excessive tension on the suture lines.18,22–25

LEAFLET PERFORATION OR DETACHMENT

This lesion affects primarily the anterior leaflet. A common clinical presentation is a simultaneous aortic and mitral endocarditis. After adequate debridement, the leaflet defect is repaired with a patch of autologous pericardium. A piece of pericardium is preserved in 0.625% glutaraldehyde for 10 minutes and then rinsed in a saline bath for a total of 15 minutes. The patch is fixed to the remaining leaflet with polypropylene suture (Fig. 39-6). The smooth surface of the pericardium is turned toward the atrium to decrease the potential risk of thromboembolic complication. Occasionally, a large surface area of the anterior leaflet is destroyed in the setting of aortic and mitral valve endocarditis. If a homograft is used to reconstruct the aortic root, the homograft's attached mitroaortic curtain can be used to reconstruct the body of the native anterior leaflet. Mitral detachment from the fibrous skeleton can also occur in the setting of aortic and mitral endocarditis due to the extensions of aortic annular lesions. This typically occurs in a localized fashion around the anterior commissure of the mitral valve. Resuspension of the mitral apparatus to the fibrous skeleton can be accomplished in most circumstances with interrupted sutures (Fig. 39-7).



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  		FIGURE 39-6 Leaflet perforation (anterior leaflet) treated by autologous pericardial patch.

 


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  		FIGURE 39-7 Mitral detachment from the fibrous skeleton treated by resuspension using interrupted sutures.

 
POSTERIOR LEAFLET PROLAPSE

The middle scallop of the posterior segment (P2 segment) is often involved in the infectious process with one or several ruptured chordae. A quadrangular resection of P2 segment is performed. Plication or compression sutures are placed along the posterior annulus of the mitral valve. A sliding plasty of P1 and P3 segments is performed and the gap between the two scallops is closed with polypropylene suture (Fig. 39-8).



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  		FIGURE 39-8 (A) Posterior leaflet endocarditis with P2 segment prolapse. (B) P2 segment is resected. (C) Compression sutures are placed along the posterior annulus. (D) Sliding plasty of segments P1 and P3 is performed.

 
ANTERIOR LEAFLET PROLAPSE

Limited infection of the free margin of the anterior leaflet is best treated with a triangular resection followed by closure with interrupted polypropylene suture. In the event of chordal rupture, chordal transfer of the secondary chordae of anterior leaflet to the free margin or chordal transposition from the posterior leaflet may be required to provide adequate support.

COMMISSURAL PROLAPSE

When the commissure is involved, the prolapsed area is resected and reconstructed using leaflet sliding plasty (Fig. 39-9).



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  		FIGURE 39-9 (A) Anterior commissure endocarditis with prolapse. (B) Infected area is resected and compression sutures are placed. (C) Sliding commissuroplasty in the paracommissural area is performed.

 
ANNULOPLASTY

In the setting of mitral valve endocarditis, prosthetic ring annuloplasty following reconstruction remains controversial. In patients with acute endocarditis without annular dilatation or deformation, the use of a prosthetic ring can be avoided. However, in patients with chronic mitral regurgitation and dilated annulus, prosthetic ring annuloplasty should be utilized to restore proper coaptation and assure long-term durability of the repair. Alternatively, in the setting of acute endocarditis, a pericardial strip fixed in glutaraldehyde can be used to fashion a posterior annuloplasty.

Prosthetic Mitral Valve Endocarditis

Reoperative mitral valve surgery can be performed through a redo sternotomy or right anterolateral thoracotomy. In patients with previous isolated mitral valve surgery, either redo sternotomy or right anterolateral thoracotomy (provided that the aortic valve is not affected by the infectious process) can be performed safely with low operative risk. Redo sternotomy is the approach of choice if concomitant procedures such as coronary artery bypass grafting and/or aortic valve surgery are required. Right anterolateral thoracotomy is the preferred approach if the patient presents with multiple previous sternotomies, history of bypass grafting with patent grafts, or possibility of severe mediastinal adhesions (recent sternotomy, mediastinitis, and mediastinal radiation).26,27 The latter approach is relatively contraindicated in the setting of previous right-sided chest surgery, severe chronic obstructive pulmonary disease, or moderate to severe aortic insufficiency.

REDO STERNOTOMY

Femoral vessels are exposed in selective cases (e.g., suspicion of severe mediastinal adhesions or prior bypass surgery with patent grafts). If the femoral artery is not suitable because of atheroslerotic disease, the axillary artery may be used for an arterial cannulation site. After redo sternotomy, mediastinal dissection is limited to the ascending aorta and the right lateral aspect of the heart. Further dissection of the left side of the heart to drop the left ventricular apex may improve mitral valve exposure in some patients.

RIGHT ANTEROLATERAL THORACOTOMY

An anterolateral thoracotomy is performed through the 4th intercostal space. The interatrial groove and the right superior pulmonary vein are dissected. Direct cannulation of the ascending aorta and percutaneous femoral vein and direct superior vena cava cannulation are performed. If the ascending aorta is not suitable for cannulation (inaccessible, inadequate exposure, calcification), the femoral or axillary arteries are alternative sites for arterial cannulation. Peripheral cannulation is done using the Seldinger technique with a small, high-flow cannula specifically designed for percutaneous insertion. Cardiopulmonary bypass is instituted with vacuum-assisted drainage and the temperature is lowered. Once the heart fibrillates, the left atrium is opened. Brief periods of low-flow bypass may be necessary to ensure adequate exposure of the mitral valve in the presence of mild aortic regurgitation, particularly when operating near the anterior commissure.

MITRAL VALVE EXPOSURE

In both redo sternotomy and right anterolateral thoracotomy approaches, the mitral valve can be exposed transseptally28 or via a left atriotomy through the interatrial groove. The left atrium approach is the preferred technique. A complete dissection of the interatrial groove, which enables a left atriotomy closer to the valve, and posterior extension of the atriotomy are two maneuvers that significantly improve the valve exposure. The transseptal approach is useful in the setting of a small left atrium, prior aortic valve replacement, or when concomitant tricuspid valve surgery is also required.

RECONSTRUCTION OF THE MITRAL ANNULUS

Following mitral valve exposure, the infected prostheses should be excised. Because prosthetic valve endocarditis typically causes partial or total destruction of the mitral annulus, one may need to reconstruct the annulus before performing a reoperative mitral valve replacement. There are numerous techniques for annular reconstruction.

Mitral annular reconstruction using autologous or glutaraldehyde-fixed bovine pericardium (David technique)29,30 In patients with posterior annular destruction, a semicircular-shaped pericardial patch is used to reconstruct the annulus. While ensuring the patch is large enough to completely cover the defect, one side of the patch is sutured to the endocardium of the left ventricle and the other side is used to secure the prosthetic valve.

In patients with complete destruction of the annulus, a circumferential patch is tailored for annular reconstruction.

Mitral annular reconstruction using figure-of-eight atrial and ventricular sutures (Carpentier technique)31 With this technique, after careful debridement, the AV junction is reconstructed by a series of figure-of-eight 2-0 braided sutures placed into the atrial and ventricular edges. These sutures are the brought out on the atrial side. The ventricular bites of theses sutures should only involve one third of the thickness of the myocardial wall and be as wide as possible, taking advantage of any fibrous tissue present on the surface of the myocardium. Exerting traction on these sutures reduces the size of the annulus and closes the AV groove without injury to the circumflex vessels. The closure of the AV groove is facilitated by downward displacement of the atrial edge toward the ventricular edge with forceps. By means of this technique the circumflex vessels and surrounding fat are displaced outward and the AV junction is restored as a firm fibrous structure available for valve replacement.

If the infectious process involves the ventricular myocardium, the atrial edge is dissected free to mobilize an atrial flap (sliding atrium technique), which is used to cover the destroyed area. The fat and connective tissue surrounding the circumflex vessels are left attached to the ventricular side. Figure-of-eight sutures as described earlier are used to reconstruct the annulus and cover the ventricular area.

After mitral annular reconstruction, mitral valve replacement is performed using a standard technique.


   RESULTS
 
Hospital mortality rates ranging to approximately 50% have been previously reported in patients with mitral valve endocarditis, although recent series described improved results with mortality rates typically ranging between 0% and 20%.4,6,7,10,18,22–25,32,33 Several variables, including improvements in antimicrobial therapy, patient selection, myocardial protection, and surgical techniques, have all likely contributed to decreasing the operative mortality rate. Prosthetic valve endocarditis remains associated with a much higher operative mortality rate than native valve endocarditis (Fig. 39-10).4,6,7,33 Interestingly, the activity of mitral endocarditis (i.e., active vs. healed) does not appear to have an effect on short- or long-term survival, and therefore the activity of endocarditis is not of primary concern in the decision-making process regarding timing of surgery (Fig. 39-11).4 In patients with native mitral valve endocarditis, valve repair is preferable to valve replacement whenever feasible, because repair is associated with a lower hospital mortality and improved long-term survival (Fig. 39-12).24 Series from Broussais Hospital and the Cleveland Clinic have reported repair rates of 80% and 45%, respectively, demonstrating the feasibility of an aggressive approach to valve repair in patients with mitral valve endocarditis.18,24 Several recent series have documented outstanding results with valve repair in the setting of mitral endocarditis, with mortality rates ranging between 0% and 9%.18,22–25 In terms of infection-free survival, mitral valve repair is associated with a less than 1% per year reinfection rate, and appears to be preferable to mitral valve replacement.24 Preserving native mitral valve tissue by means of repair and avoiding a valve prosthesis in the setting of active infection most likely accounts for this observation.



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  		FIGURE 39-10 Kaplan-Meier survival curves for discharged native valve endocarditis (NVE) and prosthetic valve endocarditis (PVE) patients. (Reproduced with permission from Aranki SF, Adams DH, Rizzo RJ, et al: Determinants of early mortality and late survival in mitral valve endocarditis. Circulation 1995; 92(suppl II): II-143.)

 


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  		FIGURE 39-11 Kaplan-Meier survival curves for discharged active and healed endocarditis patients. (Reproduced with permission from Aranki SF, Adams DH, Rizzo RJ, et al: Determinants of early mortality and late survival in mitral valve endocarditis. Circulation 1995; 92(suppl II):II-143.)

 


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  		FIGURE 39-12 Event-free survival for all patients with endocarditis undergoing mitral valve repair or replacement. (Reproduced with permission from Muehrcke DD, Cosgrove DM III, Lytle BW, et al: Is there an advantage to repairing infected mitral valves? Ann Thorac Surg 1997;63:1718.)

 

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