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Desai ND, Christakis GT. Stented Mechanical/Bioprosthetic Aortic Valve Replacement.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:825856.

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Chapter 32

Stented Mechanical/Bioprosthetic Aortic Valve Replacement

Nimesh D. Desai/ George T. Christakis

NATURAL HISTORY AND INDICATIONS FOR OPERATION
????Aortic Stenosis
????????SYMPTOMATIC PATIENTS
????????ASYMPTOMATIC PATIENTS
????????LOW-GRADIENT SEVERE AORTIC STENOSIS
????????INDICATIONS FOR OPERATION
????Aortic Regurgitation
????????ACUTE AORTIC REGURGITATION
????????CHRONIC AORTIC REGURGITATION
????????SYMPTOMATIC CHRONIC AORTIC REGURGITATION
????????ASYMPTOMATIC CHRONIC AORTIC REGURGITATION
????????INDICATIONS FOR OPERATION
CORONARY ANGIOGRAPHY AND AORTIC VALVE REPLACEMENT
TECHNIQUE OF OPERATION
????Myocardial Protection and Cardiopulmonary Bypass
????Aortotomy, Valve Excision, and Debridement
????Valve Implantation
????De-airing
????Technical Considerations with Concomitant Coronary Artery Bypass Grafting
????Aortic Root Enlargement Procedures
????Reoperative Aortic Valve Surgery
????Aortic Balloon Valvotomy
POSTOPERATIVE MANAGEMENT
AORTIC VALVE REPLACEMENT DEVICES
????Mechanical Prostheses
????????CAGED-BALL PROSTHESIS
????????TILTING MONOLEAFLET PROSTHESES
????????BILEAFLET PROSTHESES
????Stented Bioprostheses
????????FIRST-GENERATION PROSTHESES
????????SECOND-GENERATION PROSTHESES
????????THIRD-GENERATION PROSTHESES
OUTCOMES OF AORTIC VALVE REPLACEMENT
????Operative Mortality
????Long-Term Survival
????Valve-Related Mortality
????Nonfatal Valve Events
????Structural Valve Deterioration
????????MECHANICAL PROSTHESES
????????STENTED BIOPROSTHESES
????Freedom from Reoperation
????Optimal Antithrombotic Therapy
????????MECHANICAL VALVES
????????BIOPROSTHETIC VALVES
????Prosthesis Thrombosis
????Prosthetic Valve Endocarditis
????Paravalvular Leak and Hemolysis
HEMODYNAMIC PERFORMANCE AND VENTRICULAR REMODELLING
????Patient-Prosthesis Mismatch
PROSTHESIS SELECTION
????Mechanical versus Stented Biologic Valves
????Stented versus Stentless Biologic Valves
REFERENCES

?? INTRODUCTION
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This chapter provides an overview of aortic valve replacement with mechanical and stented bioprostheses. Detailed anatomy and pathophysiology of aortic valve disease are presented in previous chapters. The indications for aortic valve surgery are reviewed with an emphasis on evidence-based guidelines. The techniques of aortic valve implantation are illustrated for mechanical and stented bioprostheses, and postoperative medical management is reviewed. Currently approved mechanical and stented aortic prostheses are described. Clinical and physiologic outcomes of aortic valve surgery are reviewed to create a rational basis for prosthesis selection. Techniques of allograft and stentless bioprosthesis implantation, advanced surgery of the aortic root, and aortic valve repair are presented in subsequent chapters.


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Aortic Stenosis

Aortic stenosis may be caused by degenerative calcification, congenital malformations, or rheumatic fever. It may also be found in association with systemic diseases such as Paget's disease of bone and end-stage renal disease. Congenital malformations include unicommisural and, more commonly, bicuspid valves. Detailed descriptions of these pathologies are presented earlier in this volume. Regardless of the initial pathology, there is a progressive reduction of effective orifice area caused by cusp calcification and/or commissural fusion.1,2 The normal human aortic valve has an area between 3.0 and 4.0 cm2. Mild, moderate, and severe aortic stenosis are defined as aortic valve areas greater than 1.5 cm2, 1.0 to 1.5 cm2, and less than 1.0 cm2, respectively.3 In the presence of normal cardiac output, transvalvular gradient is greater than 50 mm Hg when the aortic valve area is less than 1.0 cm2.4 There is a rapid increase in transvalvular gradient when the aortic valve area is less than 0.8 cm2.5 Exposure to elevated intracavitary pressures causes increased wall stress leading to parallel replication of sarcomeres and concentric hypertrophy.6,7 Concentric hypertrophy compensates for the obstruction to flow created by the reduced orifice area of the aortic valve and maintains normal cardiac output. With progressive hypertrophy, the compliance of the ventricle decreases and end-diastolic pressure rises.8,9 In this situation, the contribution of atrial contraction to preload becomes more significant and loss of sinus rhythm may lead to rapid progression of symptoms.7

SYMPTOMATIC PATIENTS

Hemodynamically significant aortic stenosis is initially counteracted by left ventricular hypertrophy. Progression of outflow obstruction and ventricular hypertrophy lead to the cardinal symptoms of aortic stenosis: angina, syncope, and congestive heart failure. The average aortic valve area is 0.6 cm2 at the onset of symptoms.7 Classic natural history studies have shown that the average life expectancy in patients with hemodynamically significant aortic stenosis is 4 years if anginal symptoms are present, 3 years if they have experienced syncope, and 2 years with the onset of congestive heart failure.10 Symptomatic patients should therefore undergo aortic valve replacement (AVR)in a timely fashion.11 Excessive waiting periods for AVR in symptomatic patients are associated with increased mortality. The rate of sudden death is greater than 10% per year in symptomatic patients. Once a patient is symptomatic, average survival is less than 3 years.1215

ASYMPTOMATIC PATIENTS

Managing asymptomatic patients with hemodynamically significant aortic stenosis can be a challenging problem as there is often a prolonged latent period before symptoms emerge. During the latent period, there is a progression of concentric left ventricular hypertrophy as the ventricle adapts to elevated chamber pressures. Studies by Otto et al have shown that 7% of asymptomatic patients experience death or aortic valve surgery within 1 year after diagnosis.16 After 5 years, the incidence of death or aortic valve surgery increases to 38%. The average decrease in aortic valve area is 0.12 cm2 per year, while the average increase in transvalvular pressure is often 10 to 15 mm Hg per year.17 Sudden death is quite uncommon and occurs in asymptomatic patients at a rate of approximately 0.4% per year.18 The vast majority of patients who experience sudden death will become symptomatic in the months prior to death.19 There is considerable variation in disease progression and many patients do not experience any change in gradient for several years. Rosenhek et al identified that, among asymptomatic patients, patients with an increase in peak jet velocity greater than 0.45 m/s per year on serial echocardiography were substantially more likely to need operation than patients with lesser changes in jet velocity.20

LOW-GRADIENT SEVERE AORTIC STENOSIS

The significance of aortic stenosis is often unclear in patients with very poor ventricular function (ejection fraction less than 20%) who have severely stenotic valves but small (mm Hg) transvalvular gradients. The compromised left ventricular function in these patients may be caused by afterload mismatch created by the stenotic valve, or by an intrinsic cardiomyopathy, particularly in the setting of chronic ischemia from diffuse coronary disease. In these patients, measurement of transvalvular gradient and valve area at rest and with positive inotropy (i.e., dobutamine infusion) may distinguish whether cardiomyopathy or true valvular stenosis is the most responsible lesion. Patients with a preponderance of cardiomyopathy often do not experience significant benefit from valve replacement.21 Hwang et al, using a multivariate analysis to determine factors that predict poor functional outcome after aortic valve replacement for aortic stenosis, identified that poor preoperative left ventricular function was the most significant predictor, followed by preoperative myocardial infarction, preoperative low transvalvular gradient, and incomplete coronary revascularization.22

INDICATIONS FOR OPERATION

In 1998, a joint task force of the American College of Cardiology (ACC) and the American Heart Association (AHA) developed evidence-based consensus guidelines for management of valvular heart disease.23 Their recommendations for aortic valve replacement in the setting of aortic stenosis are summarized in Table 32-1. A class I recommendation indicates there is good evidence and general agreement that the treatment is useful and effective; class IIA indicates there may be some disagreement but the weight of evidence supports the usefulness/efficacy of the treatment in that setting; class IIB indicates that the usefulness/efficacy of the treatment is less well established; and a class III recommendation indicates that the treatment is either not useful or may be potentially harmful.


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TABLE 32-1 ACC/AHA guidelines for aortic valve replacement in patients with aortic stenosis

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Aortic valve replacement is indicated in all symptomatic patients or patients with severe asymptomatic aortic stenosis who require concomitant coronary bypass, aortic surgery, or other valve replacement. It is our practice to perform aortic valve replacement on patients with moderate aortic stenosis requiring concomitant cardiac surgery. We do not routinely perform aortic valve replacement in patients with mild aortic stenosis undergoing concomitant cardiac surgery. Aortic valve replacement should be performed in otherwise asymptomatic patients with severe aortic stenosis and severe left ventricular dysfunction, exercise-induced symptoms, significant hypertrophy, or ventricular arrhythmia. Asymptomatic patients with very high transvalvular gradients (>60 mm Hg) or highly stenotic valves (valve area less than 0.6 cm2) are at higher risk for progression to symptoms and should have valve replacement prior to significant ventricular decompensation or sudden death.

Aortic Regurgitation

ACUTE AORTIC REGURGITATION

Acute aortic regurgitation occurs in the setting of acute aortic dissection, infective endocarditis, trauma, active connective tissue disease, aortic cusp prolapse associated with ventricular septal defects, aortitis (syphilitic or giant cell), Marfan syndrome, Ehlers-Danlos syndrome, or iatrogenically after aortic balloon valvotomy.7 It may be caused by acute dilatation of the aortic annulus preventing adequate cusp coaptation or by disruption of the valve cusps themselves. The heart cannot readily tolerate acute aortic regurgitation as the left ventricle is unable to cope with the sudden increase in end-diastolic volume caused by the regurgitant volume load. The normal ventricular chamber cannot acutely dilate sufficiently to prevent the Frank-Starling mechanism from being overwhelmed.24 Hence, a dramatic reduction in forward stroke volume occurs. If there is poor left ventricular compliance from hypertrophy prior to the onset of acute aortic regurgitation, hemodynamic decompensation is significantly more dramatic.

To compensate for the acute decline in forward stroke volume, tachycardia ensues. Volume overload causes the left ventricular diastolic pressure to acutely rise above left atrial pressure resulting in early closure of the mitral valve.25 While early mitral valve closure protects the pulmonary venous circulation from high end-diastolic pressures, rapid progression of pulmonary edema and cardiogenic shock are often unavoidable.

Death is the common end point of all etiologies of acute aortic regurgitation. Progressive cardiogenic shock and malignant ventricular arrhythmias are common causes of death. Urgent surgical treatment is warranted for all causes of hemodynamically significant acute aortic regurgitation.

CHRONIC AORTIC REGURGITATION

Chronic aortic regurgitation is caused by either slow enlargement of the aortic root or dysfunction of the valve cusps. Common etiologies include congenital abnormalities, calcific cusp degeneration, rheumatic fever, endocarditis, degenerative aortic dilatation as seen in the elderly, Marfan syndrome, Ehlers-Danlos syndrome, myxomatous proliferation, osteogenesis imperfecta, ankylosing spondylitis, Behcet syndrome, Reiter syndrome, psoriatic arthritis, severe systemic hypertension, and idiopathic aortic root dilatation.7 The anorectic drugs fenfluramine and dexfenfluramine have been implicated in left- and right-sided valvular disease, including aortic regurgitation.26,27 Bicuspid aortic valve is the most common congenital abnormality, but unicommissural, quadricuspid, and fenestrated valves may also occur.28

Chronic aortic regurgitation causes a chronic volume overload of the left ventricle. This leads to progressive chamber enlargement without increasing end-diastolic pressure during the asymptomatic phase of the disease.29 Progressive chamber enlargement is accompanied by eccentric hypertrophy, with sarcomere replication and elongation of myocytes.30 The combination of chamber dilatation and hypertrophy leads to a massive increase in left ventricular mass. Initially, the ratio of wall thickness to chamber diameter, ejection fraction, and fractional shortening are all maintained.31 However, this degenerates into a repetitive cycle of enlarging chamber radius with continually increasing wall stress. This wall stress is compensated by ventricular hypertrophy. Interstitial fibrosis limits the ability of the ventricle to further dilate and this cycle becomes overwhelmed, leading to elevated end-diastolic pressure, left ventricular systolic dysfunction, and congestive heart failure.32 Vasodilator therapy may delay progression of ventricular dysfunction by decreasing afterload and decreasing regurgitant flow. This therapy is not recommended in patients with severe aortic regurgitation and left ventricular dysfunction as it does not improve survival.33 Vasodilator therapy is currently indicated in patients with severe left ventricular dysfunction who are not operative candidates, asymptomatic patients with hypertension, asymptomatic patients with severe aortic regurgitation, ventricular dilatation, and preserved systolic function, and for short-term hemodynamic tailoring prior to operation.33

SYMPTOMATIC CHRONIC AORTIC REGURGITATION

The time course from diagnosis of aortic regurgitation to the development of symptoms is highly variable. Since symptoms, such as angina and dyspnea, develop only after significant ventricular decompensation, surgery is advocated prior to the symptomatic phase of the disease. Symptomatic patients experience greater than 10% mortality per year without surgical management.34,35

ASYMPTOMATIC CHRONIC AORTIC REGURGITATION

Natural history studies of asymptomatic aortic regurgitation show that symptoms, left ventricular dysfunction, or both develop in less than 6% of patients per year.36 Progression to asymptomatic left ventricular dysfunction occurs in less than 4% of patients per year.37 Sudden death occurs in less than 0.2% per year.38 Age, left ventricular end-systolic dimension, rate of change in end-systolic dimension, and rest ejection fraction are all independent predictors of progression to symptoms, left ventricular dysfunction, or death in asymptomatic patients.39 Asymptomatic patients with left ventricular systolic dysfunction experience onset of symptoms at a rate exceeding 25% per year.40

INDICATIONS FOR OPERATION

A summary of the ACC/AHA Task Force guidelines for aortic valve replacement for aortic regurgitation is presented in Table 32-2.41 Symptomatic patients (NYHA class II or higher) with mild to moderate left ventricular systolic dysfunction (ejection fraction >20% to 30% or end-systolic dimension aortic valve replacement. Mild to moderately symptomatic patients with significant ventricular dysfunction often experience significant benefit from surgery. Patients with more severe symptoms or left ventricular dysfunction have decreased survival due to irreversible changes to the ventricle including hypertrophy and interstitial fibrosis.42 Aortic valve replacement in patients with NYHA class IV symptoms and severe left ventricular dysfunction is associated with increased perioperative mortality and poor prognosis.42,43 The decision to operate on such patients is dependent on individual variables as the outcomes are poor with surgery or medical therapy.


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TABLE 32-2 AHA/ACC recommendations for aortic valve replacement in chronic severe aortic regurgitation

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All patients with moderate to severe symptoms (NYHA class III or IV) and preserved left ventricular function should undergo aortic valve replacement. Patients with mild symptoms should have valve replacement if there is evidence of declining left ventricular systolic function (ejection fraction approaching 50%) or increasing chamber size (end-systolic diameter approaching 55 mm, end-diastolic dimension approaching 70 mm) on serial assessment.

Asymptomatic patients with systolic dysfunction (ejection fraction diameter >55 mm, end-diastolic dimension >70 mm) should have aortic valve replacement. Patients with serial deterioration of ventricular function or chamber size should have valve replacement prior to the onset of irreversible ventricular depression. Hwang et al identified poor preoperative left ventricular function and left ventricular systolic pressure as determinants of poor postoperative functional outcome in patients undergoing aortic valve replacement for aortic regurgitation.44


?? CORONARY ANGIOGRAPHY AND AORTIC VALVE REPLACEMENT
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Many patients requiring aortic valve replacement have coexistent coronary artery disease. At our institution, more than one third of aortic valve replacement procedures are combined with coronary bypass surgery. This proportion may increase as the surgical population continues to age. Risk assessment for ischemic heart disease is complicated in patients with aortic valve disease since angina may be related to true ischemia from hemodynamically significant coronary lesions or other causes such as left ventricular wall stress with subendocardial ischemia or chamber enlargement in the setting of reduced coronary flow reserve. Since traditional coronary risk stratification is unreliable in aortic valve patients, it is our practice to routinely perform diagnostic coronary angiography on all patients over the age of 35. ACC/AHA Task Force guidelines for preoperative angiography are presented in Table 32-3.45


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TABLE 32-3 ACC/AHA task force guidelines on coronary angiography in patients with valvular heart disease

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?? TECHNIQUE OF OPERATION
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Myocardial Protection and Cardiopulmonary Bypass

Isolated aortic valve replacement is performed using a single two-stage venous cannula inserted into the right atrium for venous return and a standard arterial cannula into the ascending aorta for systemic perfusion of oxygenated blood. A venting cannula is placed in the right superior pulmonary vein to ensure a bloodless field. After the cross-clamp is applied, myocardial protection is initially delivered as a single dose of high-potassium blood through the ascending aorta.4648 This will achieve prompt diastolic arrest unless there is significant aortic regurgitation. Our group does not routinely use retrograde cardioplegia for all aortic valve cases, but this strategy is helpful in patients with significant aortic regurgitation or severe concomitant coronary disease.49 Myocardial protection is maintained by continuous infusion of tepid oxygenated blood delivered via direct cannulation of both coronary ostia after the aorta has been opened.50 If retrograde perfusion is employed, this is also used in a continuous manner. Right ventricular myocardial protection via retrograde perfusion is often inadequate and can lead to significant right ventricular dysfunction after cardiopulmonary bypass is discontinued.5154

Aortotomy, Valve Excision, and Debridement

The aorta and pulmonary artery are dissected to expose the anterior aortic root to the left coronary artery prior to initiating cardioplegia. After arrest has been achieved, the aorta is opened with a transverse incision approximately 5 mm above the origin of the right coronary artery that may be extended posteriorly to the noncoronary sinus of Valsalva (Fig. 32-1). Morphology of the valve is then inspected (Fig. 32-2). Excision of the valve cusps starts at the commisure between the right and noncoronary cusps (Fig. 32-3). Mayo scissors are usually used at this stage. A moistened radioopaque sponge is placed into the outflow area to catch debris. Thorough decalcification to soft tissue improves seating of the prosthesis, and decreases the incidence of paravalvular leak and dehiscense. Care must be taken to prevent aortic perforation while all calcific deposits are debrided off the aortic wall, particularly at the commissure between the left and noncoronary cusps. Careful use of a scalpel or rongieurs may also be required. It is important to note that the bundle of His (conduction system) is located below the junction of the right and noncoronary cusp at the membranous septum. The anterior leaflet of the mitral valve is in direct continuity with the left aortic valve cusp. If it is damaged during decalcification, an autologous pericardial patch is used to repair the defect.



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FIGURE 32-1 Exposure and aortotomy incision. A two-stage venous cannula is in place in the right atrial appendage. The aortotomy (dashed line) is started approximately 5 mm above the origin of the right coronary artery. (Courtesy of Dr. C. Hayman.)

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FIGURE 32-2 The exposed aortic valve. (Courtesy of Dr. C. Hayman.)

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FIGURE 32-3 The aortic valve after debridement. (Courtesy of Dr. C. Hayman.)

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Valve Implantation

After the native valve has been excised, the annulus is sized with a valve sizer appropriate to the selected mechanical or bioprosthetic device. The valve is secured to the annulus using 12 to 16 double-needled interrupted 2-0 synthetic braided pledgeted sutures. The pledgets can be left on the inflow/ventricular side or the outflow/aortic side of the aortic annulus (Figs. 32-4 and 32-5). Placing the pledgets on the inflow side of the annulus allows the placement of a larger prosthesis and this technique is routinely used at our institution. The aorta is closed with a double row of synthetic polypropelene sutures.



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FIGURE 32-4 Placement of sutures with pledgets below the annulus. (Courtesy of Dr. C. Hayman.)

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FIGURE 32-5 Placement of sutures with pledgets above the annulus. (Courtesy of Dr. C. Hayman.)

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De-airing

During AVR, air may be entrained into the left atrium and ventricle and the aorta. This must be removed to prevent potential catastrophic air embolization. Immediately prior to tying the suture of the aortotomy, the heart is allowed to fill, the vent in the superior pulmonary vein is stopped, the lungs are inflated, and the cross-clamp is briefly partially opened. The subsequent influx of blood should expel most air from these cavities out of the partially open aortotomy. Closure of the aortotomy is then completed and the cross-clamp is fully removed. The cardioplegia cannula in the ascending aorta and the LV vent are then placed on suction to remove any residual air as the heart begins electrical activity. A small needle (21 gauge) is used to aspirate the apex of the left ventricle and the dome of the left atrium.

Technical Considerations with Concomitant Coronary Artery Bypass Grafting

Operative technique is modified to optimize myocardial protection when there is concomitant coronary disease. Distal anastomoses are performed prior to aortic valve replacement so that cardioplegia may be administered through these grafts during the operation. We routinely use the left internal thoracic artery for revascularization of the left anterior descending artery as this may improve long-term survival.55 This anastomosis is performed after the aortotomy is closed to ensure that the coronary circulation is not exposed to systemic circulation during cardioplegic arrest and to prevent trauma to the anastomosis during manipulation of the heart. All surgeons at our institution use a single cross-clamp technique for performing proximal anastomoses.

Aortic Root Enlargement Procedures

Detailed descriptions of aortic root enlargement procedures are presented in a later chapter. Either an anterior or posterior annular enlargement procedure may be performed in a patient with small aortic root to allow for implantation of a larger valve. The posterior approach is the most commonly used aortic root enlargement procedure in adults and can increase the annular diameter by 2 to 4 mm. With the posterior approach, first described by Nicks et al in 1970, the aortotomy is extended downward through the noncoronary cusp, through the aortic annulus, and into the anterior mitral leaftlet.56 Manouguian, in 1979, described a procedure extending the aortotomy incision in a downward direction through the commissure between the left and noncoronary cusps into the interleaflet triangle and anterior leaflet of the mitral valve.57,58 The anterior approach is generally used in the pediatric population. Described by Konno et al in 1975, this technique, which is also known as aortoventriculoplasty, is used when greater than 4 mm of annular enlargement is required.59 Instead of a transverse incision, a longitudinal incision is made in the anterior aorta and extended to the right coronary sinus of Valsalva and then through the anterior wall of the right ventricle to open the right ventricular outflow tract. The ventricular septum is incised allowing significant expansion of the aortic annulus and left ventricular outflow tract.

Reoperative Aortic Valve Surgery

Repeat sternotomy after aortic valve replacement may be performed for valve-related complications, progressive ascending aortic disease, or coronary disease. Valve-related causes include structural valve deterioration, prosthetic endocarditis, prosthesis thrombosis, or paravalular leak. Chest reentry is the most hazardous portion of any repeat cardiac procedure. It is our practice to obtain an adequate lateral chest roentgenogram to determine the proximetry of cardiac structures to the posterior sternum. If the right ventricle or an ascending aortic graft is close to the sternum, a computed tomography scan is performed to accurately determine the risk of injury upon entry. Cardiopulmonary bypass is instituted through the femoral vessels when there is concern about chest reentry. An oscillating saw is used to open the sternum and the dissection is kept as limited as possible. Extreme caution must be employed during dissection when there are patent bypass grafts.

The prosthesis is excised with sharp dissection. Care must be taken to remove all sutures and pledgets from the annulus. Annular injuries caused while excising the prosthesis are repaired with pledgeted interrupted sutures.

In the setting of endocarditis, aggressive debridement of infected tissue must be performed with appropriate annular reconstruction with pericardium when root abscesses are present.60,61 All foreign graft material, including Dacron aortic grafts, must be excised in the presence of active endocarditis.62

In the presence of a Dacron prosthesis in the ascending aorta, chest reentry is extremely hazardous since exsanguination will occur if the graft is accidentally opened during dissection. To limit the systemic consequences of exsanguination at normothermia, the patient should be placed on femoral-femoral cardiopulmonary bypasss and cooled to 20?C prior to chest reentry.63 If the Dacron graft is accidentally opened, local control of the bleeding is established and cardiopulmonary bypass is stopped. Under circulatory arrest, atrial venous cannulation is instituted and the graft is controlled distal to the tear. Cardiopulmonary bypass may then be restarted.

In all repeat aortic procedures, rigorous myocardial protection must be applied because these procedures often have very long ischemic times. Antegrade cold blood cardioplegia is usually employed in a continuous fashion throughout the case by selective cannulation of the coronary ostia.

Aortic Balloon Valvotomy

Aortic balloon valvotomy may be performed percutaneously via a femoral artery puncture in the interventional angiography suite to treat aortic stenosis.64 Inflation of the balloon within the valve orifice can stretch the annular tissue and fracture calcified areas or open fused commissures. There is no role for valvotomy in the patient with significant aortic regurgitation as this will become significantly worse after the procedure.6567 Balloon valvotomy is rarely successful if significant calcification is present and carries a prohibitive risk of stroke from calcific emboli.67,68 The long-term outcomes of this procedure in adult patients are dismal, with restenosis usually occurring within 1 year.67,69,70 Patients with severe symptomatic aortic stenosis who are too hemodynamically unstable to tolerate operation or have comorbid illnesses, such as advanced malignancy, which contraindicate operation, may benefit from palliative balloon valvotomy.7174


?? POSTOPERATIVE MANAGEMENT
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Special consideration must be given to the underlying pathologic changes to the ventricle during the immediate postoperative period. The severely hypertrophied, noncompliant left ventricle found in aortic stenosis is highly dependent on sufficient preload for adequate filling. Filling pressures should be carefully titrated between 15 mm Hg and 18 mm Hg with intravenous volume infusion. Maintenance of sinus rhythm is also essential as up to one third of cardiac output is derived from atrial contraction in a noncompliant ventricle. Up to 10% of patients will experience low cardiac output syndrome in the immediate postoperative period.75 If pacing is required postoperatively, synchronous atrioventricular pacing is beneficial in preventing low cardiac output syndrome. In cases of severe hypertrophy, subvalvular left ventricular outflow obstruction with systolic anterior wall motion of the mitral valve may occur. Intravenous beta-adrenergic blockade may relieve this obstruction by decreasing inotropy. In extreme cases, surgical myectomy may be required.62

Profound peripheral vasodilation, often seen in patients with aortic insufficiency, is treated with vasoconstrictors including alpha-adrenergic agonists or vasopressin. Adequate filling of the dilated left ventricle may also require volume infusion.

Complete heart block occurs in 3% to 5% of AVR patients. This complication may be due to suture placement or injury from aggressive debridement near the conduction system. Transient complete heart block caused by perioperative edema usually resolves in 4 to 6 days, after which insertion of a permanent pacemaker is recommended. Optimal antithrombotic therapy will be addressed later in this chapter.


?? AORTIC VALVE REPLACEMENT DEVICES
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Mechanical Prostheses

Currently available mechanical prostheses include caged-ball, single tilting disc, and bileaflet prostheses.

CAGED-BALL PROSTHESIS

The Starr-Edwards caged-ball prosthesis was developed in the early 1960s and was the first commercially available heart valve. Although it initially underwent minor modifications, it has not been changed since 1965 and is still actively implanted throughout the world. It is associated with a very low incidence of mechanical failure but may have a higher risk of thromboembolism than other currently available mechanical prostheses.33

TILTING MONOLEAFLET PROSTHESES

Tilting monoleaflet prostheses were initially developed in the late 1960s and current models include the Medtronic Hall (Medtronic, Minneapolis, MN), Omnicarbon (MedicalCV, Inc., Inver Grove Heights, MN), and Allcarbon Monodisc (Sorin Biomedica, Saluggia, Italy) prostheses. These valves incorporate a single pyrolite carbon-coated tungsten-impregnated leaflet into a titanium or solid pyrolite housing. The leaflet of the Medtronic Hall valve slides along an open-ended central guide strut. The leaflet of Omnicarbon valve rotates about pivots located in the housing, while the leaflet of the Allcarbon Monodisc valve is contained by struts from the valve housing. The opening angle of these monoleaflet valves is between 75? and 80?.

BILEAFLET PROSTHESES

Bileaflet prostheses currently available in North America include the St. Jude Medical Standard, Masters, Regent, and Hemodynamic Plus valves (St. Jude Medical Inc., Minneapolis, Minnesota); Carbomedics and Top-Hat Supra-annular valves (Sulzer Carbomedics, Inc., Austin, Texas); ATS valve (ATS Medical Inc., Minneapolis, Minnesota); Bicarbon valve (Sorin Biomedica, Saluggia, Italy); Edwards MIRA valve (Edwards Lifesciences, Irvine CA.); and the On-X valve (Medical Carbon Research Institute, Austin, Texas). Modern bileaflet prostheses are typically comprised of two pyrolite-carbon coated leaflets made of radiopaque tungsten-impregnated graphite substrate inside a solid pyrolite carbon or pyrolite carbon-coated titanium housing. The leaflets rotate around pivots located within the housing. Retrograde washing decreases thrombogenicity by decreasing stasis of blood around the valve and pivot mechanisms.

Recent design changes include the ability to rotate the valve within the housing for optimum alignment of the leaflets. Most bileaflet valves have opening angles between 75? and 85?. Modifications to the sewing cuffs of current prostheses include narrower sewing cuffs to increase valve internal diameter and allow supra-annular placement. Several valves including the Edwards MIRA and Bicarbon valves incorporate curved leaflets to potentially improve laminar flow and allow for faster closure.

Stented Bioprostheses

Stented biologic prostheses may be constructed of porcine aortic valves or bovine pericardium. Over the past 40 years, advances in tissue fixation methodology and chemical treatments to prevent calcification have yielded improvements in the longevity of bioprostheses. All heterograft valves are preserved with glutaraldehyde, which cross-links collagen fibers and reduces the antigenicity of the tissue. Glutaraldehyde also reduces the rate of in vivo enzymatic degradation and causes the loss of cell viability, thereby preventing normal turnover and remodeling of extracellular matrix tissues.76,77 Calcification occurs when nonviable glutaraldehyde-fixed cells cannot maintain low intracellular calcium.78 Calcium-phosphate crystals form at the phospholipid-rich membranes and their remnants, and collagen also calcifies.79

Glutaraldehyde fixation in porcine valves can be performed at high pressure (6080 mm Hg), low pressure (0.12 mm Hg), or zero pressure (0 mm Hg). Pericardial prostheses are fixed in pressure-free conditions. Porcine prostheses fixed at zero pressure retain the collagen architecture of the relaxed aortic valve cusp.80 Higher fixation pressures cause tissue flattening and compression with loss of transverse cuspal ridges and collagen crimp.8183

Multiple chemical treatments have been proposed to decrease the calcification process that invariably leads to material failure and valvular dysfunction. These include sodium dodecyl sulfate, polysorbate-80, Triton X-100 and N-lauryl sarcosine, amino-oleic acid, aminopropanehydroxydiphosphonate, toluidine blue, controlled-release diphosphonates, ferric chloride, aluminum chloride, and phosphocitrate.8498

FIRST-GENERATION PROSTHESES

First-generation bioprostheses were preserved with high-pressure fixation and were placed in the annular position. They include the Medtronic Hancock Standard and Modified Orifice (Medtronic, Minneapolis, MN) and Carpentier-Edwards Standard porcine prostheses (Edwards Lifesciences, Irvine, CA).

SECOND-GENERATION PROSTHESES

Second-generation prostheses are treated with low- or zero-pressure fixation. Several second-generation prostheses may also be placed in the supra-annular position, which allows placement of a slightly larger prosthesis. Porcine second-generation prostheses include the Medtronic Hancock II (Medtronic, Minneapolis, MN) and Carpentier-Edwards Supra-annular (SAV) (Edwards Lifesciences, Irvine, CA) valves. Second-generation pericardial prostheses include the Carpentier-Edwards Perimount (Edwards Lifesciences, Irvine, CA) and Mitroflow Synergy (Sulzer Carbomedics, Austin, TX) valves.

THIRD-GENERATION PROSTHESES

Newer generation prostheses incorporate zero- or low-pressure fixation with antimineralization processes that are designed to reduce material fatigue and calcification. They include the Medtronic Mosiac porcine (Medtronic, Minneapolis, MN), Medtronic Intact porcine (Medtronic, Minneapolis, MN), St. Jude Medical X-Cell porcine (St. Jude Medical, Minneapolis, MN), Sulzer Synergy ST porcine (Sulzer Carbomedics, Austin, TX), and Pericarbon MORE (Sorin Biomedica Saluggia, Italy) pericardial valves.


?? OUTCOMES OF AORTIC VALVE REPLACEMENT
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Operative Mortality

Operative mortality is defined as all-cause mortality within 30 days of operation or during the same hospital admission.99 Contemporary series describe a low or very low operative mortality for isolated aortic valve replacement. The mortality from aortic valve replacement varies between 1% and 6%, depending on the patient population and era of study.100111 A recent publication from the Society of Thoracic Surgeons database reviewing the results of 86,580 valve procedures found an overall mortality of 4.3% for isolated aortic valve replacement and 8.0% for aortic valve replacement with coronary bypass surgery.110 Aortic valve replacement with ascending aortic aneurysm repair had an operative mortality of 9.7%.110 The results of this study are summarized in Table 32-4. It is important to note that information in this database is voluntarily submitted and includes academic, nonacademic, low-volume, and high-volume centers.


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TABLE 32-4 Operative mortality rates for aortic valve procedures from the Society of Thoracic Surgeons' database

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Advanced patient age, poor preoperative left ventricular function, NYHA class IV symptoms, concomitant coronary artery disease, severe preoperative renal dysfunction, active endocarditis, female sex, emergent or salvage operation, and previous aortic valve replacement have been associated with increased operative mortality in several series.75,102,110117 In the absence of major comorbidities and preserved left ventricular function, isolated aortic valve replacement can be performed with an expected mortality of less than 1%.62 Kouchoukos et al have shown that operative mortality is not further increased if simple resection of an ascending aortic aneurysm is performed at an experienced center.118 Concomitant coronary bypass surgery is associated with approximately double the operative mortality of isolated aortic valve replacement.109,110,119121 Table 32-5 presents the preoperative risk factors of operative mortality derived from the Society of Thoracic Surgeons database. Most early deaths are attributable to postoperative low cardiac output syndrome, neurologic injury, or infection.


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TABLE 32-5 Independent risk factors for operative mortality (odds ratios) for isolated aortic valve replacement and aortic valve replacement plus coronary artery bypass from the Society of Thoracic Surgeons' database

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Long-Term Survival

Longitudinal analysis shows there is no difference in survival over 10 years of follow-up between patients receiving mechanical and bioprosthetic valves when they are implanted in similar age cohorts.122 However, after 15 years of follow-up, structural valve deterioration in bioprosthetic valves leads to a survival benefit for patients with mechanical valves. In a prospective trial by Hammermeister et al, 11-year mortality was 62% and 57% for bioprosthetic and mechanical valves, respectively.123 At 15 years, mortality in the bioprosthetic group rose to 79% while mortality in the mechanical valve group rose to 66%.124 There were substantially more bleeding events in patients with mechanical valves. In is important to note that the effect of bioprosthetic structural deterioration on mortality in this series was influenced by the actual prosthesis used in the study (Medtronic Hancock porcine). This is a first-generation prosthesis and may be more prone to structural failure than new devices.125,126

In most published series, the expected survival after aortic valve replacement is approximately 80% to 85% at 5 years, 65% to 75% at 10 years, and 45% to 55% at 15 years.125,127129 The outcomes of AVR are highly dependent on the functional status and comorbidities of each individual patient.129,130 Cohen et al studied the impact of age, concomitant coronary artery disease, left ventricular dysfunction, and poor functional status on survival after bioprosthetic aortic valve replacement. Their results, presented in Table 32-6, show an additive risk for each of these comorbid factors.131 Other studies have shown that concomitant renal disease, female gender, concomitant cardiac or vascular procedure, and atrial fibrillation are also risk factors for late mortality.102,120,130,132,133


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TABLE 32-6 Survival probability calculated from the accelerated time failure model with the log-logistic distribution for combinations of risk factors

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Valve-Related Mortality

Long-term survival data distinguishes between valve-related mortality, nonvalve-related cardiac mortality, and mortality from other causes. A revised consensus document from the Society of Thoracic Surgeons (STS) and the American Association of Thoracic Surgeons (AATS) was published in 1996 outlining a standardized method to report valve-related complications in prosthetic and repaired heart valves.134 This panel defined valve-related mortality as all deaths caused by structural valve deterioration, nonstructural valve dysfunction, valve thrombosis, embolism, bleeding event, operated valvular endocarditis, or death related to reoperation of an operated valve. Sudden, unexplained, unexpected deaths of patients with an operated valve are included as valve-related mortality. Deaths caused by progressive heart failure in patients with satisfactorily functioning cardiac valves are not included. In the Hammermeister series, valve-related deaths accounted for 37% of all deaths in patients with a mechanical valve and 41% of all deaths in patients with a bioprosthesis at 15 years.124 Nonvalvular cardiac deaths accounted for 17% and 21% of deaths at 15 years in patients with mechanical valves and bioprostheses, respectively.124

Nonfatal Valve Events

The joint STS/AATS panel defined specific guidelines for reporting outcomes on structural and nonstructural valve deterioration, valve thrombosis, embolic events, bleeding events, and prosthetic endocarditis.135 These definitions are summarized below.

  1. Structural valve deterioration: Any change in function of an operated valve resulting from an intrinsic abnormality of the valve that causes stenosis or regurgitation, such as wear, leaflet tears, or suture line disruption of components.
  2. Nonstructural dysfunction: Any abnormality of an operated valve resulting in stenosis or regurgitation that is caused by factors not intrinsic to the valve itself, such as pannus overgrowth, inappropriate sizing, or paravalvular leak.
  3. Valve thrombosis: Any thrombus attached to or near an operated valve that interferes with valve function in the absence of infection.
  4. Embolism: Any embolic event that occurs after the immediate postoperative period when perioperative anesthesia has been completely reversed. Emboli may be peripheral (noncerebral) or cerebral. Myocardial infarction is excluded unless the event occurs after the perioperative period and coronary artery embolus is unequivocally documented.
    Cerebral embolic events are subclassified into:
    1. Transient ischemic attacks: Fully reversible neurologic events lasting less than 24 hours.
    2. Reversible ischemic neurological deficit: Fully reversible neurologic events lasting more than 24 hours and less than 3 weeks.
    3. Stroke: Permanent neurologic deficit lasting longer than three weeks or causing death.

  5. Bleeding event: Any episode of major internal or external bleeding that causes death, hospitalization, or permanent injury, or requires transfusion regardless of the patient's anticoagulation status. This does not include embolic stroke followed by hemorrhagic transformation and intracranial bleed.
  6. Operated valvular endocarditis: Any infection involving an operated valve. Any structural/nonstructural valvular dysfunction, thrombosis, or embolic event associated with operated valvular endocarditis is included only in this category.

Time-related analysis of nonfatal complications is often expressed by the Kaplan-Meier actuarial method or by the recently described cumulative incidence method proposed by Grunkemeier.136 Cumulative incidence (or actual) reporting provides more meaningful information as it censors the impact of mortality on nonfatal outcomes. This is most relevant in higher risk groups such as elderly patients, in which many patients will die from other causes prior to the occurrence of nonfatal valve-related events. Kaplan-Meier actuarial methods tend to exaggerate nonfatal events by continuing to assume that patients who have died are still at risk for these nonfatal events.

Structural Valve Deterioration

MECHANICAL PROSTHESES

Currently available mechanical prosthesis are extremely resistant to material fatigue or structural valve deterioration (SVD). Long-term follow-up in the Starr-Edwards caged-ball prosthesis, the Medtronic Hall tilting disc prosthesis, and the St. Jude bileaflet mechanical prosthesis show that these valves are exceedingly resilient to structural failure. Some discontinued mechanical prostheses, such as the Bjork-Shiley convexo-concave valve, had high rates of structural failure due to fracture of the outlet strut.137

STENTED BIOPROSTHESES

There are several large series describing long-term follow-up of first- and second-generation bioprostheses. Most of these series are not comparable to each other as they took place in different patient populations or in different eras. Structural valve deterioration is the most common nonfatal valve-related complication in bioprosthetic aortic valves. Table 32-7 summarizes the long-term SVD outcomes of commonly used first- and second-generation stented bioprostheses. Long-term follow-up of currently available second-generation stented bioprostheses, including the Medtronic Hancock II porcine and Carpentier-Edwards pericardial valves, show that these prostheses have a freedom from structural valve deterioration greater than 90% at 12-year follow-up.125,127,138


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TABLE 32-7 Structural deterioration of stented bioprosthetic valves in the aortic position: long-term follow-up over 1215 years

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There is an important predisposition for premature bioprosthetic SVD in younger patients, particularly those under the age of 40 years.139,140 Table 32-8 summarizes the effect of patient age on structural valve deterioration. SVD may be less common in elderly patients due to decreased hemodynamic stress placed on the valve. Also, the freedom from SVD may be underestimated in the literature since most series report SVD by the actuarial method instead of the actual or cumulative incidence method.136 Actuarial statistical analysis overestimates SVD in older patients since it assumes that patients who have died of other causes will continue to be at risk for SVD.141


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TABLE 32-8 Bioprosthetic valve failure 10 years after valve replacement according to the patient's age at the time of implantation

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Freedom from Reoperation

Freedom from reoperation for currently available mechanical valves is greater than 95% at 10 years and greater than 90% at 15 years.124,142147 Bioprostheses have a significantly higher rate of reoperation due to structural valve dysfunction. In large series, freedom from reoperation is greater than 95% at 5 years, greater than 90% at 10 years, but less than 70% at 15 years.138,148166 The long-term freedom from reoperation for several commonly available valves is presented in Table 32-7.

Optimal Antithrombotic Therapy

MECHANICAL VALVES

All mechanical valves require formal anticoagulation with warfarin for the lifetime of the patient as these valves are inherently thrombogenic. The overall linearized risk of thromboembolism in patients on warfarin therapy is 1% to 2% per year in most published series.124,167184 A meta-analysis of over 13,000 patients showed that the incidence of major embolism in mechanical valves without antithrombotic therapy was 4 per 100 patient-years.185 With antiplatelet therapy this risk was 2.2 per 100 patient-years, and with warfarin therapy it was reduced to 1 per 100 patient-years. The incidence of thromboembolism was slightly higher in patients with caged-ball prostheses than other mechanical prostheses.186

The embolic risk is highest in the first few months, before the exposed cloth sewing ring and valve components have fully endothelialized.187 Antithrombotic therapy is initiated on the second postoperative day with oral warfarin. In the presence of complicating factors such as gastrointestinal or mediastinal bleeding or perioperative neurologic injury, anticoagulation may be held initially. If the target level of anticoagulation is not achieved by the fourth postoperative day, intravenous heparin is instituted to achieve a partial thromboplastin time (PTT) between 60 and 90 seconds. If the patient is at high risk for thromboembolism, heparin is started concurrently with warfarin on the second postoperative day. High-risk patients include those with atrial fibrillation, intracardiac thrombus, left atrial enlargement, severe left ventricular dysfunction, and history of systemic emboli or hypercoagulable state.33

The target level of anticoagulation for each individual patient is dependent on the thrombotic risk profile and the type of valve employed. It is our practice to establish an international normalized ratio (INR) of 3.0 (acceptable range 2.5 to 3.5) for high-risk patients with mechanical valves and additionally institute low-dose aspirin therapy (80100 mg once daily). For lower risk patients, the target INR is 2.5 (acceptable range 2.0 to 3.0) and low-dose aspirin is started on an individual basis.

Several articles suggest that caged-ball valves in the aortic position require a higher level of anticoagulation than tilting monoleaflet or bileaflet prostheses.33,179 These valves should be anticoagulated to an INR of 3.5 to 4.5. Although older tilting monoleaftlet prostheses were associated with an increased rate of thromboembolism, currently available prostheses, such as the Medtronic Hall valve, do not appear to have increased thomboembolism risk versus bileaflet prostheses and should have the same target INR.182,188,189

Aspirin, an antiplatelet agent, is routinely used at a low dose to minimize the risk of thromboembolic events. Randomized trials have shown that low-dose aspirin significantly reduces fatal cardiovascular and embolic events for all patients with mechanical valves, particularly in patients with concomitant coronary or vascular disease.190193 There are increased bleeding events when higher doses of aspirin are used in patients formally anticoagulated with warfarin.194,195 The linearized risk of a bleeding event is 0.1% to 3.5% per year depending on how these events are defined, the range of anticoagulation used, and how often coagulation parameters are measured.194,196198

BIOPROSTHETIC VALVES

Bioprosthetic valves are less thrombogenic than mechanical prostheses and do not require long-term anticoagulation with warfarin unless the patient is at high risk for thromboembolism or has had a thromboembolic event with their prosthesis.199 Stented bioprostheses have a linearized risk for thromboembolism between 0.5% and 1% per year.100,138,149,200203 This risk appears to be lower in patients with stentless heterograft, allograft, or autograft valves.204209 Anticoagulant management of bioprostheses during the first three months after implantation remains variable between institutions. There is an increased hazard function for thromboembolism before the exposed surfaces of stented bioprosthesis endothelialize.187 The current American College of Cardiology/American Heart Association guidelines recommend anticoagulation with warfarin to an INR between 2.0 and 3.0 for the first 3 months for bioprosthetic valves.33 This is discontinued at the end of the third month unless the patient is at high risk for thromboembolism. Low-dose aspirin is continued as monotherapy in low-risk patients and in conjunction with warfarin in high-risk patients for the lifetime of the patient. Combined aspirin and warfarin have a survival benefit over warfarin alone in high-risk patients with bioprosthetic heart valves.33 Aspirin significantly decreases the risk of thromboembolism in low-risk patients with bioprostheses versus no antiplatelet therapy.199,210212 If a patient has identified high-risk factors for thrombosis preoperatively, a mechanical prosthesis should be implanted unless the risk factor is amenable to correction, because formal anticoagulation with warfarin will still be necessary. With aspirin, patients with bioprosthetic valves have approximately the same risk of thromboembolism as patients with mechanical valves on full anticoagulation, with fewer bleeding complications.33

Prosthesis Thrombosis

Prosthesis thrombosis is a rare but potentially devastating outcome after aortic valve replacement. The incidence of prosthesis thrombosis is less than 0.2% per year and it occurs more often in mechanical prostheses.213215 Thrombolytic therapy may be used in some patients but it is often ineffective. Thrombolysis is recommended in patients with left-sided thrombosis who are experiencing significant heart failure (NYHA class III or higher) and are considered too high risk for surgery.33,216 Cerebral or peripheral thromboembolism occurs in 12% of patients after thrombolytic therapy.33 Surgical treatment includes replacement of the valve or open thrombectomy, and mortality from either procedure is similar at approximately 10% to 15%.217 Recurrent thrombosis after declotting occurs in up to 40% of patients, and we recommend valve replacement in virtually all patients who are managed operatively.218

Prosthetic Valve Endocarditis

Prosthetic valve endocarditis (PVE) is separated into two time frames: early (less than 60 days postimplantation) and late (greater than 60 days postimplantation). Early PVE is usually a sequela of perioperative bacterial seeding of the valve either during implantation or postoperatively from wound or intravascular catheter infections.62 Staphylococcus aureus, Staphylococcus epidermidis, gram-negative bacteria, and fungal infections are common in this period.33,219223 Although most cases of late PVE are caused by septicemia from noncardiac sources, a small proportion of late PVE in the first year is attributable to less virulent organisms introduced in the perioperative period, particularly Staphylococcus epidermidis.224 Organisms responsible for late PVE include Streptococcus and Staphylococcus species and other organisms commonly found in native valve infectious endocarditis.33 All unexplained fevers should be meticulously investigated for PVE with serial blood cultures and transesophageal and/or transthoracic echocardiography. Transesophageal echocardiography provides more detailed anatomic information such as the presence of vegetations, abscesses, and fistulas, but often does not provide adequate views of the anterior portion of the valve.225 Transthoracic views may be helpful in these cases. Mechanical valves are particularly difficult to visualize by echocardiography due to shadowing created by valve components.

The annual risk of PVE in the aortic position is 0.6% to 0.9% per patient-year.10,138,180,188,201,202,226234 The 5-year freedom from PVE reported in many major series is greater than 97%.100,127,235,236 Mechanical valves have a slightly higher early hazard for PVE than stented bioprostheses.237 However, there is no difference in risk between patients with mechanical and stented bioprostheses after the early phase. Stentless porcine heterografts and human allografts are less likely to develop PVE since they have less prosthetic material that may serve as a nidus of infection.238245 These valves may be particularly helpful in valve re-replacement for PVE.

Outcome for patients with PVE is very poor. Invasive paravalvular infection occurs in up to 40% of cases of PVE.246 Early PVE is associated with 30% to 80% mortality while late PVE is associated with 20% to 40% mortality.62,247

Surgery is indicated for PVE in the following circumstances:

  1. All cases of early (endocarditis.
  2. Concomitant heart failure and valvular dysfunction.
  3. Paravalvular leak or partial dehiscence, even in a stable patient, requires operative management, particularly if more than 40% of the valve annular circumference is involved.
  4. The presence of a new conduction defect, abscess, aneurysm, or fistula mandates operative management. All fungal infections and those caused by the most virulent strains of Staphylococcus aureus, Serratia marcescens, and Pseudomonas aeruginosa also require operation as these organisms are highly invasive and antibiotic therapy is generally ineffective.
  5. Any case of persistent bacteremia despite a maximum of 5 days of appropriate antibiotic therapy and no other source of infection.
  6. Vegetations larger than10 mm are not well penetrated by antibiotics and usually need operative management.
  7. Multiple systemic emboli.

Paravalvular Leak and Hemolysis

Paravalvular leak is uncommon outside of the setting of infective endocarditis. Technical errors may result in inappropriately large gaps between sutures, leaving a small portion of the prosthesis unattached to the annulus. If paravalvular leak is sufficient to cause significant hemolysis, surgical correction may be performed with a few interrupted pledgeted sutures. Hemolysis is uncommon with the currently available mechanical or stented bioprosthetic valves if they are functioning well. Pannus overgrowth and prosthetic structural degeneration interfering with normal valve opening and closure may cause hemolysis severe enough to warrant reoperation. Milder cases of hemolysis may be managed conservatively by dietary supplementation with iron and folic acid and routine measurement of hemoglobin, serum haptoglobin, and lactate dehydrogenase (LDH).


?? HEMODYNAMIC PERFORMANCE AND VENTRICULAR REMODELLING
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Pressure and/or volume overloading caused by aortic valve disease leads to increased intracavitary left ventricular pressures and compensatory left ventricular hypertrophy. Severe aortic regurgitation causes volume overload with an increase in left ventricular end-diastolic volume and eccentric hypertrophy, but may not change the ratio of ventricular wall thickness to cavity radius. In severe aortic stenosis, concentric ventricular hypertrophy occurs without increasing end-diastolic dimension until late in the disease process, thus increasing the ventricular wall thickness to cavity radius ratio.

Both pathologies result in an increase in left ventricular mass. Studies from the hypertension literature indicate that increased left ventricular mass has a strong negative prognostic effect. Several reports, including the Framingham Heart Study, indicate that increased left ventricular mass was a predictor of all cardiac events including sudden cardiac death.248250 The overall goal of aortic valve replacement is to alleviate the pressure and volume overload on the left ventricle allowing myocardial remodeling and regression of left ventricular mass.

The clinical impact of left ventricular mass regression is not as well understood, despite its widespread acceptance as a measure of outcome after aortic valve surgery. Smaller studies have shown that in hypertensive patients undergoing medical treatment, patients with a reduction of left ventricular mass had fewer cardiac events than those whose left ventricular mass did not change or increased.251 The prognostic implications of left ventricular mass regression after aortic valve surgery have not been rigorously studied, but logic would suggest that poor left ventricular mass regression is associated with poor clinical outcome. There are no studies showing that there is incremental clinical benefit with greater degrees of ventricular mass regression.

Left ventricular mass regresses significantly over the first 18 months and returns to within normal limits in many patients after aortic valve replacement for isolated aortic stenosis.252257 Ventricular mass regression may continue for up to 5 years after valve replacement.258 However, some patients do not experience adequate ventricular mass regression and may experience poorer prognosis. Several authors have identified a situation, referred to as patient-prosthesis mismatch, in which the poor hemodynamic performance of a prosthesis results in poor regression of left ventricular hypertrophy and poor patient outcome.

Patient-Prosthesis Mismatch

The term patient-prosthesis mismatch has been applied to several different clinical situations. It has been used to describe absolute small valve size (i.e., less than 21 mm), small valve size in a patient with a large body surface area, excessive transvalvular gradient immediately postimplantation, increased transvalvular gradient with exercise, indexed effective orifice area (IEOA), and various combinations of these variables (Table 32-9).


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TABLE 32-9 The effective orifice area and mean systolic gradient of commonly available bioprostheses

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IEOA is calculated by dividing the echocardiographically determined effective orifice area (EOA) by the body surface area (BSA). Effective orifice area is calculated by a reconfiguration of the continuity equation:

where EOA is effective orifice area in cm2, CSALVOT is the cross-sectional area of the left ventricular outflow tract (LVOT) in cm2 determined by two-dimensional measurement of the LVOT diameter, TVILVOT is the velocity time integral of forward blood flow in cm derived from pulse-wave Doppler in the LVOT, and TVIAO is the velocity time integral of forward blood flow in cm derived from software integration of transvalvular continuous wave Doppler.259 Although the aortic annular dimensions can be used instead of LVOT, several studies have shown that LVOT is a more accurate measure for estimating effective orifice area in bioprosthetic heart valves.260,261

Rahimtoola defined patient-prosthesis mismatch as a condition that occurs when the valve area of a prosthetic valve is less than the area of that patient's normal valve.262 In this situation, the prosthesis may be too small for the patient's cardiac output requirements, as estimated by their body surface area. The prosthesis creates a residual stenosis that results in an elevated transvalvular gradient.

To some extent, all mechanical and stented biological prostheses are inherently stenotic.62 The presence of rigid sewing rings and, in the case of stented bioprostheses, struts to hold the valve commissures causes obstruction to outflow and will therefore cause a residual gradient despite normal prosthesis function. The problem is exacerbated by annular fibrosis, annular calcification, and left ventricular hypertrophy, as seen in aortic stenosis, which cause contraction of the native annulus leading to the implantation of a smaller prosthesis. Larger patients are also more likely to have lower IEOA based on their larger body surface areas. The significance of patient-prosthesis mismatch is controversial as there is little evidence that lower IEOA causes diminished clinical results in many patients.

Several authors suggest that patient-prosthesis mismatch occurs at an indexed effective orifice area of less than 0.85 cm2/m2.263,264 This definition is based on the assumption that transvalvular gradients begin to rise substantially at IEOA below this value and these elevated gradients cause increased left ventricular work that prevents adequate regression of left ventricular hypertrophy.265

Using this criteria, Pibarot and Dumesnil prospectively studied 72 patients over 7 years and found no difference in survival between patients with patient-prosthesis mismatch and those without.266 Mean gradients were higher in the patient-prosthesis mismatch group (22 ? 8 mm Hg vs. 15 ? 7 mm Hg). The clinical relevance of a 7 mm Hg difference in gradient in otherwise asymptomatic patients is unclear and certainly would not warrant any treatment. Also, the difference in gradient is within the measurement error for this echocardiographically derived variable. In this study, lower IEOA was an independent predictor of poorer NYHA class early after aortic valve replacement, but this relationship was not present at 7-year follow up. No objective testing of function was performed on these patients.

Rao et al studied patient-prosthesis mismatch in patients undergoing aortic valve replacement.267 A total of 2145 patients were reviewed including 227 patients with patient-prosthesis mismatch and 1927 without. Overall survival was the same in both groups, but valve-related mortality was higher in the patient-prosthesis mismatch group at 10 years. This retrospective study was not randomized, and valve-related mortality included mechanisms of death that are totally unrelated to patient-prosthesis mismatch (embolic stroke, valve failure, endocarditis, bleeding, reoperation). Furthermore, this study had no echocardiographic data. Effective orifice area was obtained from in vitro data supplied by the manufacturers according to the valve size implanted. Patient-prosthesis mismatch was simply assumed on the basis of calculated numbers unrelated to individual patients.

Several well-designed multivariate studies have not shown that patient-prosthesis mismatch influences survival. Medalion et al studied 892 aortic valve replacements and demonstrated that although 25% of patients received valves with an indexed internal orifice area less than two standard deviations below predicted normal aortic valve size, there were no differences in 15-year survival between patients with or without patient-prosthesis mismatch.268

We have recently reported our institutional experience with patient-prosthesis mismatch in 1129 patients who were prospectively studied over a 10-year period.269 We defined patient-prosthesis mismatch as an IEOA less than the 90th percentile in our patient population. The cutoff value for IEOA to define patient-prosthesis mismatch was 0.6 cm2/m2, which would be considered very severe by most groups. Preoperative patient characteristics comparing those with normal and abnormal gradients are presented in Table 32-10. The only preoperative predictor of abnormal gradient was small valve size. Postoperative mean and peak gradients are outlined in Figure 32-6. Figures 32-7 and 32-8 illustrate that there were no differences in left ventricular mass index or survival at midterm follow-up between patients with normal and abnormal gradients. Thus, although valve size is a predictor of abnormal postoperative gradient, no clinical significance can be correlated to this finding. The distribution of indexed effective orifice areas in these patients is presented in Figure 32-9. Figures 32-10 and 32-11 show that there were no differences in left ventricular mass index or survival at midterm follow-up between patients with or without patient-prosthesis mismatch defined as IEOA less than 0.6 cm2/m2.


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TABLE 32-10 Patient-prosthesis mismatch: patient characteristics by postoperative gradient

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FIGURE 32-6 Distribution of postoperative peak gradients and mean gradients. (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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FIGURE 32-7 Left ventricular mass index in the normal gradient group and the abnormal gradient group. There was no significant difference between the two groups. LVMI = left ventricular mass index; preop. = preoperative. (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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FIGURE 32-8 Actuarial survival and freedom from New York Heart Association (NYHA) class III or IV in the normal gradient group and the abnormal gradient group. Seven-year survival was 91.2% ? 1.5% (normal gradient) and 95.0% ? 2.2% (abnormal gradient). Seven-year freedom from NYHA class III or IV was 74.5% ? 3.1% and 74.6% ? 6.2%, respectively. There were no significant differences in the two groups. (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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FIGURE 32-9 Distribution of postoperative indexed effective orifice area (IEOA). (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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FIGURE 32-10 Left ventricular mass index (LVMI) in the mismatch and the nonmismatch group. There were no significant differences in the two groups. preop. = preoperative. (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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FIGURE 32-11 Actuarial survival and freedom from New York Heart Association (NYHA) class III or IV in the nonmismatch group and the mismatch group. Seven-year survival was 94.7% ? 3.0% (nonmismatch group) and 95.1% ? 1.3% (mismatch group). Seven-year freedom from New York Heart Association class III or IV was 79.3% ? 6.6% and 74.5% ? 2.5%, respectively. There were no significant differences in the two groups. (Reproduced with permission from Hanayama N, Christakis GT, Mallidi HR, et al: Patient prosthesis mismatch is rare after aortic valve replacement: valve size may be irrelevant. Ann Thorac Surg 2002; 73:1822.)

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Many authors have expressed concern about a high incidence of patient-prosthesis mismatch in the small aortic root. He et al assessed 30-year survival after aortic valve replacement in the small aortic root and concluded that body surface area in this high-risk group influenced survival only in patients with concomitant coronary artery bypass grafting.270 Sawant et al demonstrated that in patients with small aortic roots, body surface area and valve size were not determinants of long-term survival.271

Studies by De Paulis et al have shown that there was no difference in left ventricular mass regression between patients receiving 19-mm and 21-mm mechanical valves and those with 23-mm or 25-mm valves.272 Hence, there is little clinical benefit derived from implantation of a one-size larger prosthesis, particularly if the potential operative morbidity is increased to do this. There is no evidence in the literature suggesting that small differences in the degree of left ventricular mass regression have any clinical significance in patients after aortic valve replacement or hypertension.

Foster et al showed that in patients with 17-mm and 19-mm prostheses who had resting transvalvular gradients greater than 30 mm Hg, 93% were in NYHA class I at late follow-up.273 Kratz et al also reported that small valve size was not predictive of congestive heart failure or late death.274 Khan et al studied 19-mm to 23-mm Carpentier-Edwards pericardial valves and found that significant left ventricular mass regression occurred with each valve size, including 19-mm valves.275

Complex operations of the aortic root including root enlargement procedures and stentless porcine prostheses have been proposed to enable the implantation of valves with a larger IEOA. The rationale for choosing a more complex operation, which carries an increased perioperative risk, is predicated on the assumption that the patient will experience improved long-term outcome. However, there is no clear evidence to suggest that a patient receiving a prosthesis with an IEOA as low as 0.6 cm2/m2 will experience any decrease in life expectancy based on prosthesis size.269

Aortic root enlargement procedures may carry excessive mortality, particularly when performed by less experienced surgeons. In a large series, David et al performed aortic root enlargement procedures in almost 20% of aortic valve replacements without any increase in mortality.276 The prognostic benefit of root enlargement procedures in decreasing left ventricular mass or preventing cardiac events has not been established.277

Walther et al performed a small randomized trial comparing the ability of stented porcine and stentless porcine valves to cause regression of left ventricular hypertrophy.278 They showed that despite equivalent annular dimensions in the stented and stentless groups, larger valves (by labeled size) were implanted in the stentless group. The patients receiving stentless valves had a greater degree of left ventricular mass regression than those receiving stented valves. No clinical follow-up was provided.

Rao et al compared hemodynamic data among 19-mm to 23-mm Carpentier-Edwards pericardial valves and Toronto SPV stentless valves of equivalent internal diameter and found no hemodynamic differences in peak or mean gradient.49 At the same institution, Cohen et al randomized patients to receive Carpentier-Edwards pericardial valves and Toronto SPV stentless valves and compared clinical outcomes.279 There were no differences in the size of the aortic root between the two groups. Postoperative echocardiography showed that there was no difference in indexed effective orifice area or left ventricular mass regression between groups (Fig. 32-12). They also found no difference in functional outcome between valves at 1-year follow-up (Fig. 32-13). These findings challenge the notion that stentless porcine valves provide increased IEOA, or either hemodynamic or clinically significant benefits. Some reports have shown that transvalvular gradients in patients with lower IEOA often increase substantially with exercise.280,281 Although the majority of patients undergoing aortic valve replacement are elderly and unlikely to experience function limitations from this situation, in younger, highly active patients either root enlargement or stentless prostheses may provide better functional outcome.



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FIGURE 32-12 Indexed ventricular mass regression in both groups over time. CE = Carpentier-Edwards stented valve; LVMI = left ventricular mass index; SPV = Toronto stentless porcine valve. (Reproduced with permission from Cohen G, Christakis GT, Joyner CD, et al: Are stentless valves hemodynamically superior to stented valves? A prospective randomized trial. Ann Thorac Surg 2002; 73:767.)

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FIGURE 32-13 Change in Duke Activity Status Index (D.A.S.I.) scores in both groups over time. CE = Carpentier-Edwards stented valve; SPV = Toronto stentless porcine valve; Preop = preoperative. (Reproduced with permission from Cohen G, Christakis GT, Joyner CD, et al: Are stentless valves hemodynamically superior to stented valves? A prospective randomized trial. Ann Thorac Surg 2002; 73:767.)

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?? PROSTHESIS SELECTION
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An ideal aortic prosthesis would be simple to implant, widely available, possess long-term durability, would have no intrinsic thrombogenicity, would not have a predilection for endocarditis, and would have no residual transvalvular pressure gradient. Such a valve does not currently exist. Currently available options include mechanical valves, stented biologic heterograft valves, stentless biologic heterograft valves, allograft valves, and pulmonary autograft valves. Among these options, pulmonary autograft valves and allograft valves are the most physiologic prostheses. They are less prone to thrombosis or endocarditis and have excellent hemodynamic characteristics.206,240,282288 The longevity of such valves is dependent on patient factors, the preparation of the valve, and the technical skill of the operating surgeon. Despite their potential benefits, these prostheses are not readily available and can be very technically demanding to implant compared to standard mechanical or stented bioprostheses. They are most beneficial in children and younger adults. Allograft valves may also improve the results of aortic valve replacement in active endocarditis.239 A further discussion of these valves is presented in subsequent chapters. As their use has remained confined to a few centers that perform such operations regularly, the remainder of this discussion will focus on issues regarding selection of mechanical or bioprosthetic valves.

Mechanical versus Stented Biologic Valves

When selecting between mechanical and biologic heart valves, the surgeon and patient must balance the risks and benefits of each choice. Mechanical valves are much less likely to undergo structural deterioration than bioprosthetic valves, and reoperation for structural valve deterioration is more common in patients with bioprosthetic valves. Mechanical valves are more thrombogenic than bioprosthetic valves and require formal anticoagulation with oral warfarin. Anticoagulated patients have a significantly increased risk of bleeding complications. Patients with mechanical valves and adequate anticoagulation do not have significantly greater risk of thromboembolic events than bioprosthetic valves. There is no difference in actuarial freedom from bacterial endocarditis between mechanical and bioprosthetic valves.

Patients with an absolute requirement for long-term anticoagulation such as atrial fibrillation, previous thromboembolic events, hypercoagulable state, severe left ventricular dysfunction, another mechanical heart valve in place, or intracardiac thrombus, should receive a mechanical valve regardless of age. Patients with end-stage renal failure and hypercalcemia have a significantly elevated risk for early bioprosthetic structural valve deterioration and should also receive a mechanical prosthesis unless they are not expected to outlive their bioprosthesis.

Currently available second-generation bioprostheses, such as the Medtronic Hancock II porcine and Carpentier-Edwards pericardial valves, have greater than 90% freedom from structural valve dysfunction and greater than 90% freedom from reoperation at 12-year follow-up.138,158,165 The rate of structural deterioration is lower in patients older than 65 to 70 years. Hence, patients over 70 years old at the time of surgery should receive a biologic valve. Patients between 65 and 70 years of age who have comorbidities such as coronary artery disease are less likely to outlive their prosthesis and should receive a biologic valve. Patients between 65 and 70 years old who are otherwise quite healthy and have isolated aortic valve disease without significant ventricular dysfunction are at higher risk to outlive a bioprosthesis and should receive a mechanical valve. Patients under the age of 65 years should have a mechanical prosthesis to minimize the risk of structural failure requiring repeat aortic valve replacement in an octogenarian. Also, patients in whom anticoagulation is contraindicated, such as women of childbearing age wishing to become pregnant, or those who refuse anticoagulation, should receive a bioprosthesis.

A detailed discussion of these risks and benefits of prosthesis selection should occur with all patients and their families prior to surgery.

Stented versus Stentless Biologic Valves

Stentless porcine valves have gained popularity in cardiac surgery due to pioneering work by David at the Toronto General Hospital in 1988.289 Since they do not have obstructive stents and strut posts, stentless valves provide residual gradients and effective orifice areas that are similar to freehand allografts. Since stentless valves are more difficult to implant and require a longer cross-clamp time, the risks of operation must be matched to a specific benefit the patient may receive with a stentless valve. As discussed earlier in this chapter, there is conflicting evidence that the use of stentless valves results in improved left ventricular mass regression over stented bioprostheses. Several studies have shown adequate left ventricular mass regression in patients receiving small stented bioprostheses. There is also no evidence that incremental improvements in left ventricular mass provide additional clinical benefit. Thus, the routine use of stentless bioprostheses cannot be recommended for most patients with small aortic roots with the currently available data. At this time, stentless porcine valves are most useful in a relatively younger patient with a small aortic root who is active and likely to be limited by the elevated residual gradient a stented bioprosthesis will create. Long-term durability data are not available to fairly compare current generation stented and stentless bioprostheses. There are reports of decreased thromboembolic events in stentless valves.290 The final role of stentless aortic valves will be decided based on their long-term freedom from structural valve deterioration and clinical outcomes.


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