This chapter provides an overview of aortic valve replacement (AVR) with stented bioprostheses. The indications for aortic valve surgery are reviewed with an emphasis on evidence-based guidelines and contemporary clinical and physiologic outcomes of aortic valve surgery with currently available stented bioprostheses.

Aortic Stenosis

NATURAL HISTORY

Aortic stenosis (AS) is primarily caused by degenerative calcification in patients over 70 years of age and bicuspid aortic valve in patients under 70 years of age in the developed world. Rheumatic valve disease is the third most common cause of AS affecting patients across the age spectrum. AS is also associated with systemic diseases such as Paget’s disease of bone and end-stage renal disease. The pathogenetic mechanisms of aortic valve calcification include valvular interstitial cell transformation, inflammation and lipid accumulation, reminiscent of the pathogenesis of atherosclerotic plaques.¹ The overall incidence of calcific AS is rising with the aging population in developed countries. A population-based study of Olmstead County reported the increase in prevalence of degenerative AS and other valvulopathy in patients with age from 55 to 64 (0.6%), 65 to 74 (1.4%) and ≥75 years (4.6%; p < .0001, Fig. 28-1).²

Valvular degenerative calcification is characterized as a progressive reduction of orifice cross-sectional area caused by calcification of the cusps. The normal human aortic valve area (AVA) is between 3.0 and 4.0 cm² with minimal to no gradient. AS is defined as mild, moderate, severe and very severe with the corresponding AVA, mean gradients and peak jet velocities as shown (Table 28-1). In the presence of normal cardiac output, transvalvular gradient is usually greater than 50 mm Hg when the AVA is less than 1.0 cm².³ A rapid increase in transvalvular gradient is seen with AVAs between 0.7 and 1.0 cm². However, discordant echocardiographic parameters are not uncommon. Minners et al⁴ examined 3483 echocardiographic studies with severe AVA, 25% had less-than-severe mean gradient and 30% has less-than-severe peak velocities leaving only 40% of patients with all echocardiographic criteria consistent with severe AS. Thus, echocardiographic data require careful assessment of images and correlation with hemodynamic parameters such as preload and afterload conditions.

Hemodynamic obstruction to flow created by the reduced orifice area of the aortic valve elevates intracavitary pressures. The resultant wall stress and ischemia-induced myocardial fibrosis leads to compensatory concentric left ventricular hypertrophy (LVH) to normalize wall tension and to maintain cardiac output.⁵ With progressive LVH, ventricular compliance decreases and end-diastolic pressure rises.⁶ The contribution of atrial contraction to preload becomes more significant and loss of sinus rhythm to atrial fibrillation may lead to rapid progression of symptoms.

SYMPTOMATIC PATIENTS

As AS progresses to become hemodynamically significant, progressive LVH leads to the cardinal symptoms of AS, those being (1) angina, (2) syncope, and (3) dyspnea or congestive heart failure (CHF). The average AVA is 0.6 to 0.8 cm² at the onset of symptoms.⁵ Classic natural history studies have demonstrated that average life expectancy in patients with hemodynamically significant AS is 4 years with angina, 3 years with syncope, and 2 years with CHF.⁷ Symptom development in the context of AS is an absolute indication for surgical intervention.⁸ Excessive delay of AVR in symptomatic patients is associated with rate of sudden death of >10% per year. Once a patient is symptomatic, average survival is less than 3 years typically from ventricular arrhythmia or CHF.⁹

ASYMPTOMATIC PATIENTS

The management of asymptomatic patients with hemodynamically significant AS remains a challenge. First, such patients should be exercised to confirm whether they are in fact asymptomatic. Symptoms on exertion will be unveiled in approximately one-third of patients during exercise testing. For truly asymptomatic patients, when considering AVR, the risk of sudden death and progressive ventricular remodeling should be weighed against the institutional surgical outcomes or the Society of Thoracic Surgeons Adult Cardiac Surgery Database (STS ACSD) surgical mortality of 3.9%, if appropriate.¹⁰ For uncorrected AS, the average decrease in AVA is 0.12 cm² per year, while the average increase in transvalvular pressure is often 10 to 15 mm Hg per year.¹¹ Overall, up to 7% of patients with asymptomatic AS experience death or surgery 1 year after diagnosis which rises to 38% at 5 years.¹² Furthermore, freedom from death or AVR was 67% at 1 year, 56% at 2 years, and 33% at 4 years. However, the high-risk patient subset with very severe AS (jet velocity ≥ 5m/s) progressed much more rapidly with event-free survival of 64% at 1 year, 36% at 2 years, 12% at 4 years and 3% at 6 years.¹³

Early surgery in asymptomatic severe AS may limit and even reverse concentric myocardial injury and fibrosis. In high-volume centers, the operative mortality for isolated AVR is significantly lower than that reported mortality in the STS ACSD.¹⁰ Furthermore, loss to follow up and delay from the time of symptoms to surgical referral are also of concern. For these reasons, early surgery may a reasonable strategy, particularly for young patients who are unlikely to escape the need for surgical valve replacement.

On the other hand, there is considerable variation in the rate of disease progression, there can exist a prolonged and stochastic latent period before symptoms emerge and many patients do not experience any change in gradient for several years. Sudden death is rather uncommon in the asymptomatic patient with AS and even with severe AS, the rate is less than 1% per year.¹² Furthermore, the vast majority of patients who experience sudden death will become symptomatic in the months immediately prior. In addition, early and late outcomes were similar among patients with severe AS who underwent surgery with symptoms or without.¹⁴ Thus, watchful waiting with close clinical and echocardiographic follow up may also be considered for those with asymptomatic AS.

It is difficult to predict who will eventually need surgical intervention and to identify asymptomatic patient subsets that will benefit from an early surgical approach. As mentioned, asymptomatic patients with increases in high peak velocity jet are substantially more likely to need an operation.¹³ Patients with very severe AS (AVA ≤ 0.75 cm² and jet velocity ≥ 4.5 m/s or mean gradient ≥ 50 mm Hg) have lower-mid-term all-cause mortality (2 ± 1% vs 32 ± 6%, p < .001) with early surgery versus conventional treatment.¹⁵ Severe LVH (left ventricular mass [LVM] index ≥ 180 g/m²) and enlarged left atrium (≥5.0-cm diameter) are markers of longstanding AS and are associated with reduced survival post-AVR.¹⁶ B-type natriuretic peptide (BNP) is released in response to increased myocardial wall stress and is a well-established marker of heart failure. Several groups have shown BNP to be a marker of symptomatic AS and an independent and objective predictor of outcome in patients with AS.^17-19 Further clinical studies will be needed to determine the clinical value of such echocardiographic measurements and biomarkers as triggers to guide the timing of surgical intervention.

LOW-GRADIENT AORTIC STENOSIS

Patients with very poor ventricular function (ejection fraction < 50%) who have severely stenotic valves but nonsevere (<40 mm Hg) transvalvular gradients or jet velocity (<4 m/s) are termed low-gradient AS (LGAS). Compromised left ventricular function in these patients may be caused by afterload mismatch created by the stenotic valve or by intrinsic cardiomyopathy, or both, 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 (eg, dobutamine stress echocardiography) may distinguish cardiomyopathy versus true valvular stenosis as the most responsible diagnosis. Those patients with contractile reserve that experience an increase in valve gradient (≥40 mm Hg) or jet velocity (≥4 m/s) with dobutamine inotropy are considered to have true LGAS. An increase in augmented flow resulting in only a mild increase in transvalvular gradient but an increase in valve area by ≥0.2 cm² suggests pseudosevere LGAS. The lack of increase in gradient nor AVA with dobutamine suggests pseudosevere LGAS lacking contractile reserve. Severe diastolic dysfunction with EF ≥50% and indexed AVA ≤ 0.6 cm² but mean gradient < 40 mm Hg, jet velocity < 4 m/s and indexed stroke volume < 30 cc/m² is termed paradoxical LGAS. The latter is associated with pronounced left ventricular concentric remodeling, moderate-to-severe diastolic dysfunction, decreased longitudinal strain and reduced stroke volume.

Patients with LGAS are a high-risk patient population with lower 5-year survival compared with those with high gradient severe AS. A retrospective study of 1154 patients with severe AS confirmed higher operative mortalities with LGAS (6.3%) and paradoxical LGAS (6.3%) compared with normal flow severe AS (1.8%).²⁰ However, such patients experience a significant survival benefit from valve replacement compared with medical management alone (Fig. 28-2).²¹ Tribouilloy et al²² report a high operative mortality (22%) but in survivors, an improved propensity-matched 5-year survival with AVR (65 ± 11% vs 11 ± 7%, p = .019). Thus, patients with LGAS should be carefully selected but can benefit from surgical AVR.

MEDICAL THERAPY

Medical therapy for afterload reduction may be beneficial in AS but there is no known medical therapy that has been shown to alter its natural history. Hypertension is associated with greater cardiovascular events and improved survival, and thus medical treatment for hypertension is reasonable.²³ Afterload reduction may be considered for patient with AS in heart failure but should be initiated and titrated cautiously as a sudden decrease in systemic vascular resistance can result in an acute reduction in cardiac output.²⁴ With regard to targeted therapy, three randomized controlled trials (RCTs) did not show a benefit of statins in did not halting or lowering the rate of disease progression in AS.^25-27 The importance of osteogenic processes as key mechanisms in AS has suggested potential targets for therapy but these studies are still very much in the experimental stages.²⁸

INDICATIONS FOR SURGERY

In 2014, 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 patients with valvular heart disease.²⁹ These guidelines encompass several important overarching changes since the 2006AHA/ACC guidelines and the 2008 updates:^30,31

1. 
   

   Regarding AS and aortic regurgitation (AR), the revised guidelines include a new classification of heart valve diseases based on valve anatomy, valve hemodynamics, hemodynamic consequences, and symptoms. There are four stages with treatment recommendations for each stage: (A) at risk; (B) progressive asymptomatic; (C) severe asymptomatic (C1, with ventricular compensation; C2, with ventricular decompensation); and (D) severe symptomatic.

   
   
2. 
   

   Symptomatic severe AS is subdivided into high gradient (V_max ≥ 4 m/s or mean gradient ≥ 40 mm Hg), LGAS with reduced left ventricular ejection fraction (LVEF) (severe leaflet calcification with severely reduced motion, effective orifice area [EOA] ≤ 1.0 cm², and V_max < 4 m/s or gradient < 40 mm Hg with LVEF < 50%, and EOA remaining ≤1.0 cm², but V_max ≥ 4 m/s at any flow rate during dobutamine echocardiography), and paradoxical LGAS with normal LVEF (severe leaflet calcification with severely reduced motion, EOA ≤ 1.0 cm² and V_max < 4 m/s or gradient < 40 mm Hg with LVEF ≥ 50%).

   
   
3. 
   

   A focus on the Heart Team approach for clinical decision-making, particularly given the availability of surgical and transcatheter interventions.

   
   
4. 
   

   An integrative approach to the procedural risk, which incorporates risk scoring, frailty, major organ system dysfunction and procedural impediments.

The specific recommendations for AVR for patients with AS are shown (Table 28-2 and Fig. 28-3).²⁹ To summarize, AVR should be performed in all symptomatic patients with severe AS or in patients with severe asymptomatic AS who require concomitant cardiac surgery or with left ventricular dysfunction (LVD; LVEF < 50%). It is reasonable to perform AVR in patients with moderate AS requiring concomitant cardiac surgery. AVR is reasonable in otherwise asymptomatic patients with very severe AS (valve area < 0.6 cm² and jet velocities ≥ 5 m/s), severe AS and exercise-induced symptoms, and in those with true or paradoxical LGAS. Asymptomatic patients with severe AS with rapid progression may be considered for valve replacement prior to significant ventricular decompensation or sudden death.

Aortic Regurgitation

ACUTE AORTIC REGURGITATION

Acute AR is caused by (1) acute dilatation of the aortic annulus or sinotubular junction or both, preventing adequate cusp coaptation or by (2) disruption of the valve cusps themselves. The specific causes of AR include aortic dissection, infective endocarditis, trauma, aortic cusp prolapse secondary to VSD, aortitis or arteritis (eg, syphilitic, giant cell, Takayasu) and iatrogenesis (eg, postaortic balloon valvotomy).

The heart is relatively intolerant to acute AR, as the left ventricle is unable to compensate for the sudden increase in end-diastolic volume caused by a large regurgitant volume load. A dramatic reduction in forward stroke volume ensues. In the context of a hypertrophic and poorly compliant left ventricle, hemodynamic decompensation is significantly more dramatic. Tachycardia is the initial compensatory response to acute decline in forward stroke volume. Progressive volume overload causes the left ventricular end-diastolic pressure to acutely rise above left atrial pressure resulting in early closure of the mitral valve.³² Although this protects the pulmonary venous circulation from excessively high end-diastolic pressures, rapid progression of pulmonary edema and cardiogenic shock is unavoidable. Death secondary to progressive cardiogenic shock and malignant ventricular arrhythmias are the commonest endpoints of acute AR regardless of etiology. Thus urgent surgical treatment is warranted for all causes of hemodynamically significant acute AR.

CHRONIC AORTIC REGURGITATION

Chronic AR is caused by either slow enlargement of the aortic root or dysfunction of the valve cusps. Common causes of chronic AR include congenital abnormalities (eg, bicuspid, unicuspid, quadricuspid aortic valve), calcific cusp degeneration, rheumatic fever, endocarditis, Marfan syndrome, Ehlers-Danlos syndrome, myxomatous proliferation, osteogenesis imperfect and ankylosing spondylitis. The echocardiographic and catheter-based parameters for AR are shown (Table 28-3).

Chronic AR causes a persistent volume overload of the left ventricle. Initially, the ratio of wall thickness to chamber diameter, ejection fraction, and fractional shortening are maintained.³³ However, this volume burden eventually leads to progressive chamber enlargement without increasing end-diastolic pressure during the asymptomatic phase of the disease. Chamber enlargement is accompanied by adaptive eccentric hypertrophy, associated at the cellular level with sarcomere replication and elongation of myocytes. The combination of chamber dilatation and hypertrophy leads to a massive increase in left ventricular mass. A vicious cycle of chamber enlargement, continually increasing wall stress and maladaptive ventricular hypertrophy ensues. Development of interstitial fibrosis is an important pathogenic mechanism that limits further ventricular dilation elevating end-diastolic pressure and leading to left ventricular systolic dysfunction, and CHF.³⁴ Natural history studies of AR show that symptoms, LVD, or both develop in <6% of patients per year.³⁵ Progression to LVD without symptoms occurs in <4% of patients per year and sudden death occurs in <0.2% per year.³⁶ Independent predictors of progression to symptoms, LVD, or death in asymptomatic patients include age, left ventricular end-systolic dimension, rate of change in end-systolic dimension, and resting ejection fraction.³⁷ Once LVD develops, the onset of symptoms occur at a rate exceeding 25% per year.³⁸

The decision to operate on patients with AR and LVD is indeed challenging since the outcomes are poor with surgery and with medical therapy. Patients with more severe LVD have decreased perioperative and late survival due to irreversible ventricular remodeling including hypertrophy and interstitial fibrosis.^39,40 Vasodilator therapy may delay progression of ventricular dysfunction by decreasing afterload thus reducing regurgitant flow. This is currently indicated in asymptomatic patients with hypertension; asymptomatic patients with severe AR, ventricular dilatation, and preserved systolic function; and for short-term hemodynamic tailoring prior to operation. This therapy is not recommended in patients with severe AR and LVD, as it does not improve survival but may be considered if such patients are considered inoperable.

INDICATIONS FOR OPERATION

A summary of the 2014 ACC/AHA Guidelines for AVR for chronic AR is presented in Table 28-4 and Fig. 28-4.²⁹ Symptomatic patients experience > 10% mortality per year thus surgery is absolutely indicated.³⁹ Since symptoms, such as angina and dyspnea, develop only after significant ventricular decompensation has occurred, surgery is advocated prior to the symptomatic phase of the disease. Surgical intervention for asymptomatic patients is based on the identification of subtle but measurable changes in myocardial function before they become irreversible and negatively affect the patient’s long-term prognosis.

Many patients requiring AVR have coexistent coronary artery disease (CAD). In North America, more than one-third of AVR procedures are accompanied with coronary artery bypass graft surgery.¹⁰ 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, or both.

According to the 2014 ACC/AHA Guidelines, during preoperative planning for AVR, coronary catheterization should be performed for the presence of angina, ischemia, LVD, or history of CAD; males > 40 years old; and postmenopausal women (Class I, Level of Evidence C). CT coronary angiography may be performed with low or intermediate pretest probability of CAD (Class IIa, Level of Evidence B).²⁹

Technique of Operation

MYOCARDIAL PROTECTION AND CARDIOPULMONARY BYPASS

Isolated AVR is performed using a single, two-stage right atrial venous cannula and an arterial cannula into the ascending aorta for systemic perfusion of oxygenated blood. A retrograde cardioplegia cannula may be placed into the coronary sinus via the right atrium. A left ventricular vent cannula may be placed in the right superior pulmonary vein and advanced into the left ventricle to ensure a bloodless field and to prevent ventricular distention with aortic insufficiency. Alternatively, a vent may be placed into the pulmonary artery or directly in the left ventricular outflow tract (LVOT) via the aortotomy. Once cardiopulmonary bypass (CPB) is initiated, careful dissection of the pulmonary artery from the aorta ensures that the cross-clamp will be fully occlusive on the aorta and prevents inadvertent opening of the pulmonary artery with the aortotomy incision. Care is needed to prevent pulmonary artery injury, as this tissue is substantially more friable than the aorta.

After the cross-clamp is applied, myocardial protection is initially delivered as a single dose of high potassium blood through the ascending aorta. This will trigger prompt diastolic arrest unless there is moderate-to-severe AR in which arrest can be achieved with direct ostial or retrograde cardioplegia. Myocardial protection is maintained by continuous infusion of cold or tepid oxygenated blood cardioplegia delivered via direct cannulation of both coronary ostia after the aorta has been opened. The angiogram should be examined to rule out a short left main coronary artery, in which case, direct ostial antegrade cannulation may preferentially perfuse either the LAD or circumflex system. In the presence of severe CAD, antegrade cardioplegia may not perfuse myocardial segments distal to significant coronary obstruction. Furthermore, direct cannulation of left main coronary artery risks endothelial injury and potential dissection or promotion of atherosclerosis development.

An alternative method of cardioprotection in aortic valve cases is retrograde cardioplegia, in either intermittent or continuous forms and utilized in isolation or in combination with antegrade cardioplegia. This is helpful in patients with significant AR or severe concomitant coronary disease. However, there are some questions regarding the quality of right ventricular perfusion using retrograde alone. If a retrograde cannula cannot be guided into the coronary sinus, conversion to bicaval cannulation will allow opening the right atrium and direct placement of the cannula into the coronary sinus. Do not place the retrograde cannula beyond the origin of the right coronary vein ostium in the coronary sinus to ensure adequate right ventricular myocardial protection.

Right ventricular myocardial protection can be a challenge for a small nondominant right coronary artery (RCA) that will not accept a direct ostial cannula. One solution is to drift the patient’s temperature to 28°C with cold topical slush and frequent retrograde cardioplegia.

AORTOTOMY, VALVE EXCISION, AND DEBRIDEMENT

Once the cross-clamp has been applied and cardioplegic arrest has been achieved, the aorta is opened either with a transverse or oblique aortotomy. The low transverse aortotomy is a common approach to the aortic valve when using stented bioprostheses or mechanical valves. The aortotomy is started approximately 10 to 15 mm above the origin of the RCA and extended anteriorly and posteriorly. The initial transverse incision over the RCA may also be extended obliquely in the posterior direction into the noncoronary sinus or the commissure between the left and noncoronary cusps (Fig. 28-5). The oblique incision is often used in patients with small aortic roots, in whom root enlargement procedures may be required.

Morphology of the valve is then inspected (Fig. 28-6). The valve cusps are incised with scissors at the right cusp between the right coronary ostium and the commissure between the right and noncoronary cusps using Mayo scissors or special right-angled valve scissors (Fig. 28-7). One to two millimeters of tissue is left behind to support a sewing surface. Right cusp excision is carried first toward the left coronary cusp and then toward the noncoronary cusp and the cusp is removed as a single piece if possible. A moistened radiopaque sponge may be placed into the outflow area to catch calcific debris, which must be removed before placing the valve sutures. Thorough decalcification is then performed with a scalpel or rongeur. Debridement of all calcium deposits back to soft tissue improves seating of the prosthesis and decreases the incidence of paravalvular leak and dehiscence.

Care must be taken to prevent aortic perforation while calcific deposits are debrided from the aortic wall, particularly at the commissure between the left and noncoronary cusps, where perforation is most likely. Several anatomic relationships must be respected during valve excision (Fig. 28-8). The bundle of His (conduction system) is located below the junction of the right and noncoronary cusps in the membranous septum. Deep debridement in this area can result in permanent heart block. 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 can be used to repair the defect.

Once debridement is completed, the aortic root is copiously flushed with saline while the left ventricular vent is stopped. To prevent pushing debris into the left ventricle, saline in a bulb syringe is flushed through the left ventricular vent and out the aortic valve in an antegrade manner instead of retrograde through the valve. The irrigation solution is suctioned with the external wall suction and not into the cardiotomy suction.

VALVE IMPLANTATION

The annulus is sized with a valve-sizer designed for the selected prosthetic device. The valve is secured to the annulus using 12 to 16 double-needled interrupted 2-0 synthetic braided pledgeted sutures that are alternating in color. The pledgets can be left on the inflow/ventricular side or the outflow/aortic side of the aortic annulus (Figs. 28-9 and 28-10). Placing the pledgets on the inside of the annulus allows supra-annular placement of the valve and generally will allow implantation of as slightly larger prosthesis. If the coronary ostia are close to the annulus, supra-annular placement may only be possible along the noncoronary cusp. Mattress sutures are first placed in the three commissures and retracted to assist visualization. Some surgeons will place the commissural suture between the right and noncoronary cusps from the outside of the aorta (ie, the pledget is left on the outside of the aorta) to prevent injury to the conduction system. Pledgeted mattress sutures are then placed in a clockwise fashion typically starting in the noncoronary cusp. Sutures may be placed into the sewing ring of the prosthetic valve with each annular suture or after all annular sutures are placed. The sutures for each of the three cusps are held separately with three hemostats and retracted while the prosthesis is slid into the annulus. Sutures are then tied down in a balanced fashion alternating among the three cusps.

AORTIC CLOSURE AND DE-AIRING

The aorta is closed with a double row of synthetic 4-0 polypropylene sutures. The first suture line is started on the right side at the posterior end of the aortotomy and the double-needled suture is secured slightly beyond the incision to ensure there is no leak in this region. One end of the suture is run as a horizontal mattress anteriorly to the midpoint of the aortotomy, and then the second end of the suture is run anteriorly, slightly superficial to the horizontal mattress suture, in an over-and-over manner. On the left side, a similar technique is performed, the aorta is de-aired, and the two sutures are tied to themselves and to each other at the aortotomy midpoint.

During AVR, air is entrained into the left atrium and ventricle, and aorta. This must be removed to prevent 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 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 left ventricular vent are then placed on suction to remove any residual air as the heart begins electrical activity. A small needle (21-gauge) can be used to aspirate the apex of the left ventricle and the dome of the left atrium. To prevent air entrainment, the left ventricular vent must be removed while the pericardium is filled with saline irrigation. De-airing maneuvers are verified with visualization using transesophageal echocardiography. Vigorous shaking and careful manual compression of the heart while suctioning through the aortic vent (ie, cardioplegia tack) is helpful to remove air trapped within trabeculations. Once de-airing is complete, the aortic vent is removed. The patient is then weaned from CPB and decannulated in the standard fashion. If patients are pacemaker dependent when weaned from CPB in the operating room, it is recommended to insert atrial pacing wires to allow for synchronous atrioventricular pacing.

CONCOMITANT CORONARY ARTERY BYPASS GRAFTING

Operative technique is modified when there is concomitant CAD to optimize myocardial protection. Distal anastomoses are performed prior to AVR so that antegrade cardioplegiamay be administered through these grafts during the operation. The left internal mammary artery should be used for revascularization of the left anterior descending artery. 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.

The 2014 ACC/AHA Guidelines recommend concomitant surgical revascularization for coronary stenosis ≥ 70% or left main stenosis ≥ 50% (Class IIa, Level of Evidence C).²⁹ The benefit of revascularization should be balanced with the increased operative mortality, which increases from 3.9 to 5.9% for combined CABG/AVR according to the STS ACSD.¹⁰ Concomitant CABG at the time of AVR is common as reported rates were 30% in patients 51 to 60 years of age, 41% in 61 to 70 years of age and 50% in >71 years of age.⁴¹

CONCOMITANT ASCENDING AORTIC REPLACEMENT

The threshold for concomitant replacement of the ascending aorta at the time of AVR is an area of debate. Borger et al,⁴² reviewed patients with bicuspid aortic valve undergoing AVR and report 15-year freedom from aorta-related complications was 86, 81, and 43% in patients with an aortic diameter of <4.0 cm, 4.0 to 4.4 cm, and 4.5 to 4.9 cm, respectively (Fig. 28-11). Extrapolating from these data and others to all patients with concomitant ascending aortic dilation, the current 2014 ACC/AHA Guidelines recommend aorta replacement when maximal diameter exceeds 4.5 cm for patients undergoing aortic valve surgery (Class IIa, Level of Evidence C).²⁹ In patients with Marfan or Loeys-Dietz Syndromes, the aortopathy is much more aggressive and a lower trigger point for replacement may be appropriate. Given the lack of data, there are currently no recommendations for concomitant replacement of ascending aorta when replacing a tricuspid aortic valve. Clearly the threshold should be between 4.5 and 5.5 cm. The decision is left to the surgeon and should be based on the additive risk of the procedure, patient’s age, comorbidities, and overall life expectancy.

AORTIC ROOT ENLARGEMENT PROCEDURES

Detailed descriptions of aortic root enlargement procedures are presented in a later chapter. Briefly, either an anterior or posterior annular enlargement procedure may be performed in a patient with a 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. Nicks and colleagues in 1970 described a technique of root enlargement in which the aortotomy is extended downward through the noncoronary cusp, through the aortic annulus to the anterior mitral leaflet with patch augmentation.⁴³ In 1979, Manouguian and Seybold-Epting 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 into the anterior leaflet of the mitral valve with patch augmentation.⁴⁴ The anterior approach is generally used in the pediatric population. Described by Konno and colleagues in 1975, this technique, which is also known as aortoventriculoplasty, is used when more than 4 mm of annular enlargement is required.⁴⁵ 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

Reoperative AVR may be performed for prosthetic valve-related complications or commonly for progressive AS post-CABG. Prosthetic valve-related causes include structural valve deterioration, prosthetic endocarditis, prosthesis thrombosis, or paravalvular leak. Chest reentry is the most hazardous portion of any repeat cardiac procedure. The proximity of cardiac structures to the posterior sternum must be assessed prior to redo sternotomy. This can be accomplished by lateral chest x-ray (CXR), computed tomography (CT) scan, or magnetic resonance imaging (MRI). Before making an incision, there should be blood transfusion units in the room, external defibrillator pads on the patient and the CPB pump should be primed. Femoral or axillary vessels may be exposed or CPB may be instituted through the peripheral vessels in the case of high-risk chest reentry. An oscillating saw is used to open the sternum and as little tissue as possible is dissected. Extreme caution must be employed during dissection when there are patent bypass grafts that cross the midline.

Once cardioplegic arrest is established, the old prosthesis is excised with sharp dissection. Care must be taken to count and remove all sutures and pledgets from the annulus. Annular injuries caused while excising the prosthesis are repaired with pledgeted interrupted sutures or with a patch, typically of treated bovine pericardium. Removal of stentless prostheses may be particularly difficult. In the setting of endocarditis, aggressive debridement of all infected tissue must be performed with annular and aortic root reconstruction with pericardium when root abscesses are present.⁴⁶ Any foreign material can be seeded with bacteria, including Dacron aortic grafts, must be excised in the presence of active endocarditis as grafts can be seeded with bacteria.

In the presence of a Dacron prosthesis in the ascending aorta, chest reentry may be extremely hazardous since exsanguination will occur if the graft is inadvertently opened during dissection. To limit the systemic consequences of exsanguination at normothermia, the patient may be placed on femoro-femoral CPB and cooled to 18 to 20°C prior to chest reentry. If the Dacron graft is accidentally opened, local control of the bleeding is established and CPB is stopped. Under circulatory arrest, the graft is repaired or replaced. CPB may then be restarted. In all repeat aortic procedures, rigorous myocardial protection must be applied since 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. Retrograde cardioplegia may have benefit in the setting of patent old saphenous vein grafts.⁴⁷ More and more patients with previous cardiac surgery that require high-risk reoperative AVR are increasingly being referred to Heart Teams for consideration of transcatheter aortic valve replacement (TAVR).

PORCELAIN AORTA

Porcelain aorta is the most severe form of aortic atherosclerosis. The major risk of manipulation of a calcified aorta is atheroemboli with stroke being the most common clinical sequelae.³⁶ Calcified or porcelain aorta is found in approximately 1 to 2% of cases and can be diagnosed based on preoperative imaging or intraoperative assessment. A history of risk factors such as smoking, hypercholesterolemia, diabetes, hypertension, or stroke as well as imaging demonstrating ostial coronary disease, peripheral vascular disease or carotid disease should trigger a high index of suspicion for aortic atheroma. Preoperative imaging to demonstrate aortic calcification includes CXR, transthoracic echocardiogram, angiogram, CT, or MRI. Intraoperative assessment includes direct palpation, transesophageal echocardiography and epiaortic ultrasound. Of these, epiaortic ultrasound is the most sensitive modality to detect aortic calcification, particularly for soft, nonechogenic, and nonpalpable plaque components.³⁷

The key strategic decisions are (1) central versus peripheral cannulation, (2) cross-clamp versus circulatory arrest, and (3) isolated AVR versus AVR and RAA. Gillinov et al⁴⁸ reported a series of patients with severe aortic calcification and AS treated with endarterectomy, replacement of ascending aorta, cross-clamp during DHCA and balloon occlusion of aorta via aortotomy with Foley catheter. Cannulation sites were aorta (34%), femoral artery (34%), axillary artery (24%), and innominate artery (8%), and all patients underwent circulatory arrest. More recently, TAVR has changed the landscape, offering an alternative to surgical valve replacement in this high-risk patient subset. In fact, porcelain aorta is the primary indication in approximately 10 to 15% of patients that undergo TAVR.⁴⁹

Special consideration must be given to the underlying pathologic changes to the ventricle during the immediate postoperative period. The severely hypertrophied, noncompliant left ventricle resulting from AS is highly dependent on sufficient preload for adequate filling. Filling pressures should be carefully titrated between 15 and 18 mm Hg with intravenous volume infusion. Subvalvular left ventricular outflow obstruction with systolic anterior wall motion of the mitral valve should be avoided. Intravenous beta-adrenergic blockade may relieve this obstruction by decreasing inotropy and chronotropy. In extreme cases reoperation and surgical myectomy may be required.

Maintenance of sinus rhythm is also essential since 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. If pacing is required postoperatively, synchronous atrioventricular pacing is beneficial in preventing low cardiac output syndrome.

Complete heart block occurs in 3 to 5% of AVR patients. This complication may be due to suture placement or injury from debridement near the conduction system at highest risk inferior to the right-non commissure. Transient complete heart block caused by perioperative edema usually resolves in 4 to 6 days. After this time, insertion of a permanent pacemaker is recommended if there is no resolution.

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.

Stented bioprostheses may be constructed with porcine aortic valves or bovine pericardium. Over the past 40 years, advances in tissue fixation methodology and various proprietary chemical treatments have been developed to prevent extracellular matrix and calcium deposition. All heterograft valves are preserved with glutaraldehyde, which acts by cross-linking collagen fibers to reduce tissue antigenicity. Glutaraldehyde also ameliorates in vivo enzymatic degradation and causes the loss of cell viability, thereby preventing extracellular matrix turnover.⁵⁰ Glutaraldehyde fixation of porcine valves can be performed at high pressure (60 to 80 mm Hg), low pressure (0.1 to 2 mm Hg), or zero pressure (0 mm Hg). Porcine prostheses fixed at zero pressure retain the collagen architecture of the relaxed aortic valve cusp.⁵¹ Pericardial prostheses are fixed in low- or zero-pressure conditions.