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Aortic Valve Replacement (Mechanical, Bioprosthetic, Stentless)

Jordan Hoffman, Muhammad Aftab, David A. Fullerton

Abstract

First performed in 1960, surgical aortic valve replacement (AVR) remains the principal option by which the valve is replaced, although transcatheter techniques for AVR are now available in select patients. The decision to replace the diseased valve with either a mechanical valve or a bioprosthetic valve is individualized, and consideration must be given to issues pertaining to anticoagulation and the durability of the prosthesis for a given patient. Like all cardiac operations, the risks of the procedure are related to patient-specific risk factors. Nonetheless, the operative procedure may be performed safely with very low rates of morbidity and mortality. Following AVR, patients must be followed for prosthetic valve-related problems such as structural valve deterioration, prosthetic valve endocarditis, and complications of anticoagulation. Nonetheless, the long-term prognosis following AVR is excellent.

Introduction

The most common indication for AVR is aortic stenosis (AS), which is the third most common cardiovascular disease and the most common indication for heart valve replacement.[1] AS is a disease of aging, and approximately 3% to 6% of the population over the age of 70 years carry the diagnosis.[2] The etiology of AS is not well understood, but it has long been considered a degenerative disease of the aortic valve in which the valve leaflets progressively calcify, leading to fusion of leaflets and stenosis or narrowing of the valve.[3] Recently, laboratory data suggest that AS may be a disease of chronic inflammation.[4]

Aortic regurgitation (AR) is far less common that AS. The most common etiologies for isolated AR include calcification of the valve leaflets causing fusion at the commissures (acquired “bicuspid” aortic valve [BAV]), congenital BAV, postinflammatory scarring (in the case of rheumatic valve disease), infective endocarditis, and aorto-annular ectasia.[5]

Both AS and AR are mechanical problems and require replacement of the valve; no other therapies have been identified. Therefore, AVR plays a prominent role in the treatment of these structural heart defects.

Surgical Anatomy of the Aortic Valve

The normal aortic valve is comprised of 3 thin, pliable valve leaflets (cusps) attached to the heart at the junction of the aorta and the left ventricle. (Figure 1) Inferiorly, the aortic valve is bordered by the left ventricular outflow tract (LVOT), which represents the caudal most aspect of the ventriculo-aortic junction. The transition from left ventricle to aorta is anatomically demarcated by a “virtual” ring called the aortic valve annulus, which serves as a point of attachment for the nadir of the aortic valve cusps. The leaflets are attached within the 3 sinuses of Valsalva to the proximal aorta and joined together in 3 commissures that create the shape of a coronet. Superiorly, the sinotubular junction signifies the transition from aortic root to ascending aorta. The sinotubular junction is anatomically demarcated by a thickened rim of tissue called the supra-aortic ridge and represents the upper most aspect of the sinuses of Valsalva.[6],[7]

Figure 1
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Surgical anatomy of the aortic valve.

The coronary arteries originate within 2 of the 3 sinuses of Valsalva. The right and left coronary leaflets correspond to the location of the right and left coronary ostia, respectively. The noncoronary leaflet is usually located posterior-laterally and is not associated with a coronary artery ostium. The distance of the coronary ostium from the base of the corresponding valve leaflet is variable and typically between 9 and 20 mm superior to the leaflet nadir.[6]

The commissure between the right coronary and noncoronary cusps provides an important surgical landmark related to the conduction system of the heart. The atrioventricular (AV) node originates from the apex of the triangle of Koch in the right atrium. The bundle of His arises from the AV node and pierces the membranous interventricular septum in proximity to the central fibrous body that lies beneath the commissure between the right coronary and noncoronary cusps. Hence, the conduction system may be injured at the time of AVR.

Bicuspid Valve

In approximately 1% of the population, the aortic valve is bicuspid instead of tricuspid. The BAV is commonly associated with other cardiac conditions, including coarctation of the aorta, patent ductus arteriosus, septal defects, and aortopathy, leading to aortic aneurysms.[8] Truly bicuspid aortic valves are uncommon, representing only 6% of all bicuspid valves.[9] Most surgical bicuspid valve specimens demonstrate fusion of the right and left coronary leaflets (71%), or right coronary and noncoronary leaflets (15%).[10]

Patients with a BAV have aberrant coronary anatomy more often than patients with a tricuspid valve. Common variations include a short left main coronary artery, separate ostia of the circumflex and left anterior descending coronary arteries, and a left dominant circulation.[11] Right and left coronary ostia are typically separated by either a commissure or raphe, but the distance between the ostia is often less than in a trileaflet valve. This may impact the implantation of a prosthetic valve. In a truly bicuspid aortic valve with an anterior-posterior valve leaflet orientation, representing 2% of all surgical specimens, both coronary arteries may originate from a common anterior valve cusp.[10]

BAV is associated with aortopathy.[9] The prevalence of aortic dilation in patients with a BAV ranges from 20% to 84%.[12] The diameter of the aorta tends to increase more commonly in these patients when compared to patients with tricuspid aortic valves, and aortic dissection is reported to occur more commonly in patients with a bicuspid aortic valve.[8]

Current guidelines recommend that patients with BAVs undergo elective repair of the aortic root or ascending aorta if the aortic diameter of these structures exceeds 5.0 cm; however, if patients with BAV undergo elective valve replacement, consideration should be given to aortic repair if the diameter is greater than 4.5 cm.[13]

Diagnostic Considerations

Aortic Stenosis

The classic symptoms of AS are angina, syncope, and heart failure.[14] In clinical practice, the most common initial symptoms are early signs of heart failure such as loss of exercise tolerance, easy fatigue, and dyspnea on exertion. Patients may not develop symptoms until the aortic valve area (AVA) is approximately 1 cm2; this usually requires years. When this degree of stenosis has been reached, however, symptoms are typically present.

AS produces a systolic murmur best heard at the base of the heart that radiates into the carotid arteries; it may be difficult to distinguish the murmur of AS from a bruit in the carotid artery. This murmur is associated with a slow, prolonged rise in the arterial pulse, called pulsus parvus et tardus. The murmur of severe AS is soft and high-pitched and is often described as a seagull murmur.[15]

The diagnosis is confirmed and the severity of AS is determined by echocardiography.[16] The normal AVA is 3 to 4 cm2 and has little or no transvalvular gradient until the AVA has been reduced by approximately one-half. Therefore, the flow velocity across the normal aortic valve (determined by Doppler echocardiography) is less than or equal to 1.0 m/s. With mild AS, the AVA is decreased to greater than 1.5 cm2, and the flow velocity across the valve is increased to 2.5 m/s to 2.9 m/s. AS is considered moderate when AVA is reduced to 1.0 cm2 to 1.5 cm2 and the flow velocity across the valve increases to 3.0 to 4.0 m/s. Severe AS is diagnosed by an AVA less than 1.0 cm2 and a velocity across the valve of greater than 4.0 m/s. When normalized for patient body surface area, severe AS is an AVA less than or equal to 0.60 cm2/m2.

Aortic Regurgitation

The myocardial compensatory mechanisms of AR are such that patients may be asymptomatic for a long period of time; however, as these compensatory mechanisms begin to fail, patients experience symptoms of heart failure such as dyspnea on exertion, loss of exercise tolerance, orthopnea, and paroxysmal nocturnal dyspnea. Nocturnal angina may occur as a result of a slow heart rate and an exceedingly low diastolic pressure, with resultant poor coronary arterial perfusion.

The physical examination of patients with AR is distinctive because of the wide pulse pressure. The peripheral pulses rise and fall abruptly (Corrigan pulse or Watson’s water hammer pulse), the head may bob with each systole (de Musset sign), and the capillaries may pulsate visibly (Quincke sign). The murmur of AR is a decrescendo, diastolic murmur. A mid- to late diastolic rumble may sometimes be heard (Austin-Flint murmur); this represents rapid antegrade flow across the mitral valve that closes prematurely as a result of rapid ventricular filling secondary to the AR.[15]

Echocardiography is the mainstay for the confirmation of the diagnosis and the determination of severity of AR. The echocardiographic criteria for the diagnosis of severe AR include a regurgitant jet with a diameter of at least 65% of the LVOT, holodiastolic flow reversal in the descending thoracic aorta, and vena contracta greater than 0.6 cm.[5]

Pathophysiology

Aortic Stenosis

AS is generally a chronic disease manifest by a progressive narrowing of the aortic valve orifice. It is characterized by calcification of the valve leaflets and fusion of the commissures. This progressive narrowing of the valve orifice steadily increases afterload on the left ventricle. The appropriate compensatory response to this increasing afterload by the left ventricle is hypertrophy. As the ventricle hypertrophies, it becomes stiffer as its compliance decreases; a higher left ventricular end-diastolic pressure is needed to maintain the same volume of cardiac output. To achieve a sufficiently high left ventricular end-diastolic pressure (diastolic loading), left ventricular output becomes increasingly dependent on its intraluminal volume and on the atrial kick; loss of the atrial kick, as occurs with atrial fibrillation, may result in a significant decline in cardiac output and acute hemodynamic decompensation.

Although left ventricular hypertrophy is an appropriate biologic response to an increasing afterload, it has detrimental effects. The hypertrophy of the left ventricle produces several changes, the combination of which will culminate in: increased myocardial oxygen demand; greater left ventricular muscle mass; decreased left ventricular compliance, resulting in greater ventricular wall tension; higher systolic ventricular pressure; and longer systolic ejection time. At the same time, coronary artery blood flow is compromised by increased wall tension compressing the vessels and higher left ventricular end-diastolic pressure, the combination of which lowers the coronary artery perfusion pressure. These factors contribute to inadequate coronary arterial perfusion of the subendocardium in the setting of increased myocardial oxygen demand, leading to chronic myocardial ischemia. In turn, chronic ischemia leads to myocardial cell death and fibrosis.[15]

Despite the obstruction to left ventricular ejection produced by AS, left ventricular hypertrophy helps the heart achieve a normal cardiac output under resting conditions. To do so, however, a pressure gradient across the valve is required. As the aortic valve orifice (valve area) becomes progressively smaller, the transvalvular gradient increases. This relationship of flow across the valve, valve area, and transvalvular pressure gradient is expressed in the Gorlin formula,[17] as follows:

AVA = F/(44.5 × √ ΔP)

where ΔP is the mean pressure gradient across the valve, F is aortic valve flow, equal to cardiac output (in mL/min) divided by systolic ejection period (in sec/min); AVA is the aortic valve area (in cm2), and C is an empirical orifice constant, 44.5. For quick calculations, this simplifies to the following:

AVA = cardiac output/(mean pressure gradient)

As the valve area decreases to 1 cm2, there is little change in the transvalvular gradient needed to generate the same flow, and patients frequently experience no symptoms; however, with a valve area of 0.8 cm2, patients typically develop symptoms.

Aortic Regurgitation

In the setting of AR, the aortic valve leaks during diastole. This, in turn, lowers diastolic pressure and widens the pulse pressure. Because coronary blood flow occurs primarily in diastole, the decrease in diastolic blood pressure lowers coronary perfusion pressure. Unlike AS, in which the pathologic process is left ventricular pressure overload, the pathophysiology of aortic insufficiency derives from left ventricular volume overload. The left ventricular end-diastolic volume (preload) is increased by the regurgitation of blood through the incompetent aortic valve. The normal compensatory response of the left ventricle to the volume overload is left ventricular dilation. Patients with chronic aortic insufficiency may have the greatest left ventricular end-diastolic volume among patients with any form of heart disease. Because left ventricular compliance is often increased, at least initially in the course of the disease, left ventricular end-diastolic pressure may or may not be elevated.

The compensatory mechanism of left ventricular dilation maintains forward stroke volume and ejection fraction via increased left ventricular end-diastolic and end-systolic volumes. Thus, even though the left ventricular volumes are increased, the left ventricular ejection fraction (LVEF), known as the percentage of the end-diastolic volume that is ejected with each beat, may be maintained as long as the myocardium may compensate.

However, the law of Laplace dictates that this left ventricular dilation results in an increase in the left ventricular wall tension in order to develop the requisite systolic pressure. Such increased wall stress not only increases myocardial oxygen demand but also initiates left ventricular hypertrophy and increases left ventricular wall mass. As with AS, this left ventricular hypertrophy ultimately leads to myocardial fibrosis.[15]

With well-compensated aortic insufficiency, exercise may be tolerated because peripheral vascular resistance declines during exercise, thereby lowering the left ventricular afterload and increasing effective forward flow. At the same time, the heart rate increases, which shortens diastolic time, thereby decreasing the regurgitant volume. But because the left ventricular myocardium ultimately decompensates, the left ventricular systolic function begins to decline; as it does, its ejection fraction decreases. This decline in ejection fraction results in an increase in left ventricular end-diastolic volume, even without an increase in aortic regurgitant volume. The decline in left ventricular systolic function leads to a decline in stroke volume with a resultant increase in the end-systolic volume. Left ventricular emptying is impaired and the ventricle fails.

In severe AR, increased myocardial oxygen demand exceeds myocardial oxygen supply, causing ischemia despite normal coronary arteries. Increased left ventricular mass and wall tension occur concurrently with low diastolic pressures (low coronary perfusion pressure). Consequently, and particularly with exercise when the diastolic period shortens, coronary blood flow may not meet demand. Although no longer commonly seen in the clinical setting, patients with severe AR may therefore experience angina.[15]

Natural History and Indications for Operation

Aortic Stenosis

Over a period of years, the valve progressively narrows. During this “latent” period, patients are typically asymptomatic; however, the progressive narrowing of the valve is not linear; it occurs in an unpredictable, stepwise fashion. Patient survival is not significantly diminished until symptoms develop. (Figure 2) Thereafter, survival is quite limited. The 3 principal symptoms of AS are angina, syncope, and heart failure.[14],[18],[19],[20] With the onset of angina, the mean survival of a patient with AS is 4.7 years. Once a patient develops syncope, the mean survival is typically less than 3 years. Patients with dyspnea and heart failure have a mean survival between 1 and 2 years. Heart failure is the presenting symptom in at least one-third of patients with AS. Once a patient crosses the threshold from asymptomatic to symptomatic, the risk of mortality promptly increases and approximately 3% to 5% of patients will die within weeks to months. Hence, it is extremely important to accurately identify the presence of symptoms. The presence of symptoms in a patient with AS is an indication for an AVR. Management of the asymptomatic patient is discussed below.

Figure 2
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Survival curve of patients with aortic stenosis. Reproduced with permission from: Braunwald and Ross: Circulation 1968; 38 (suppl V): 61-67)

Aortic Regurgitation

Patients with mild to moderate AR are typically asymptomatic and have an excellent prognosis without surgery.[5],[21] The prognosis worsens, however, with the onset of symptoms and/or changes in left ventricular function or dimensions.

Symptomatic AR is an indication for AVR. But given the insidious progression of left ventricular changes, left ventricular changes may develop in the absence of symptoms. Hence, even in the absence of symptoms, the degree of left ventricular dilation may be an indication for valve replacement and a left ventricular end-systolic diameter greater than 50 mm or end-diastolic diameter greater than 65 mm are indications for AVR.[5] As the left ventricle dilates, its systolic function may irreversibly decline. Therefore, evidence of left ventricular dysfunction with an LVEF less than 50% in the setting of severe AR may be an indication for valve replacement.[5]

History of Aortic Valve Replacement

The first attempt to treat AS is attributed to Tuffier, in 1912, in Paris, when he unsuccessfully attempted transaortic digital dilation of a stenotic aortic valve.[15],[22] It would be another 36 years before the first successful valvotomy for AS would be performed. In 1948, Smithy performed the first successful aortic valvotomy in Charleston, South Carolina, in a 21-year-old woman who traveled to the Medical University of South Carolina from Ohio. Ironically, Smithy died later that same year of AS at the age of 34 years. Three years later, in Philadelphia, Bailey reported a successful aortic valvotomy by insertion of a mechanical dilator across the stenotic valve of patients to open-fused commissures. In 1952, Hufnagel and Harvey at Georgetown University placed the first prosthetic ball valve into the descending aorta of a patient with aortic insufficiency. In 1955, Swann performed the first successful aortic valvotomy using hypothermia and inflow occlusion at the University of Colorado in Denver. Surgery on the aortic valve under direct vision required the development of cardiopulmonary bypass by Gibbon (1954). The initial open aortic valve operations were limited to aortic valve commissurotomy and debridement of calcified aortic valve leaflets. But in 1962, Ross successfully performed an orthotopic homograft valve replacement in London. The modern era of AVR began when Harken, in Boston in 1960, and Starr, in Portland, Oregon, in 1963, reported replacement of the aortic valve with a prosthesis. In 1967, Ross performed the first pulmonary autograft procedure (Ross procedure) for correction of AS. In the mid-1960s, stent-mounted porcine aortic valves were implanted, but these formaldehyde-fixed valves degenerated rapidly. But in 1974, Carpentier, in Paris, reported superior longevity of the glutaraldehyde-preserved porcine valve; thereafter, their usage was well established. By 1981, bileaflet mechanical valves became widely implanted in the aortic and mitral positions and largely supplanted the use of ball-cage mechanical valves. In the mid-1990s, a new generation of bovine pericardial valves were shown to have durability similar to porcine valves, and both types of bioprostheses became widely implanted. By the mid- to late 1990s, stentless bioprosthetic valves came into widespread use. Within 15 years, however, concerns about the durability of stentless valves led to a decrease in their use. By the early 2000s the flow dynamics and durability of tissue valves were recognized as improved and, at the same time, the complications of anticoagulation were better appreciated. Thus, by 2004, most valves implanted in patients in the United States were tissue valves. Many assumed that surgical AVR would remain the only effective treatment of aortic valve disease. But in 2002, transcatheter aortic valve replacement (TAVR) was performed in a patient with AS by Cribier in Rouen, France. Today, both AVR and TAVR provide surgical options for the treatment of aortic valve disease.

Preoperative Decision-Making

Once AVR is indicated, careful evaluation of the patient is required. The decisions that must be made are focused on the operative risk for a given patient and the choice of prosthetic valve to implant.

Preoperative Risk Assessment

AVR may be performed safely. According to The Society of Thoracic Surgeons (STS) Adult Cardiac Surgery Database (ACSD), the operative and in-hospital mortality rate for isolated AVR is now 2.1% and 1.6%, respectively.[23] The risk of an AVR for a given patient, however, requires consideration of patient-specific risk factors.

The STS Predicted Risk of Operative Mortality (PROM) calculator for the valve surgery is one of the most commonly used tools for prediction of an individual patient’s risk for AVR.[24] Use of the STS PROM permits stratification of mortality risk for AVR into high (>8%), intermediate (3%-8%) and low risk (< 3%). The STS PROM may be accessed online at www.sts.org and permits a rapid estimation of an individual patient’s risk. As with other cardiac operations, patient-specific risk factors for AVR include prior cardiac operation, renal failure, history of stroke, need for concomitant procedure, and endocarditis. It is important to recognize, however, that some patient-specific risk factors may significantly increase the risk of AVR but are not included in the STS PROM. Examples include cirrhosis, significant pulmonary hypertension, and frailty.

Choice of Prosthetic Aortic Valve

The choice of prosthesis should be individualized and patient specific. Factors that should be considered in preoperative decision-making include patient age, comorbid conditions, valve durability, short- and long-term valve specific risks, anticoagulation strategy, indication for surgery, and patient preference.[16]

Recent guidelines have now lowered the age at which a mechanical prosthesis may be preferred. The 2017 American Heart Association/American College of Cardiology (AHA/ACC) provided a focused update of the 2014 AHA/ACC guidelines for the treatment of valvular heart disease and suggest that it may be reasonable to consider a mechanical valve for implantation in patients 50 years or younger and a bioprosthetic valve in patients 70 years or older[5]; however, the choice of valve becomes less straightforward in patients between the ages of 50 and 70 years. In these patients, reliance on additional factors and patient preferences are heavily weighed.

The operative risks of cardiac valve replacement are not associated with the choice of prosthesis. Further, the hemodynamic performances of contemporary valves are similar. The choice of aortic valve prosthesis has traditionally focused on whether a patient would be committed to the risks of life-long anticoagulation (mechanical valve) or the presumed need for reoperation for structural valve deterioration (bioprosthetic valve); however, this approach is an oversimplification and the choice of prosthetic valve must be patient specific. In addition to appropriate consideration of a given patient’s comorbidities, one of the most important considerations is the age of the patient at valve implantation. In this light, it is important to recognize that approximately 80% of all valve replacements in the United States are performed in patients above the age of 60 years. Currently, the use of bioprosthetic valves has risen to 80% of all implanted valves.[16]

Operative Technique

The standard surgical approach used by the authors for AVR that has been previously described[16] is via a median sternotomy (Figure 3). Cardiopulmonary bypass is established by aortic and right atrial cannulation. After initiation of cardiopulmonary bypass, the aortic root is vented and a left ventricular vent is inserted via the right superior pulmonary vein. If the aortic valve is competent, cardiac arrest may be achieved by antegrade cardioplegia with subsequent administration of cardioplegia in retrograde fashion. Otherwise, all cardioplegia may be administered retrograde. The myocardial temperature is monitored in the interventricular septum and kept below 10oC by administration of cold blood cardioplegia every 20 minutes throughout the period of aortic occlusion. Systemic hypothermia is routinely employed by cooling the patient to a bladder temperature of 28oC to 32oC, although there is variability in the approaches to temperature monitoring and to cooling protocols.

Figure 3
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Operative technique for aortic valve replacement.

There are several important technical caveats. First, it is important to prevent the introduction of air into the left atrium with the insertion of left ventricular vent via the right superior pulmonary vein. This can be done by temporary partial occlusion of the venous line, thereby filling the left atrium with blood. Second, the ascending aorta in patients undergoing AVR may be very thin because of post-stenotic dilatation, advanced age, annulo-aortic ectasia, or other factors. Hence, aortic cannulation stitches must be placed very carefully to avoid tearing the aorta; they should be placed in the media of the aortic wall and should not be full thickness. Third, when operating for AR, the heart is prone to ventricular fibrillation once cardiopulmonary bypass and systemic cooling have been initiated. If the heart fibrillates, the left ventricle will immediately distend, which could be potentially lethal. Therefore, avoid systemic cooling until the left ventricular vent has been placed.

Once cardiopulmonary bypass has been initiated, the plane between the aorta and pulmonary artery is dissected. This is important to optimize visualization of the aortic valve and to facilitate aortic closure. An important technical nuance is to identify the surface anatomy of the right coronary artery as it originates from the right sinus of Valsalva. This may be done by gentle dissection of the fat pad overlying the right sinus of Valsalva. One must be confident the aortotomy is not too close to the right coronary ostium, for the ostium may be damaged or distorted with aortic closure or by the new valve itself. The aortotomy should be approximately 2 to 2.5 cm distal to the origin of the right coronary artery. As the patient is systemically cooled, the heart will fibrillate. The aortic cross-clamp is then applied, and cardioplegia is administered.

A small, transverse aortotomy is made. Through this initial aortotomy, one may visualize the aortic valve. The aortotomy is then extended transversely across the anterior surface of the aorta. It is important to stay approximately 1 cm distal to the zenith of the commissures of the aortic valve leaflets. Having extended the aortotomy to the patient’s right, once the incision is exactly over the halfway point of the noncoronary leaflet, the aortotomy incision is directed in the axis of the aorta down toward the aortic annulus. This portion of the aortotomy incision should stop at least 1 cm distal to the aortic annulus.

The aortic valve is best visualized with the operating table in a reverse Trendelenberg position and rotated a bit to the patient’s right. Traction sutures are then placed through the top of each commissure and snapped to the surgical drapes. This brings the aortic valve up toward the surgeon. The aortic valve leaflets are then excised with scissors. After the leaflets have been removed, a sponge is placed in the outflow track and a rongeur instrument is then used to gently debride the annulus of calcium. During this process, it is helpful for the assistant to follow along with an open-tipped suction catheter to help sweep up any small pieces of calcium. Once the annulus has been sufficiently debrided of calcium, the sponge is removed from within the ventricle, and the lumen of the left ventricle is liberally irrigated with cold saline to flush out any calcium debris.

Horizontal pledgetted mattress sutures are placed in the aortic annulus with the pledgets in the subannular position. Note that the annular size will be somewhat smaller once all the valve sutures have been placed. Therefore, the annulus should be sized and the choice of valve size should be finalized after all the valve sutures have been placed. It is very important not to attempt to implant an oversized valve. The aortic valve prosthesis is then brought to the operative field and the sutures passed through the valve sewing ring. To facilitate symmetrical suture placement, it is helpful to mark the sewing ring in thirds.

Once the sutures are passed through the sewing ring, the valve is seated into the aortic annulus, and the sutures tied. In order to minimize difficulty in seating the valve, the sutures at each of the 3 commissures should be tied first. Next, a suture midway between each commissure should be tied. In this manner, the surgeon may be assured that the valve will seat appropriately. Once the valve is sewn in place, the aortotomy is closed with 5-0 polypropylene sutures in 2 layers. The first layer is a running horizontal mattress stitch, and the second is an over-and-over running stitch.

Stentless Valve Implantation

AVR with a stentless valve offers the theoretical advantage of a lower residual gradient across the valve; however, the use of stentless valves is not common in contemporary surgical practice. In large part this may be because the implantation of a stentless aortic valve prosthesis may be technically challenging. Stentless valves are commonly implanted using the subcoronary technique.

To implant a stentless valve using the subcoronary technique, the aorta is transected approximately 1 cm distal to the sinotubular junction, and the patient’s aortic valve leaflets are excised; the aortic annulus is debrided of calcium. The ostia of the left and right coronaries are identified. With the implantation of a stentless valve, it must be oriented in such a way to avoid occlusion of the coronary ostia. (Figure 4)

Figure 4
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Operative technique for AVR with a stentless bioprosthesis.

Using the commercial valve sizer, the appropriately sized prosthesis is chosen. A double-armed suture is placed at the midpoint of each cusp of the patient’s aortic annulus. The other needle of each suture is then placed in the sewing ring at the midpoint of each cusp of the prosthesis. The surgeon must be confident that these suture placements will orient the prosthesis such that the coronary ostia ultimately sit in the midpoints of the left and right prosthetic valve cusps. A series of single sutures are then placed and tied in order to sew the sewing ring of the prosthesis to the aortic valve annulus.

The superior edge of the sewing prosthesis is then sewn to the aortic valve. A double-armed polypropylene suture is placed at the midpoint of the superior edge of the sewing ring of each cusp, sewing the device to the wall of the aorta. Beginning under the ostium of the left coronary artery, and using a running suture technique, the device is sewn to the inside of the aortic wall. Each end of the sutures is sewn using a running suture technique toward a commissure of the prosthesis. When the suture line reaches the commissure, the commissure is sewn to the aortic wall by passing the needle through the aortic wall. At each commissure, the needles of the sutures are passed through a felt pledget, and the sutures are tied. (Figure 4)

Postoperative Management

Aortic Stenosis

The postoperative management of patients following AVR for AS typically requires little more than is routinely required for other cardiac surgical patients; however, because these patients have left ventricular hypertrophy, their cardiac output will be very sensitive to left ventricular preload (preload dependent). In the early postoperative period, it is often helpful to continuously monitor the pulmonary artery diastolic pressure as a parameter of left ventricular end-diastolic pressure (preload) via a pulmonary artery catheter. This should be placed in the operating room before initiating the procedure. A pulmonary artery catheter that provides a continuous readout of the mixed venous oxygen saturation is especially helpful in monitoring the total body oxygen-supply balance. If volume administration is required to maintain preload, either crystalloid or colloid may be used.

Because these patients have a noncompliant left ventricle and are preload-dependent, the left ventricle requires sufficient diastolic filling time. Hence, tachycardia may not be well tolerated and often leads to a fall in cardiac output. This is especially true of atrial fibrillation. With the new onset of postoperative atrial fibrillation, not only is the atrial kick lost but the ventricular rate-response is often uncontrolled and rapid. The combination of these 2 things may decrease left ventricular preload with a resultant fall in cardiac output. It is therefore helpful to initiate β-Blockers as soon as feasible postoperatively as prophylaxis against atrial fibrillation.

Aortic Regurgitation

As with the postoperative management of patients with AS, the management of patients undergoing AVR for AR must focus on maintaining an adequate left ventricular preload. For this reason, it is important to maintain sinus rhythm. Additionally, the patient with AR may commonly have preoperative evidence of left ventricular systolic dysfunction. Such patients are more likely to require inotropic support postoperatively. The inotropic agent of choice varies from one institution to the next, but epinephrine or dobutamine are often recommended in this setting.

If a patient is progressing normally on the first or second day following AVR for AR, it may be appropriate to initiate diuretic therapy (furosemide) to help reverse the patient’s preoperative and operative volume-overloaded state.

Outcomes and Complications

Early Surgical Outcomes

Operative mortality

The STS PROM[24] permits the stratification of patients undergoing AVR for AS into those predicted to have low risk of mortality (< 3%), intermediate risk (3%-8%) and high risk (>8%). In contemporary surgical practice, the majority of patients undergoing isolated AVR fall into the low-risk category. As such, the STS ACSD reports that that the average operative mortality for isolated AVR done as an elective procedure is approximately 2%.[23] Obviously, the risk is higher among those with patient-specific risk factors such as emergency status, active endocarditis, renal failure, history of stroke, or prior cardiac operation.

Operative complications

The complication rate associated with AVR is low and is often a function of patient-specific factors. Stroke, in particular, remains a morbid complication and occurs in 1% to 2% of low-risk patients.[23] Although it may occur in patients without obvious risk factors for stroke, some patients are known to be at higher risk, including those undergoing concomitant CABG and those with diffuse atherosclerotic disease involving the aorta and/or carotid arteries. Use of the STS PROM allows for the risk stratification of stroke for an individual patient; as the patient-specific risk factors increase, the risk of perioperative stroke steadily increases.[25] To help minimize the risk of stroke, special attention should be paid not to lose any calcium fragments during the valve resection and debridement. Furthermore, adequate removal of air from the heart should be accomplished under transesophageal echocardiographic (TEE) guidance upon closing the aortotomy.

The risk for reoperation for bleeding after AVR ranges between 3% and 5%.[23],[25] This risk is higher (6.3%) among the patients undergoing a combined AVR and CABG procedure.[23] Deep sternal wound infection or mediastinitis occurs in less than 1% of cases.[23] The risk of postoperative renal failure ranges from 2% to 4% and is higher in patients with preoperative renal insufficiency.[23] Given the proximity of the aortic valve to the conduction system, postoperative complete heart block occurs in approximately 5% of patients.

Long-Term Outcomes

Following AVR, the median survival for patients less than 80 years is approximately 11 years; for octogenarians, it is approximately 6 years. The 10-year survival for patients following AVR ranges from 40% to 70%, with an average in the literature of 50%. The type of prosthesis does not impact survival, but other patient-specific factors such as age at operation and presence or absence of coronary artery disease do impact survival following AVR. Regardless of the type of prosthetic valve implanted, approximately one-third of patients die of valve-related causes. Given that valve-related complications occur at a frequency of about 3% to 6% per year, it is important to ask if the risks in a specific patient may be minimized by the choice of a mechanical vs a bioprosthetic valve. The choice of valve prosthesis must be individualized.

Mortality among heart valve recipients is valve related in approximately 30% of patients. The principal causes of valve-related death following valve implantation include thromboembolism (12%), reoperation (10%), bleeding (4%), and prosthetic valve endocarditis (PVE) (3%).[15] The risk of PVE is not different between mechanical or tissue valves. It is approximately 4% spread over the patient’s lifetime; however, if PVE does occur, it is associated with up to a 50% mortality rate.[26]

The leading cause of valve-related death is thromboembolism. Largely because mechanical valves are thrombogenic, the risk of thromboembolism is greater with mechanical valves. At 10 years following AVR, the risk of thromboembolism is 20% for mechanical valves and 9% for bioprosthetic valves.[15]

Because a mechanical valve obligates the patient to chronic anticoagulation therapy (warfarin sodium), the choice of a prosthetic valve must consider the risks of chronic anticoagulation. The risk of bleeding complications from chronic anticoagulation is between 1% and 2% per year. In fact, 4% of valve-related deaths result from bleeding. Mechanical valves should be avoided in patients with contraindications to anticoagulation because of occupation or because of coexistent medical conditions. Likewise, patients who are medically noncompliant or whose level of anticoagulation may not be closely monitored should not receive mechanical valves.

Ten percent of valve-related deaths result from reoperation. It was traditionally assumed that following implantation of a tissue valve, patients would require reoperation for structural valve deterioration. Mechanical valves were therefore recommended for patients with a life expectancy longer than 10 years. This reasoning requires refinement. First, placement of a mechanical valve does not eliminate the potential for subsequent valve reoperation. Although mechanical valves will not structurally fail, upwards of 10% of mechanical aortic valves require reoperation within 5 to 10 years, primarily for paravalvular leak, endocarditis, or nonstructural valve dysfunction such as scar tissue or pannus ingrowth.[27] Second, the structural durability of newer bioprosthetic valves is superior to prior generations of valves. Third, it is now appreciated that on average, patient death (all-cause mortality) occurs before reoperation for structural valve deterioration. In fact, use of actual rather than actuarial statistical methodology demonstrates the incidence of reoperation for structural valve deterioration of a bioprosthetic valve is less than 15% for patients older than 60 years.[28] One option now available to mitigate the risk of reoperation for the structural valve deterioration of a bioprosthetic valve is the performance of a “valve-in-valve” TAVR procedure.

The Small Aortic Annulus

The use of a prosthetic valve may produce some degree of residual obstruction to left ventricular outflow because of the sewing ring and/or stents. It is therefore important to implant a valve that is appropriately sized for the patient’s cardiac output. Otherwise, a high residual transvalvular gradient may exist should a prosthesis that is too small be implanted, creating the phenomenon of “prosthesis-patient mismatch.” The term “prosthesis-patient mismatch” (PPM) was coined in 1978 by Rahimtoola[29] and used to describe his observation that a patient’s AS may not be relieved by a prosthesis. This concern has led to persistent controversy over the management of the small aortic annulus.

Although some authors have demonstrated that implantation of small aortic valve sizes has no effect on long-term survival, others have suggested otherwise.[30] One factor confounding the interpretation of these data is the fact that the sizing of prosthetic valves is inconsistent from one manufacturer to the next. For example, a size 19 valve may vary in effective orifice area (EOA) from 1.0 cm2 to 1.3 cm2, depending on the manufacturer.[31] Another confounding factor is the fact that populations of study patients (with particular regard to patient age, gender, and size) has varied from one report to the next. A small prosthesis implanted in a small, elderly patient may be perfectly adequate for the patient’s cardiac output, but the same size valve may be inadequate for a more active, larger patient with a higher cardiac output.

The patient’s size (body surface area, BSA) and age must therefore be considered when choosing the appropriate aortic valve prosthesis. This may be done by use of an index, which normalizes the EOA of the prosthesis to the BSA of the patient (EOA/BSAi). Acknowledging some of the uncertainties provided by the literature in this area, one should avoid implantation of an aortic prosthesis with a calculated EOA/BSAi less than 0.8 cm2/m[2],[32]; it is generally accepted that the likelihood of PPM is minimized if the prosthesis provides the patient with an EOA/BSAi greater than 0.85 cm2/m2. An EOA/BSAi of 0.65 cm2/m2 to 0.85 cm2/m2 is considered moderate PPM, and less than 0.65 cm2/m2 is considered severe PPM. This recommendation is derived from the fact that an AVA of 0.6 cm2/m2 is considered severe AS. Use of this guideline is helpful as it places the consideration of valve size in the context of the patient’s hemodynamic needs, rather than in absolute terms.

The use of this strategy assumes that the patient with a larger BSA will require a higher flow/minutes across the valve (cardiac output) than will the patient with a smaller BSA. The EOA for each prosthesis may be obtained from the manufacturer, which in turn allows calculation of the EOA/BSAi for a given prosthesis. A difference in survival among patients with PPM may not be apparent for 5 to 7 years postoperatively.[30] Therefore, other patient-specific factors must be considered in the determination of an appropriately sized prosthesis, such as age and activity level; the 60-year-old distance runner will require a larger EOA that the 80-year-old sedentary person. Nonetheless, this strategy serves as a useful guideline in choosing valve size.

The challenge of the need for a large valve relative to the small aortic annulus may be difficult to reconcile. Within a few years of the first AVR by Harken in 1960, surgical techniques to surmount the problem by enlargement of the annulus emerged. By the end of the 1970s, Nicks,[33] Konno,[34] and Manouguian[35] had each described techniques to enlarge the annulus so that a larger valve could be implanted. Nicks (1970) and Manouguian (1979) each described techniques of patch enlargement of the posterior aspect of the aortic annulus. Konno described a more extensive procedure of aortoventriculoplasty of the anterior aspect of the aortic annulus in 1975. More recently, Otaki[36] described a method of patch enlargement of both the posterior and anterior aortic annulus (1997).

Implantation of stentless bioprosthetic aortic valves may be an alternative in some patients, and some hemodynamic advantages associated with their use was appreciated by 1990.[37] Because these valves lack valve struts, the design of stentless valves offers an inherently larger EOA. In most centers, stentless valves are implanted by 1 of 2 techniques: subcoronary or as a total aortic root replacement. Although some controversy exists in the literature, it is generally accepted that the hemodynamic performance of stentless bioprosthetic valves is better that of stented valves. In particular, use of the root replacement technique is felt to minimize the risk of PPM. There is, however, concern that stentless valves are less durable than stented bioprostheses.

Patch enlargement of the annulus is the easiest and most straightforward technique used to effectively avoid PPM. According to the STS National Cardiac Surgical Database, approximately 2.4% of AVR procedures include an annular enlarging procedure. Some reports raised concerns that operative mortality may be higher with use of the technique, and it has therefore been avoided by many.[38] Recent reports, however, demonstrate that surgical outcomes are probably not different from those of AVR alone.[39] The annular dimensions should be known from the preoperative echocardiogram, allowing the surgeon to plan to enlarge the annulus from the outset of the procedure. As a rule of thumb, a Nicks procedure (incision of the annulus in the midpoint of the noncoronary leaflet portion of the annulus) will generally permit 1 size larger valve. On the other hand, a Manouguian procedure (incision of the annulus through the commissure of the non- and left-valve leaflets) will generally permit placement of a valve 2 sizes larger. In most situations, a Nicks procedure is sufficient and, as previously described, is therefore the preferred technique by the authors[15] and is described below (Figure 5):

Figure 5
Descriptive text is not available for this image
Operative technique for AVR with annular enlargement.

1. Enlarge the annulus at the midway point of the noncoronary leaflet. This is accomplished by extension of the aortotomy incision.

2. Extend this incision into the fibrous apron between the mitral and aortic annuli; it is unnecessary to incise the mitral annulus or the anterior leaflet of the mitral valve.

3. Beginning at the apex of the incision, a fashioned piece of woven Dacron is sewn in place. The patch material is typically 2 cm wide and beveled at the point of insertion into the annulus. A pledgetted 5-0 polypropylene suture is brought through the patch material, then the roof of the left atrium, then the apex of the aortic incision, and tied. The patch material is sewn to the aorta for a distance of about 2 inches. A second suture line of 5-0 polypropylene suture is helpful to aid with hemostatis.

4. The valve stitches are placed. In the area over the patch material, 4 pledgetted sutures of 4-0 polypropylene suture are brought from outside-in through the patch material.

At each edge of the patch, a horizontal mattress stitch is brought outside-in with 1 needle through the aorta and the other through the patch material. Between these 2 stitches, 2 additional valve sutures are typically placed. It is preferable to use 4-0 polypropylene for these 4 valve sutures because the needle holes through the patch material are small, and therefore bleeding is less. The remainder of the valve sutures are pledgetted braided 2-0 sutures.

5. The patch material is then brought anteriorly to complete aortic closure.

If the patch material over the anterior aorta is too wide, the proximal aorta may be displaced anteriorly and caudally. In so doing, the orifice of the right coronary may be displaced and kinked. This may be avoided by cutting the patch material no wider than about 1.5 to 2 cm in this area. Should the right coronary artery ostium be distorted despite this effort, the patch material may be imbricated anteriorly in order to restore the normal position of the right coronary artery ostium.

6. Once the aorta is closed, hemostasis may be tested by the administration of antegrade cardioplegia. A small amount of oozing through the patch material is to be expected until heparin reversal. But any bleeding sites, particularly near the apex of the patch closure, should be repaired before release of the aortic cross-clamp.

Asymptomatic Aortic Stenosis

Although still somewhat controversial, the vast majority of asymptomatic patients do not require AVR; however, some do carry a low but real risk of sudden death. The challenge is the identification of the subset of asymptomatic patients in whom the risk of death is greater if AVR is not performed, or in whom the likelihood of AVR in the near term is probable.

Risks Without Operation

The risk of sudden death in asymptomatic patients is considered to be quite low[5]; however, it has been reported to be as high as approximately 6%.[40] In addition, management of the asymptomatic patient is complicated by the fact that the mortality is 3% to 4% soon (within weeks to months) after the onset of symptoms.[41]

Unmasking the Symptoms

Given the patient with significant AS diagnosed by echocardiogram, it is important to determine that the patient is truly asymptomatic. This may be objectively confirmed by exercise stress testing (treadmill). Although unnecessary and risky in the symptomatic patient with AS, exercise testing by experienced personnel has been found to be safe in asymptomatic patients. A modified Bruce protocol may be employed under careful observation. An exercise test is considered positive if symptoms occur, systolic blood pressure falls by more than 10 mm Hg, dysrhythmias occur, or ST segment changes are noted.[42] Given a positive exercise test, the patient should be considered symptomatic and offered surgery.

Outcomes of Patients with a Negative Stress Test.

Following a negative stress, patients must be closely followed for hemodynamic progression of AS. On average, the aortic flow velocity increases by 0.3 m/s per year, and the AVA decreases by 0.1 cm2 per year[18]; however, the flow velocity is largely dependent on left ventricular stroke volume and contractility, and should left ventricular function decline, velocity may not change despite a smaller AVA. Further, the rate of progression of AS is quite variable, making it difficult to predict the clinical course of a given patient. Aortic flow velocity as the most important patient-specific variable. The highest risk group are those asymptomatic patients with an aortic flow velocity of greater than 4 m/s, as less than one-third may be alive without valve replacement at 2 years.[18]

Patients with very severe AS are defined as those with a peak aortic jet velocity greater than 5 m/s, a mean gradient greater than 60 mm Hg, and a valve area less than 0.6 cm2. Asymptomatic patients with very severe AS have a very poor prognosis; event-free survival was only 64% at 1 year and 36% at 2 years.[20] In a series of 197 consecutive asymptomatic patients with very severe AS,[21] early surgery was performed in 102 patients, and a conventional treatment strategy (surgery deferred until the onset of symptoms) was followed in 95 patients. The cardiac mortality rate in the early surgery group was 0%, and 24% in the conventional treatment group at 6 years. Provided that AVR may be performed with low morbidity and mortality, asymptomatic patients with very severe AS may benefit from AVR.

In addition to the absolute baseline aortic flow velocity, longitudinal follow-up may reveal patients with a rapidly increasing flow velocity on serial echocardiograms; these patients are at risk for cardiac events. Among patients who remain asymptomatic, the average rate of progression of aortic flow velocity is approximately 0.14 m/s per year. But among those asymptomatic patients who do experience cardiac events, it may be as high as 0.45 m/s per year.[20] These data suggest that patients with rapidly increasing flow velocity are at higher risk.

Patient age and aortic valve calcification may also be important. In asymptomatic patients with an aortic flow velocity greater than 4 m/s, those above age 50 years are more likely to experience cardiac events in follow-up.[20] Interestingly, in this same group, moderate or severe aortic valve calcification was strongly associated with subsequent cardiac events.

Therefore, for the patient felt to be asymptomatic following a carefully obtained history, an exercise stress test may be obtained. Patients with a positive stress test may be offered surgery. If the stress test is negative, an asymptomatic patient may be longitudinally followed with regularly scheduled echocardiograms. Patients with very severe AS should be advised of their increased risk. AVR may also be recommended if the LVEF is less than 50% as this implies ventricular dysfunction secondary to AS.

Asymptomatic Aortic Regurgitation

AVR is clearly indicated in the patient with symptomatic AR. Conversely, the natural history of asymptomatic severe AR is not well defined. Ten years after the diagnosis of severe AR, as many as 75% of patients will have died or undergone AVR.[5] It is now clear that upon diagnosis, certain subsets of asymptomatic patients with severe AR should be offered AVR. The recommendation for AVR should be based on left ventricular size and function.

There is consensus that the asymptomatic patient with severe AR with subnormal LVEF at rest should undergo AVR. This consensus is based on a 25% progression per year to heart failure or death in these patients.[5] Evidence of left ventricular dilation is strongly associated with progression to heart failure or death; a left ventricular end-systolic dimension greater than 55 mm (or >25 mm/m2) or a left ventricular end-diastolic dimension greater than 80 mm are an indication for AVR. Likewise, if longitudinal echocardiographic follow-up reveals either rapid diminution in LVEF or a rapid increase in left ventricular dimensions, AVR is indicated. Although normal at rest, myocardial performance may be found abnormal with exercise. Hence, exercise stress testing may be used to unmask myocardial contractile dysfunction; a fall in LVEF with exercise greater than 5% is a strong relative indication for surgery.[5]

Low-Gradient Aortic Stenosis

The aortic transvalvular gradient is determined by the volume and flow rate of blood that flows across the narrowed valve. In turn, the volume of blood is determined by the left ventricular stroke volume index (LVSVI) and the systolic ejection time. Most patients with AS have a high transvalvular gradient and normal LVEF; however, some patients may have severe narrowing of the aortic valve (AVA < 1 cm2) but have a low transvalvular gradient (mean gradient < 40 mm Hg) because the volume and flow rate through the valve are low. Such “low flow” is defined as an LVSVI less than 35 mL/m2. Patients with “low-flow, low-gradient” AS may be subdivided into patients with normal LVEF or diminished LVEF.

Low-Gradient Severe Aortic Stenosis With Preserved Left Ventricular Function

This group of patients may also be referred to as patients with paradoxical low-flow, low-gradient (PLFLG) AS. Among patients with severe AS, 10% may have PLFLG AS. It is more commonly found in elderly women with a small BSA. It may also be found in the setting of severe concentric LV hypertrophy, a small LV cavity, small LV volumes and systemic hypertension.[43]

Patients with PLFLG AS have worse short- and long-term prognoses than do patients with a high gradient; it is consistently noted to be an independent predictor of mortality, with a 10-year survival of about 32%.[44] These patients, do, however, benefit from AVR as patients with PLFLG AS who undergo AVR have a better 5-year survival than those who do not (63% vs 38%)[44]; however, perhaps because of greater LV hypertrophy and fibrosis, the operative mortality rate for AVR for PLFLG may be increased. The operative mortality of 9.8% in these patients was increased compared with mortality of 3.8% in patients with high-gradient AS[44]; however, others have reported that AVR may be performed in these patients without increased perioperative mortality.[45] These patients must be managed selectively and thoughtfully.

Low-Gradient Aortic Stenosis With Left Ventricular Dysfunction

Among the most challenging patients with AS are those with a low transvalvular gradient and severe left ventricular dysfunction. Low-gradient AS in this setting is defined as less than 30 mm Hg. Treated medically, the median survival of these patients is usually less than 2 years; the 1 and 4 year survivals are 41% and 15%, respectively.[16],[46] This subset represents less than 5% of patients with AS. The clinical outcomes of AVR in these patients has not been well characterized, but the operative mortality rate for AVR in this group of patients has historically been quite high, leading some authors to recommend against surgery.

When the patient with severe left ventricular dysfunction associated with low-gradient AS is first seen, it may be difficult to know if the left ventricular dysfunction is primary or secondary. The pathogenesis of left ventricular dysfunction secondary to AS is derived from afterload mismatch. With significant AS, the left ventricle compensates for pressure overload by hypertrophy, thereby normalizing wall stress. In this manner, LVEF and cardiac output are initially maintained. When the ventricle is no longer able to compensate for the increased wall stress, left ventricular systolic function declines secondary to afterload mismatch. The transvalvular pressure gradient may be low despite the presence of severe AS. Provided the left ventricle still has the ability to contract (contractile reserve), clinical outcomes with AVR are quite good; operative mortality is acceptably low, and left ventricular function typically improves after AVR.[16]

On the other hand, left ventricular dysfunction may be primary rather than secondary to the AS. The dysfunctional left ventricle may be unable to fully open a mildly calcified aortic valve if the stroke volume is significantly decreased. This condition is termed “relative AS.”[47] These patients have a cardiomyopathy (ischemic or otherwise) with only mild aortic valve narrowing.

For the surgeon and the patient, the principal questions relate to the risks of an operation and whether the patient will be improved afterward. The answers must rely on a paucity of data regarding the clinical outcomes of patients with low-gradient AS and severe left ventricular dysfunction. Taken together, the available data suggest that patients with low-gradient AS and severe left ventricular dysfunction may be stratified according to the severity of AS and the contractile reserve of the left ventricle.[48] This can be accomplished with a dobutamine stress echocardiogram. During an infusion of dobutamine up to 40 mcg/kg per minute, the hemodynamic response may be monitored by echocardiography or cardiac catheterization. In response to dobutamine infusion, stroke volume and thereby cardiac output should increase, raising the transvalvular gradient. An increase in stroke volume of at least 20% is considered evidence of contractile reserve.[5]

The echocardiographic appearance of the aortic valve may be very helpful in the decision-making. If the valve appears densely calcified with severely restricted leaflet motion, one may be confident the patient has severe AS. Conversely, if the leaflets are not badly calcified, or the leaflet motion subjectively seems better than the patient’s clinical condition suggests, a dobutamine stress echocardiogram may be useful in 2 ways. First, if the stroke volume (and thereby cardiac output) increases by at least 20%, the patient has contractile reserve. If the increase in stroke volume is associated with an increase in transvalvular gradient, the patient will typically benefit from AVR with a postoperative improvement in LVEF and functional status. But if no increase in stroke volume and transvalvular gradient are noted with dobutamine, the patient lacks contractile reserve or may not have severe AS. In such circumstances, AVR is not recommended.

“Prophylactic” Aortic Valve Replacement

An unexpected finding of moderate AS in patients undergoing concomitant cardiac operations may create a dilemma: whether to replace the aortic valve. This may be a difficult and controversial decision, particularly in patients undergoing operations for coronary artery bypass grafting (CABG). The decision must balance the relative risks of the progression of the AS with those of performing a concomitant AVR. Proponents of “prophylactic” AVR at the time of CABG argue the AS will inevitably progress, committing the patient to a second procedure associated with morbidity and mortality. Those favoring an expectant approach argue that “prophylactic” AVR may increase the risks of the procedure and unnecessarily commit an unacceptable number of patients to the risks of valve-related morbidity and mortality. Although progression from asymptomatic to symptomatic AS in a relatively short time is clinically recognized, it is very difficult to identify those patients likely to do so. At the heart of the argument is the need for an understanding of the natural history of mild to moderate AS and the contemporary risks of AVR after previous CABG.

The natural history of moderate AS (AVA 1.0-1.5 cm2) is difficult to define but is clearly worse than that of mild AS. The strongest predictors of patient events appear to be the degree of aortic valve calcification, a peak aortic flow velocity at study entry greater than 3 m/s, age greater than 50 years, and the presence of coronary artery disease. These patients with moderate AS may experience hemodynamic progression during relatively short follow-up.

The operative mortality rate reported for AVR subsequent to CABG or other cardiac procedures has significantly diminished in recent years. Certainly, advances in myocardial protection, surgical and anesthetic techniques as well as greater collective experience with cardiac reoperations have contributed to improved outcomes. But in contemporary surgical practice, TAVR should be considered the treatment of choice for patients with severe AS and prior cardiac operation. Thus, in the patient undergoing a cardiac operation who is found to have moderate AS, the decision regarding prophylactic AVR should factor in the possibility of a future TAVR.

At the time of a concomitant cardiac operation, patients with mild AS (AVA >1.5 cm2; aortic flow velocity < 2.5 m/s) have an excellent prognosis from their aortic valve and should not have AVR. On the other hand, patients with moderate AS and an AVA less than 1.2 cm2 and/or an aortic flow velocity greater than 3m/s associated with significant aortic valve calcification are likely to have symptomatic AS within the next several years. Provided the risks of doing an AVR at the time of the cardiac operation are acceptably low in this subset of patients it is reasonable to consider AVR at the initial operation. Another option is to not replace such a valve at the time of the initial operation and to follow the patient expectantly if a subsequent TAVR procedure may be an option.

Future Directions

AS is a disease of aging. As the population continues to age, the number of cases of AS can be expected to increase. Until recently, the only effective treatment for AS was AVR. Today, however, TAVR offers an alternative treatment and is already approved by the US Food and Drug Administration for use in high- and intermediate-risk patients. Randomized clinical trials are currently underway that compare surgical AVR to TAVR for patients at low risk for AVR. Given that TAVR offers a less invasive technique with a more rapid recovery for the treatment of AS, it seems very likely that TAVR may soon be the treatment of choice for AS for many patients. As such, the role of surgical AVR in the cardiac surgical armamentarium should be expected to change. In fact, as reported by the STS, the number of TAVR procedures performed annually has now surpassed the number of AVR procedures. This gap between the number of TAVR and AVR procedures can be expected to widen.

It therefore seems likely that the primary role of surgical AVR for the treatment of AS will change but it may be performed in cases in which TAVR is not a good option. For example, such cases may include those with endocarditis, those previously treated with TAVR but who are not candidates for a valve-in-valve TAVR procedure, those with significant coronary artery disease not amenable to percutaneous coronary intervention, and those in need of a concomitant aortic procedure. Cases such as these are technically more challenging and typically higher-risk procedures than routine, elective isolated AVR procedures. As such, it will be very important for cardiothoracic surgeons to continue to refine operative techniques, strategies for myocardial protection, and skills in perioperative management.

References

  1. Lindroos M, Kupari M, Heikkilä J, et al. Prevalence of aortic valve abnormalities in the elderly: an echocardiographic study of a random population sample. J Am Coll Cardiol. 1993;21(5):1220-5.  [PMID:8459080]
  2. Sverdlov AL, Ngo DT, Chapman MJ, et al. Pathogenesis of aortic stenosis: not just a matter of wear and tear. Am J Cardiovasc Dis. 2011;1(2):185-99.  [PMID:22254198]
  3. Pawade TA, Newby DE, Dweck MR. Calcification in Aortic Stenosis: The Skeleton Key. J Am Coll Cardiol. 2015;66(5):561-77.  [PMID:26227196]
  4. Wang D, Zeng Q, Song R, et al. Ligation of ICAM-1 on human aortic valve interstitial cells induces the osteogenic response: A critical role of the Notch1-NF-κB pathway in BMP-2 expression. Biochim Biophys Acta. 2014;1843(11):2744-53.  [PMID:25101972]
  5. Nishimura RA, Otto CM, Bonow RO, et al. 2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017;135(25):e1159-e1195.  [PMID:28298458]
  6. Piazza N, de Jaegere P, Schultz C, et al. Anatomy of the aortic valvar complex and its implications for transcatheter implantation of the aortic valve. Circ Cardiovasc Interv. 2008;1(1):74-81.  [PMID:20031657]
  7. Anderson RH, Wilcox BR. Understanding cardiac anatomy: the prerequisite for optimal cardiac surgery. Ann Thorac Surg. 1995;59(6):1366-75.  [PMID:7771812]
  8. Braverman AC. The bicuspid aortic valve and associated aortic disease. In: Valvular Heart Disease. 4th ed., Otto CM, Bonow RO, eds. Philadelphia, PA: Saunders/ Elsevier;2013:179.
  9. Braverman AC. Aortic involvement in patients with a bicuspid aortic valve. Heart. 2011;97(6):506-13.  [PMID:21339321]
  10. Sievers HH, Schmidtke C. A classification system for the bicuspid aortic valve from 304 surgical specimens. J Thorac Cardiovasc Surg. 2007;133(5):1226-33.  [PMID:17467434]
  11. Koenraadt WM, Tokmaji G, DeRuiter MC, et al. Coronary anatomy as related to bicuspid aortic valve morphology. Heart. 2016;102(12):943-9.  [PMID:26864668]
  12. Verma S, Siu SC. Aortic dilatation in patients with bicuspid aortic valve. N Engl J Med. 2014;370(20):1920-9.  [PMID:24827036]
  13. Svensson LG, Adams DH, Bonow RO, et al. Aortic valve and ascending aorta guidelines for management and quality measures. Ann Thorac Surg. 2013;95(6 Suppl):S1-66.  [PMID:23688839]
  14. Ross J, Braunwald E. Aortic stenosis. Circulation. 1968;38(1 Suppl):61-7.  [PMID:4894151]
  15. Fullerton DA, Harken AH. Valvular heart disease. In: Townsend CM, Beauchamp RD, Evers BM, and Mattox KL, eds. Sabiston’s Textbook of Surgery: The Biological Basis of Modern Surgical Practice. 19th ed. Philadelphia, PA: Saunders/Elsevier;2012:1686, 1687, 1689, 1691.
  16. Fullerton DA. Aortic valve replacement. In: Kaiser LR, Kron IL, Spray TL, eds. Mastery of Cardiothoracic Surgery. 3nd Edition. New York, NY: Lippincott Williams & Wilkens;2014:458.
  17. GORLIN R, GORLIN SG. Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves, and central circulatory shunts. I. Am Heart J. 1951;41(1):1-29.  [PMID:14799435]
  18. Otto CM. Aortic stenosis--listen to the patient, look at the valve. N Engl J Med. 2000;343(9):652-4.  [PMID:10979797]
  19. Otto CM, Burwash IG, Legget ME, et al. Prospective study of asymptomatic valvular aortic stenosis. Clinical, echocardiographic, and exercise predictors of outcome. Circulation. 1997;95(9):2262-70.  [PMID:9142003]
  20. Rosenhek R, Zilberszac R, Schemper M, et al. Natural history of very severe aortic stenosis. Circulation. 2010;121(1):151-6.  [PMID:20026771]
  21. Kang DH, Park SJ, Rim JH, et al. Early surgery versus conventional treatment in asymptomatic very severe aortic stenosis. Circulation. 2010;121(13):1502-9.  [PMID:20308614]
  22. Westaby S, Bosher C. Development of surgery for valvular heart disease. In Westaby S, Bosher C, eds. Landmarks in Cardiac Surgery. Oxford, England: Isis Medical Media;2000.
  23. D'Agostino RS, Jacobs JP, Badhwar V, et al. The Society of Thoracic Surgeons Adult Cardiac Surgery Database: 2017 Update on Outcomes and Quality. Ann Thorac Surg. 2017;103(1):18-24.  [PMID:27884412]
  24. O'Brien SM, Shahian DM, Filardo G, et al. The Society of Thoracic Surgeons 2008 cardiac surgery risk models: part 2--isolated valve surgery. Ann Thorac Surg. 2009;88(1 Suppl):S23-42.  [PMID:19559823]
  25. Thourani VH, Suri RM, Gunter RL, et al. Contemporary real-world outcomes of surgical aortic valve replacement in 141,905 low-risk, intermediate-risk, and high-risk patients. Ann Thorac Surg. 2015;99(1):55-61.  [PMID:25442986]
  26. Grover FL, Cohen DJ, Oprian C, et al. Determinants of the occurrence of and survival from prosthetic valve endocarditis. Experience of the Veterans Affairs Cooperative Study on Valvular Heart Disease. J Thorac Cardiovasc Surg. 1994;108(2):207-14.  [PMID:8041168]
  27. Hammermeister K, Sethi GK, Henderson WG, et al. Outcomes 15 years after valve replacement with a mechanical versus a bioprosthetic valve: final report of the Veterans Affairs randomized trial. J Am Coll Cardiol. 2000;36(4):1152-8.  [PMID:11028464]
  28. Banbury MK, Cosgrove DM, White JA, et al. Age and valve size effect on the long-term durability of the Carpentier-Edwards aortic pericardial bioprosthesis. Ann Thorac Surg. 2001;72(3):753-7.  [PMID:11565653]
  29. Rahimtoola SH. The problem of valve prosthesis-patient mismatch. Circulation. 1978;58(1):20-4.  [PMID:348341]
  30. Rao V, Jamieson WR, Ivanov J, et al. Prosthesis-patient mismatch affects survival after aortic valve replacement. Circulation. 2000;102(19 Suppl 3):III5-9.  [PMID:11082354]
  31. Christakis GT, Buth KJ, Goldman BS, et al. Inaccurate and misleading valve sizing: a proposed standard for valve size nomenclature. Ann Thorac Surg. 1998;66(4):1198-203.  [PMID:9800806]
  32. Feindel CM. COUNTERPOINT: Aortic valve replacement: size does matter. J Thorac Cardiovasc Surg. 2009;137(2):284-5.  [PMID:19185137]
  33. Nicks R, Cartmill T, Bernstein L. Hypoplasia of the aortic root. The problem of aortic valve replacement. Thorax. 1970;25(3):339-46.  [PMID:5452289]
  34. Konno S, Imai Y, Iida Y, et al. A new method for prosthetic valve replacement in congenital aortic stenosis associated with hypoplasia of the aortic valve ring. J Thorac Cardiovasc Surg. 1975;70(5):909-17.  [PMID:127094]
  35. Manouguian S, Seybold-Epting W. Patch enlargement of the aortic valve ring by extending the aortic incision into the anterior mitral leaflet. New operative technique. J Thorac Cardiovasc Surg. 1979;78(3):402-12.  [PMID:470420]
  36. Otaki M, Oku H, Nakamoto S, et al. Two-directional aortic annular enlargement for aortic valve replacement in the small aortic annulus. Ann Thorac Surg. 1997;63(1):261-3.  [PMID:8993289]
  37. David TE, Pollick C, Bos J. Aortic valve replacement with stentless porcine aortic bioprosthesis. J Thorac Cardiovasc Surg. 1990;99(1):113-8.  [PMID:2294343]
  38. Sommers KE, David TE. Aortic valve replacement with patch enlargement of the aortic annulus. Ann Thorac Surg. 1997;63(6):1608-12.  [PMID:9205157]
  39. Peterson MD, Borger MA, Feindel CM, et al. Aortic annular enlargement during aortic valve replacement: improving results with time. Ann Thorac Surg. 2007;83(6):2044-9.  [PMID:17532393]
  40. McCann GP, Hillis WS. Surgery in asymptomatic aortic stenosis. BMJ. 2004;328(7431):63-4.  [PMID:14715580]
  41. Rosenhek R, Binder T, Porenta G, et al. Predictors of outcome in severe, asymptomatic aortic stenosis. N Engl J Med. 2000;343(9):611-7.  [PMID:10965007]
  42. Shah RV, Desai NR, O'Gara PT. Asymptomatic severe aortic stenosis: silence of the lambs? Circulation. 2010;122(17):1734-9.  [PMID:20975009]
  43. Martin RP. Severe Aortic Stenosis: It Used to Be Simple. JACC Cardiovasc Imaging. 2018;11(5):670-672.  [PMID:28528152]
  44. Mohty D, Magne J, Deltreuil M, et al. Outcome and impact of surgery in paradoxical low-flow, low-gradient severe aortic stenosis and preserved left ventricular ejection fraction: a cardiac catheterization study. Circulation. 2013;128(11 Suppl 1):S235-42.  [PMID:24030412]
  45. Lopez-Marco A, Miller H, Kumar P, et al. Outcome of isolated aortic valve replacement in patients with classic and paradoxical low-flow, low-gradient aortic stenosis. J Thorac Cardiovasc Surg. 2017;154(2):435-442.  [PMID:28412115]
  46. Pereira JJ, Lauer MS, Bashir M, et al. Survival after aortic valve replacement for severe aortic stenosis with low transvalvular gradients and severe left ventricular dysfunction. J Am Coll Cardiol. 2002;39(8):1356-63.  [PMID:11955855]
  47. Monin JL, Quéré JP, Monchi M, et al. Low-gradient aortic stenosis: operative risk stratification and predictors for long-term outcome: a multicenter study using dobutamine stress hemodynamics. Circulation. 2003;108(3):319-24.  [PMID:12835219]
  48. Carabello BA. Is it ever too late to operate on the patient with valvular heart disease? J Am Coll Cardiol. 2004;44(2):376-83.  [PMID:15261934]
Aortic Valve Replacement (Mechanical, Bioprosthetic, Stentless) is a sample topic from the Adult and Pediatric Cardiac.

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STS Cardiothoracic Surgery E-Book from The Society of Thoracic Surgeons provides expert guidance for Cardiac and Thoracic Surgery. Sections include Pearson’s General Thoracic, Esphageal, Adult Cardiac, and Pediatric and Congenital Cardiac Surgery. .

Last updated: September 14, 2020