Surgery for Acquired Cardiac Disease

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CHAPTER 30 Surgery for Acquired Cardiac Disease

* The views expressed in this chapter are those of the author and do not necessarily reflect the official policy or position of the Department of the Navy, Army, Department of Defense, or the U.S. government.

We certify that all individuals who qualify as authors have been listed; each has participated in the conception and design of this work, the analysis of data (when applicable), the writing of the document, and the approval of the submission of this version; that the document represents valid work; that if we used information derived from another source, we obtained all necessary approvals to use it and made appropriate acknowledgments in the document; and that each takes public responsibility for it.

The history of cardiac surgery dates back to the late 19th century, with the repair of pericardial and cardiac trauma by Williams of Chicago in 1893. The modern era of cardiac surgery began in earnest with the development of the cardiopulmonary bypass machine by Gibbon of Boston in 1953. The modern concepts and techniques of extracorporeal circulation were refined further by Lillehei and Kirklin in the early 1950s. Extracorporeal circulation, along with improved techniques of myocardial protection, has allowed surgeons to perform the most complex procedures in the current realm of cardiothoracic surgical practice. The most commonly performed procedure since its inception in the 1960s is coronary artery bypass graft (CABG) surgery.

The development of coronary cine angiography in the early 1960s enabled the identification of stenoses of the coronary arteries in living patients (Fig. 30-1). This identification made it possible for the directed treatment of ischemic heart disease through CABG surgery and percutaneous interventions of obstructed arteries. The treatment for coronary artery disease was revolutionized, dramatically improving the therapeutic options for patients with this commonly occurring condition.

image

image FIGURE 30-1 Coronary angiogram of right and left coronary artery systems.

(From Mayo Clinic Cardiothoracic Grand Rounds, picture used in slide presentation, 2002.)

SURGERY FOR CORONARY ARTERY DISEASE

Description and Special Anatomic Considerations

Myocardial blood flow is provided by the left and right coronary arteries, originating from the aortic root. The left main coronary artery bifurcates into the left anterior descending (LAD) and the left circumflex arteries. The left circumflex artery further branches into the obtuse marginal arteries, which together with the LAD artery provide most blood flow to the left ventricle. The right coronary artery provides blood flow to the right ventricle and terminates as the posterior descending artery, providing blood flow to the inferior wall of the left ventricle (Fig. 30-2).

image

image FIGURE 30-2 Coronary arteries of the heart.

(Redrawn from University of Utah Health Sciences Center. 2002. Available at: healthcare.utah.edu/healthinfo/adult/cardiac/arteries.htm.)

The basic goal of CABG surgery is to provide new blood flow beyond significantly stenotic epicardial vessels. Stenosis is considered hemodynamically significant when the diameter is reduced by greater than 50%, which equates to a reduction in the cross-sectional area of 75% (Fig. 30-3). The technique of CABG surgery involves four stages: (1) conduit harvest, (2) institution of extracorporeal circulation, (3) construction of vascular anastomoses, and (4) separation from cardiopulmonary bypass. Most commonly used conduits for bypass grafts include the left internal mammary artery and greater saphenous vein. Other possible conduits include the right internal mammary artery, the radial artery, the right gastroepiploic artery, and the lesser saphenous vein. Generally, arterial conduits have better long-term patency than venous grafts.

image

image FIGURE 30-3 Relationship of coronary artery stenosis in diameter and cross-sectional area.

(From Brandt PW, Partridge JB, Wattie WJ. Coronary arteriography: a method of presentation of the arteriogram report and a scoring system. Clin Radiol 1977; 28:361.)

CABG surgery is performed with the use of cardiopulmonary bypass, which provides circulatory support and gas exchange during the operation. Anticoagulation with heparin is typically used during the period of cardiopulmonary bypass. To establish a still and bloodless field on which to sew the anastomoses, the heart is arrested using hyperkalemic cardioplegia solution. The basic cardiopulmonary bypass circuit is shown in Figure 30-4. When the heart is arrested, and epicardial arteries are exposed (Fig. 30-5), the vascular anastomoses may be constructed.

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image FIGURE 30-4 Basic cardiopulmonary bypass circuit.

(Redrawn from Mayo Clinic Cardiothoracic Grand Rounds, picture used in slide presentation, 2002.)

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image FIGURE 30-5 Common cannulation and myocardial protection techniques used for cardiopulmonary bypass.

(Redrawn from Roberts AJ. Efficacy of intraoperative myocardial protection in adult cardiac surgery. In Roberts AJ [ed]. Difficult Problems in Adult Cardiac Surgery. Chicago, Year Book Medical Publishers, 1985, p 386.)

The microvascular anastomoses are constructed using fine suture material, under loupe magnification, as shown in Figure 30-6. The left internal mammary artery is most commonly placed to the LAD artery as an in-situ graft (Fig. 30-7), whereas the greater saphenous vein is placed as a reversed graft from the ascending aorta to the coronary artery (Fig. 30-8).

image

image FIGURE 30-6 A-D, Technique of anastomosis of the left internal mammary artery to the left anterior descending coronary artery.

(Redrawn from Rankin JS, Morris JJ. Utilization of autologous arterial grafts for coronary artery bypass. In Sabiston D, Spencer F [eds]. Surgery of the Chest, 6th ed. Philadelphia, Saunders, 1996, p 1913.)

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image FIGURE 30-7 In-situ left internal mammary artery graft to left anterior descending coronary artery.

(Redrawn from Rhead J, Sundt TM. What is coronary artery bypass grafting? Society of Thoracic Surgeons, 2008. Available at: www.sts.org/sections/patientinformation/adultcardiacsurgery/cabg.)

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image FIGURE 30-8 Reversed aorto–saphenous vein graft to left anterior descending coronary artery.

(Redrawn from Rhead J, Sundt TM. What is coronary artery bypass grafting? Society of Thoracic Surgeons, 2008. Available at: www.sts.org/sections/patientinformation/adultcardiacsurgery/cabg.)

The final stage of the operation involves separation of the patient from cardiopulmonary bypass and obtaining hemostasis. Protamine is typically administered to reverse heparin anticoagulation.

Indications

Over the years, accepted indications for CABG surgery have changed slightly, primarily as a result of the advent of catheter-based revascularization techniques, especially coronary artery stenting. The American Heart Association (AHA) has published comprehensive guidelines regarding the indications for CABG.1 These recommendations generally are classified into one of eight subsets of patients as shown in Table 30-1. Class I or II indications for surgery include patients with stable or unstable angina and three-vessel disease (including the main branches of the right coronary artery, LAD artery, and left circumflex artery), patients with two-vessel disease with proximal LAD artery stenosis, or asymptomatic patients with significant left main stenosis. CABG surgery after acute myocardial infarction is indicated in these same conditions and is usually delayed for 1 week, if possible, to allow myocardial recovery before surgery. Emergent CABG surgery may be indicated for cardiogenic shock secondary to acute myocardial infarction in patients younger than 75 years (which can salvage 50% of patients) or for post–percutaneous intervention complications.

TABLE 30-1 American Heart Association Recommended Indications for Coronary Artery Bypass Graft (CABG) Surgery: Clinical Subsets of Patients

From Eagle KA, Guyton RA, Davidoff R, et al. ACC/AHA 2004 guideline update for coronary artery bypass surgery: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Update the 1999 Guidelines for Coronary Artery Bypass Graft Surgery. Circulation 2004; 110:e340-e437.

Outcomes and Complications

Overall hospital mortality after CABG surgery has declined over the past 20 years and presently is 2% to 3%, according to the STS surgical database. Most in-hospital deaths after CABG surgery are due to cardiac failure. Overall 5-year survival is greater than 90%, and overall 10-year survival is 70% to 80%. The frequent use of the left internal mammary artery has favorably affected short-term and long-term survival. For patients with preoperative angina, resolution of symptoms is approximately 60% at 10 years. Recurrent angina is typically due to progression of atherosclerotic disease of the native coronary arteries or vein grafts. The aggressive use of statin therapy and β blockers can delay the progression of coronary artery or vein graft disease after CABG surgery.2

The results of three randomized prospective studies comparing CABG surgery with medical management conclusively showed survival advantages with CABG surgery, particularly among patients with three-vessel disease, left main disease, and decreased left ventricular ejection fraction (35% to 50%).35 In diabetic patients with multivessel disease, CABG surgery has been shown to be superior to percutaneous coronary interventions. In the current era of drug-eluting stents, CABG surgery has been shown to have a reduced rate of reintervention, particularly in the setting of multivessel disease.

Potential early postoperative complications after CABG surgery include cardiac failure/low cardiac output syndrome, stroke, bleeding, renal failure requiring hemodialysis, pneumonia, mediastinitis/wound infection, pericardial tamponade, and atrial fibrillation. Atrial fibrillation is the most frequent complication after cardiac surgery, seen in 15% to 30% of patients. The incidence of this arrhythmia has decreased with the use of perioperative prophylaxis with agents such as amiodarone or β blockers. Possible late complications (>2 weeks postoperatively) include delayed pericardial or pleural effusion, late saphenous vein graft failure, and wound infection (sternal or saphenectomy site).

Imaging Findings

Preoperative Planning

With the advent of selective coronary angiography by Mason Sones in 1967, and the CASS study,4 the gold standard for assessment of coronary artery anatomy and disease was established. Several projections obtained using fluoroscopic guidance allow the surgeon to obtain a three-dimensional assessment of the coronary arteries (Table 30-3). Figure 30-9 shows several commonly used projections of coronary artery catheterization. Additionally, by injecting contrast material with the catheter positioned in the left ventricle, an image of the left ventricle throughout the cardiac cycle may be obtained to assess left ventricular function.

TABLE 30-3 Standard Projectional Views for Cardiac Catheterization

The high-resolution, 64-detector CT scanner has emerged as a tool for performing coronary angiography quickly and less invasively.6 Data quality is high, and has improved with increasingly sophisticated technology. Sensitivity and specificity of CT angiography have been shown to be comparable to conventional coronary angiography in detecting stenoses in symptomatic patients.7 Positive and negative predicted values also are comparable. Current limitations of CT angiography that reduce the reliability for image interpretation include heavy vessel wall calcifications, persistent irregular heart rhythm (and the need for heart rates <70 beats/min), and existing coronary stents.8 The estimated radiation dose used for CT angiography is also higher than the dose used for conventional angiography. MR angiography is another modality used to assess coronary artery anatomy, particularly in patients with coronary anomalies.

Preoperative echocardiogram is recommended to evaluate valvular competency and ventricular function. For patients with peripheral vascular disease who are at risk for perioperative stroke, a non–contrast-enhanced CT scan of the chest to rule out aortic atheroma and a carotid duplex image to rule out significant carotid artery stenosis are useful.

SURGERY FOR AORTIC VALVULAR DISEASE

Description and Special Anatomic Considerations

Although the number of coronary artery bypass procedures has gradually declined in current cardiovascular surgical practice in the United States, the number of valve procedures has steadily increased over the last 10 years. In the executive summary of the STS Spring 2007 Report, the number of isolated aortic valve replacements (AVRs) and tricuspid valve procedures showed the greatest increase since 1997.9

Aortic Valve Anatomy

Situated centrally at the base of the heart, the aortic valve resides in a unique position because of its proximity to all chambers of the heart and the three other cardiac valves (Fig. 30-10). The aortic valve is trileaflet, consisting of three semilunar cusps and the fibrous aortic annulus to which the cusps are attached. Sinuses of Valsalva are areas of aortic dilation adjacent to the aortic valve cusps, and are identified by the respective coronary artery origination as left, right, and noncoronary (Fig. 30-11). The commissures are structures where adjacent aortic cusps abut each other and have special anatomic significance during surgery. The commissure between the noncoronary and right coronary cusps is directly cephalad to the penetration of the atrioventricular bundle and membranous septum (see Fig. 30-11). The commissure between the noncoronary and left coronary cusps bisects the aortic-mitral curtain and the anterior leaflet of the mitral valve (see Fig. 30-11). This area is of particular significance during aortic root enlargement and in cases of aortic valve endocarditis as an avenue of spread for infection to the mitral valve. The last commissure between the left and right cusps defines the adjacent pulmonary valve and right ventricular outflow tract (see Figs. 30-10 and 30-11).

image

image FIGURE 30-10 Aortic valve position in base of the heart.

(Redrawn from Miljevic T, Sayeed MR, Stamou SC, et al. Pathophysiology of aortic valve disease. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 825-840.)

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image FIGURE 30-11 Aortic annulus.

(Redrawn from Miljevic T, Sayeed MR, Stamou SC, et al. Pathophysiology of aortic valve disease. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 825-840.)

The aortic valve operates via a passive mechanism of valve opening and closing that is driven by small differences in pressure between the ascending aorta and left ventricle. This mechanism is quite different from the mitral valve discussed later in this section.

Pathophysiology of Aortic Stenosis and Regurgitation

Acquired calcific aortic valvular stenosis is most commonly due to degeneration and calcification of the aortic valve leaflets; this disease primarily affects elderly patients. In contrast, significant aortic stenosis in younger patients is most commonly due to premature calcification and degeneration of a bicuspid aortic valve, and typically occurs in the fourth or fifth decade of life. In calcific aortic stenosis, the calcification and thickening of the aortic valve leaflets occurs through an active inflammatory process, partially related to hypercholesterolemia, similar to the process of coronary atherosclerosis.1013 As the leaflets calcify and fuse together, the functional area of the valve decreases to cause a measurable obstruction to outflow. The progressive pressure overload to the left ventricle results in maladaptive left ventricular hypertrophy, and eventually results in clinically significant obstruction.

In contrast to aortic stenosis, the causes of aortic valvular regurgitation are numerous and include pathology of the aortic annulus, aortic valve, ascending aorta, or a combination. Common causes of aortic regurgitation include ascending aortic aneurysm or dissection; annuloaortic ectasia; and abnormalities of the aortic valve, such as bicuspid aortic valve, calcific degeneration, rheumatic disease, infectious endocarditis, and myxomatous degeneration. In contrast to aortic stenosis, in which there is a pressure overload, aortic regurgitation is characterized by pressure and volume overload to the left ventricle. Maladaptive compensatory mechanisms include eccentric and concentric left ventricular hypertrophy to maintain forward flow.

Over time, changes include an increase in chamber compliance to accommodate the increased volume state, with an increase in left ventricular end-diastolic and end-systolic dimensions. Eventually, left ventricular systolic dysfunction develops with progressive chamber enlargement as the left ventricular chamber conforms to a more spherical geometry from the normal ellipsoid shape. This change results in a decrease in left ventricular myocardial contractility and correlates with the onset of symptoms of heart failure.13 This process is gradual and can take many years until the development of clinically relevant aortic regurgitation. In contrast to chronic aortic regurgitation, acute severe aortic regurgitation is less well tolerated. The sudden volume overload to the ventricle creates marked hemodynamic changes frequently resulting in pulmonary edema and cardiogenic shock unless the volume overload is corrected. Infective endocarditis of the aortic valve and ascending aortic dissection are two common causes of acute severe aortic regurgitation.

Aortic Valve Replacement

The technique of AVR is similar for aortic stenosis and aortic regurgitation. Implementations of cardiopulmonary bypass and cardioplegic arrest of the heart are important steps in the successful conduct of the operation. Because of the location of the aortic valve, it is crucial to avoid injury to related structures (see Figs. 30-10 and 30-11). In all AVRs, the concept of adequate myocardial protection must be ensured. This is particularly true in operations on the aortic valve because the ventricle is hypertrophic and susceptible to injury during surgery. Delivery of cardioplegia should include antegrade cardioplegia either into the aortic root (aortic stenosis) or directly into the coronary ostia in cases of aortic regurgitation and retrograde cardioplegia into the coronary sinus for balanced myocardial protection.

The ascending aorta is opened, and the aortic valve is inspected and excised carefully (Fig. 30-12). In cases of aortic stenosis, the annulus requires débridement of calcium to seat the prosthesis and prevent paravalvular regurgitation. The aortic annulus is sized for an appropriate-sized valve. Sutures (supported with pledgets on either the ventricular or aortic side) are placed around the aortic annulus and then passed through the sewing cuff of the prosthetic valve, which is then seated (Figs. 30-13 and 30-14). After seating the prosthesis, the aortotomy is closed, the heart is deaired, and the cross-clamp is released. After confirmation of satisfactory hemodynamics and adequate prosthesis function by intraoperative transesophageal echocardiography (TEE), the patient is separated from extracorporeal circulation, and anticoagulation is reversed.

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image FIGURE 30-12 Excised aortic valve and annular débridement.

(Redrawn from Desai ND, Christakis GT. Bioprosthetic aortic valve replacement: stented pericardial and porcine valves. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 857-894.)

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image FIGURE 30-13 Suture placement for seating prosthesis.

(Redrawn from Desai ND, Christakis GT. Bioprosthetic aortic valve replacement: stented pericardial and porcine valves. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 857-894.)

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image FIGURE 30-14 Seating prosthesis.

(Redrawn from Desai ND, Christakis GT. Bioprosthetic aortic valve replacement: stented pericardial and porcine valves. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 857-894.)

Indications

The evaluation and degree of severity of aortic stenosis can be estimated using echocardiography with Doppler measurements and cardiac catheterization, and can be graded based on several parameters (Table 30-4).13 Hemodynamically, but not clinically significant obstruction occurs when the valve area decreases from the normal 3 to 4 cm2 to less than 1.5 to 2 cm2. The classic symptoms of aortic stenosis are angina; syncope; and symptoms of congestive heart failure, such as dyspnea. When symptoms occur, survival is dismal, unless the valve is replaced. About 75% of patients with symptomatic aortic stenosis die within 3 years after the onset of symptoms unless the aortic valve is replaced.10,11 Current indications for AVR as defined by the American College of Cardiology (ACC) and AHA are listed in Table 30-5.13 Asymptomatic patients with severe aortic stenosis can be observed until symptoms develop.

TABLE 30-5 Indications for Aortic Valve Replacement for Aortic Stenosis (AS)

Indication Class of Evidence*
Symptomatic
Severe AS that is symptomatic I
Asymptomatic
Severe AS and undergoing coronary artery bypass graft surgery I
Severe AS and undergoing surgery of the aorta I
Severe AS and undergoing surgery for other heart valves I
Severe AS and left ventricular systolic dysfunction (ejection fraction <50%) I
Moderate AS and undergoing other heart surgery IIa

* Class I refers to conditions for which there is evidence or general agreement (or both) that the procedure or treatment is beneficial, useful, and effective. Class IIa refers to conditions for which there is conflicting evidence or a divergence of opinion (or both). Weight of evidence/opinion is in favor of usefulness or efficacy or both.

The severity of aortic regurgitation can be quantified by echocardiography or MRI as defined by Table 30-6. Operative therapy for chronic aortic regurgitation is controversial in asymptomatic patients. Because the natural history of severe asymptomatic aortic regurgitation is a gradual decline in ventricular function, patients require close follow-up to detect the onset of clinically evident heart failure. The rate of progression and the predictors of outcome are debatable and not well defined based on randomized trials. Observational data support surgery in asymptomatic patients with evidence of ventricular enlargement or decrease in ejection fraction. Extreme left ventricular dilation (left ventricular end-diastolic dimension >80 mm) may be a risk factor for sudden death.14 The use of vasodilators in delaying the rate of progression of aortic regurgitation is controversial. Afterload-reducing agents such as calcium channel blockers and angiotensin-converting enzyme inhibitors have been examined, and the results are equivocal.15 Similarly, the regulation of serum lipid levels to delay the progression of aortic stenosis has been studied with mixed results.16

Patients with aortic regurgitation and the presence of severe symptoms, categorized as New York Heart Association class III-IV, should have aortic valve surgery. The indications of AVR for aortic regurgitation are summarized in Table 30-7.13

TABLE 30-7 Indications for Aortic Valve Replacement in Severe Aortic Regurgitation (AR)

Indication Class of Evidence*
Symptomatic
Severe AR with NYHA class III-IV I
Asymptomatic
Severe AR and evidence of LV dysfunction (EF <50%) I
Severe AR and undergoing coronary bypass graft surgery I
Severe AR and undergoing other valve or aortic surgery I
Severe AR and normal EF and evidence of LV dilation (LVEDD >75 mm or LVESD >55 mm) IIa

EF, ejection fraction; LV, left ventricular; LVEDD, left ventricular end-diastolic dimension; LVESD, left ventricular end-systolic dimension; NYHA, New York Heart Association.

* Class I refers to conditions for which there is evidence or general agreement (or both) that the procedure or treatment is beneficial, useful, and effective. Class IIa refers to conditions for which there is conflicting evidence or a divergence of opinion (or both). Weight of evidence/opinion is in favor of usefulness or efficacy or both.

Contraindications

There is no effective medical therapy for severe aortic stenosis, and given the fatality of symptomatic aortic stenosis, there are no absolute contraindications for AVR. Three situations warrant special discussion when considering the risks of AVR. (1) AVR has been shown to be lifesaving in octogenarians or older individuals in the absence of major coexisting illnesses.17 Age by itself is not a contraindication. (2) Among patients with left ventricular dysfunction and substantial transvalvular gradients (mean >40 mm Hg), the result of surgery is excellent.13 Patients with a reduced ejection fraction and a low transvalvular gradient (mean <30 mm Hg) have high operative risk and reduced survival after surgery.18 Even these high-risk patients benefit from surgery, however, and such patients should be considered for operative therapy unless prohibitive risks are encountered. (3) Asymptomatic patients with severe aortic stenosis have an excellent prognosis without valve replacement; however, there is a risk of sudden death in 1% to 2% of asymptomatic patients. In addition, the onset of symptoms can be insidious and not clinically apparent. Exercise testing and echocardiography may help identify asymptomatic patients who may benefit from early valve surgery.

Otto and colleagues12 found patients whose transvalvular velocity exceeded 4 m/s had a 70% risk of becoming symptomatic and requiring AVR in 2 years. In patients with prohibitive risk of AVR, aortic balloon valvotomy has been used as a bridge to surgery in hemodynamically unstable adults with severe left ventricular dysfunction. The acute complication rate is greater than 10%, and restenosis is rapid in most patients. This form of therapy should be limited to centers with extensive experience in this procedure.13

There are no absolute contraindications for AVR in patients with aortic regurgitation. Among patients with prohibitive risk of death because of serious comorbid conditions, vasodilator therapy may be indicated.

Outcomes and Complications

To discuss the outcomes of AVR, we first briefly discuss the various types of prostheses because the prosthesis is one of the most important determinants of long-term results. Prosthetic aortic valves are divided into two major types: tissue and mechanical. A mechanical prosthesis requires lifelong anticoagulation to prevent thromboembolic complications and is associated with long-term bleeding risk, particularly in elderly patients. Structural valve degeneration does not occur with mechanical valves, and they can last the lifetime of the patient. The evolution of mechanical valves has progressed from the “ball in cage” valve (e.g., Starr-Edwards valve) through the tilting disk valve (e.g., Björk-Shiley valve) to the current design of a bileaflet valve (e.g., St. Jude valve) (Fig. 30-15). Bileaflet anatomy of the valve provides the best flow dynamics and the least trauma to red blood cells.

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image FIGURE 30-15 Mechanical bileaflet prosthetic aortic valve.

(St. Jude Regent valve courtesy of St. Jude Medical, Minneapolis, MN.)

In contrast to mechanical valves, a tissue prosthesis provides the surgeon a variety of choices. Tissue valves can be separated into three major classes based on tissue origin: autograft, allograft, and xenograft. Xenograft tissue prosthesis (bovine or porcine) can be divided further into stent supported (Fig. 30-16A) and unsupported (see Fig. 30-16B). Nonstented valves are supported by the native aortic root and provide better hemodynamics than stented valves.

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image FIGURE 30-16 A, Stented tissue prosthetic aortic valve. B, Unstented aortic valve (cadaver homograft).

(A, Carpentier-Edwards Perimount Magna valve courtesy of Edwards Lifesciences, Irvine, CA.)

The major advantage of a tissue prosthesis is that long-term anticoagulation is not required, decreasing the risk of bleeding complications and lifestyle modifications necessary for mechanical valves. Limitations of tissue valves include structural valve degeneration that may require replacement during the lifetime of the patient. The risk of replacement is greatest in patients younger than 60 years and patients with hypercalcemic conditions, such as renal dysfunction or hyperparathyroidism. Although there is no conclusive evidence that unstented prostheses offer a survival advantage to stented valves, there are clinical situations where an unstented valve provides advantages. In cases of aortic valve endocarditis complicated by an aortic root abscess, an unstented cadaver allograft (homograft) provides native tissue to reconstruct the aortic annulus and decreases the risk of reinfection of the prosthesis compared with other types of valves. A second situation includes a small aortic root, often seen in calcific aortic stenosis among elderly women. In this situation, an unstented valve may provide a larger orifice and superior flow dynamics than a stented valve. Last, the autograft aortic valve includes the transposition of the pulmonary valve to the aortic position and reconstruction of the pulmonary valve with an unstented valve (also known as Ross procedure).

A second important consideration to AVR outcome is the concept of patient-prosthesis mismatch as described in detail by Pibarot and Dumesnil.19 Patient-prosthesis mismatch is due to the inherent limitations in effective orifice area (EOA) obligatory in all stented tissue prostheses. To overcome this problem, much technology has been invested in designing stented tissue valves with larger EOA. Although it is unclear if a particular type of stented tissue valve offers an advantage compared with another, it is important to index the EOA to the patient’s body surface area (EOA index). Generally, a minimum EOA index greater than 0.75 is necessary, and an EOA index greater than 0.85 is optimal to prevent patient-prosthesis mismatch.19 Unless an adequate-sized valve is replaced at the aortic position, continued obstruction of left ventricular outflow can result in decreased functional improvement and progression of left ventricular hypertrophy with increased short-term and long-term mortality.19 To prevent the problems related to patient-prosthesis mismatch, two options are available: aortic root enlargement or placing an unstented tissue prosthesis. Aortic root enlargement usually allows the seating of a prosthesis one size larger and is required in 10% of patients undergoing AVR.17

The results of surgery for aortic stenosis are excellent compared with medical therapy (Fig. 30-17) with improvement in long-term survival. In the executive summary of the STS Spring 2007 Report, the unadjusted aortic valve operative mortality was 3% to 4% for the last 10 years.13 If CABG surgery is required in addition to AVR, the mortality is increased to 5% to 7%. If concomitant mitral valve surgery is required, the risk of death increases further to 7% to 11%.13

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image FIGURE 30-17 Survival comparison between surgical and medical therapy for symptomatic aortic stenosis.

(From Emery RW, Emery AM, Knutsen AI, et al. Aortic valve replacement with a mechanical cardiac valve prosthesis. In Cohn LH [ed]. Cardiac Surgery in the Adult. New York, McGraw-Hill, 2008, pp 841-856.)

Specific postoperative complications of AVR can be categorized as patient-related and valve-related. All patients are at risk of perioperative stroke, with the individual rates varying according to existing medical conditions and age. Increased risk is seen in patients with advanced age, diabetes, and peripheral vascular disease. Risks of injury to adjacent structures include myocardial infarction, ventricular septal defect, pulmonary and mitral valve injury, heart block with the need for a permanent pacemaker, and aortic disruption or dissection. Valve-related complications, which are similar between mechanical and tissue prostheses, include endocarditis, paravalvular leak, and hemolysis. Long-term issues include problems related to anticoagulation, patient-prosthesis mismatch, and structural valve degeneration if a tissue prosthesis was implanted.

Imaging Findings

Preoperative Planning

All patients older than 40 years should undergo selective left heart catheterization to exclude concomitant coronary artery disease that may require bypass grafting. Among patients with severe aortic stenosis and angina, the prevalence of coronary artery disease is 40% to 50%.13 In cases where noninvasive testing is equivocal to the severity of aortic stenosis, left heart catheterization can measure transvalvular pressure gradient and calculate the aortic valve area.

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