Aortic Valve Replacement
Aortic valve replacement remains the gold standard for the treatment of patients with significant aortic valve stenosis and regurgitation. Successful aortic valve replacement requires careful preoperative assessment of the patient and an intimate understating of the aortic root anatomy. The authors understand that the operative steps may vary among surgeons; however, certain core principals exist that will ensure an optimal outcome.
Keywords: aortic valve, aortic stenosis, valve replacement, Operations for Valvular Heart Disease
Step 1. Surgical Anatomy
· The aortic valve is the last valve in the heart through which the blood is pumped before it goes to the body. The purpose of the aortic valve is to prevent backflow of blood from the aorta into the left ventricle.
· The normal aortic valve is tricuspid, with left coronary, right coronary, and noncoronary leaflets. Each leaflet is supported by a fibrous skeleton with a shallow U-shaped configuration. The portion of this skeleton that supports the left coronary leaflet is continuous with the anterior leaflet of the mitral valve, forming the aortic-mitral curtain (annulus fibrosa).
· Each leaflet is attached just beneath their corresponding sinus of Valsalva. The sinuses of Valsalva are slight dilations of the aorta above the valve that act to create the vortex of blood required for valve closure. The sinuses end at the sinotubular junction, which is the narrowest portion of the ascending aorta.
· The left main coronary artery arises from the left sinus of Valsalva. Its ostium lies directly posterior, below the level of the sinotubular junction. The left main coronary artery runs to the left, beneath the pulmonary artery. The right coronary ostium is an anterior structure located above the right coronary cusp. Its location tends to be more variable than that of the left main coronary artery.
· The ventricular septum is located beneath the right coronary cusp and contains the atrioventricular conduction system, which passes below the noncoronary cusp near the right-noncoronary commissure (Fig. 9.1).
Step 2. Preoperative Considerations
· In the vast majority of adults, aortic valve replacement (AVR) is the only effective treatment for severe aortic stenosis (AS). Although there is some lack of agreement about the optimal timing of surgery, particularly in asymptomatic patients, it is possible to develop rational guidelines for most patients.
· In the absence of serious comorbid conditions, AVR is indicated in virtually all symptomatic patients with severe AS. There are many ways in which AVR benefits these patients. These depend partly on the patient’s left ventricular (LV) function. The outcome is similar in patients with normal LV function and in those with moderate ventricular dysfunction. The depressed ejection fraction in many of these patients is caused by excessive afterload, and LV function improves after AVR. If LV dysfunction is not caused by afterload mismatch, improvement in LV function and resolution of symptoms may not be complete after valve replacement,1 but survival is still improved in this setting.2
· Symptomatic patients with angina, dyspnea, or syncope exhibit symptomatic improvement and an increase in survival after AVR.1-6
· In patients who have severe AS, even those with a low transvalvular pressure gradient, AVR results in hemodynamic improvement and better overall patient functional status.
· In summary, symptomatic patients with severe AS should undergo AVR. These patients will have improved LV function, reduced or resolved symptoms, and increased survival.
· Many clinicians are reluctant to proceed with AVR in an asymptomatic patient, whereas others are concerned about conservative treatment of a patient with severe AS. Insertion of a prosthetic aortic valve is associated with low perioperative morbidity and mortality. Despite this, some difference of opinion persists among clinicians regarding the indications for corrective surgery in asymptomatic patients. Irreversible myocardial depression or fibrosis may develop during a prolonged asymptomatic stage, and this may preclude an optimal outcome.5,7 Still others attempt to identify patients who may be at especially high risk of sudden death without surgery, although evidence supporting this approach is limited. Patients in this subgroup include those who have an abnormal response to exercise (e.g., hypotension), those with LV systolic dysfunction, those with marked or excessive LV hypertrophy, and those with evidence of very severe AS.
· We recommend that asymptomatic patients with an aortic valve area of less than 0.8 cm2 undergo valve replacement. Similarly, any evidence of impaired LV function (e.g., decreased ejection fraction, LV dilation, or significantly elevated LV diastolic pressure at rest or with exercise) is an indication for AVR. In the absence of symptoms, a peak aortic gradient of 70 mm Hg may be an indication for surgery, but this is controversial.
· Patients with moderate or more AS (mean gradient of 20 mm Hg or higher), with or without symptoms, who are undergoing coronary artery bypass grafting should undergo AVR at the time of the revascularization procedure.
· Similarly, patients with moderate or more severe AS undergoing surgery on other valves (e.g., mitral valve repair) or the aortic root should also undergo AVR as part of the surgical procedure.
Indications for Aortic Valve Replacement in Aortic Regurgitation
· AVR is recommended for patients with severe regurgitation in the presence of symptoms or any evidence of pathologic LV remodeling (e.g., impairment of LV function, LV dilation, significant elevation of LV end-diastolic pressure).
· Symptomatic patients with advanced LV dysfunction (ejection fraction < 0.25 or end-systolic dimension > 60 mm) present difficult management issues. Some patients manifest meaningful recovery of LV function after operation, but many will have developed irreversible myocardial changes. The mortality rate associated with valve replacement approaches 10% in these patients, and the postoperative mortality rate over the subsequent few years is high.
· AVR should be considered more strongly for patients with New York Heart Association (NYHA) functional class II and III symptoms, especially if symptoms and evidence of LV dysfunction are of recent onset, and intensive short-term therapy with vasodilators, diuretics, or intravenous positive inotropic agents results in substantial improvement in hemodynamics or systolic function. However, even in patients with NYHA functional class IV symptoms and an ejection fraction less than 0.25, the high risks associated with AVR and subsequent medical management of LV dysfunction are usually a better alternative than the higher risks of long-term medical management alone.8
· AVR in asymptomatic patients remains a controversial topic, but it is generally agreed that valve replacement is indicated for patients with LV systolic dysfunction.8-14 As noted previously, for the purposes of these guidelines, LV systolic dysfunction is defined as an ejection fraction below normal at rest.
· Valve replacement is also recommended for patients with severe LV dilation (end-diastolic dimension > 75 mm or end-systolic dimension > 55 mm), even if the ejection fraction is normal. Most patients with this degree of dilation have already developed systolic dysfunction because of afterload mismatch and thus are candidates for valve replacement on the basis of the depressed ejection fraction. The elevated end-systolic dimension in this regard is often a surrogate for systolic dysfunction. The relatively small number of asymptomatic patients with preserved systolic function, despite severe increases in end-systolic and end-diastolic chamber size, should be considered for surgery because they appear to represent a high-risk group with an increased incidence of sudden death15,16; the results of valve replacement in these patients have thus far been excellent. In contrast, postoperative mortality is considerable once patients with severe LV dilation develop symptoms or LV systolic dysfunction.17
Step 3. Operative Steps
· Once the cardiac structures have been exposed, the patient is heparinized, and the distal ascending aorta and right atrial appendage are cannulated. If the aorta is heavily calcified, the surgeon may consider femoral or axillary cannulation and deep hypothermia with circulatory arrest without cross-clamping to avoid stroke. Transesophageal or epiaortic echocardiography can be useful if there is some uncertainty about the state of the aorta.18 A retrograde cardioplegia cannula is placed into the coronary sinus. Cardiopulmonary bypass is instituted, and a LV vent is placed through the right superior pulmonary vein. A cannula is placed in the mid ascending aorta for the delivery of cardioplegia into the aortic root and later de-airing. The aorta is cross-clamped, and the heart is arrested with antegrade and retrograde cardioplegia. Intermittent doses of cardioplegia are given throughout the procedure. In patients with significant aortic insufficiency, antegrade cardioplegia is often not effective, and arrest can be initiated with retrograde cardioplegia, followed by direct injection of cardioplegia into the coronary ostia.
· Access to the aortic valve can be through an oblique or a transverse aortotomy. The aortotomy is placed at least 1 cm above the sinotubular junction, above the right coronary ostium. This circumvents compromising or injuring the right coronary artery during closure of the aortotomy. The aortotomy can be extended to the noncoronary sinus of Valsalva for greater exposure (Fig. 9.2).
· Traction sutures can be placed at the sinotubular junction above the commissures. This provides maximum exposure of the annulus. The instillation of carbon dioxide into the operative field while the aorta is open may reduce intracardiac air when the cross-clamp is removed.
· With the aortic valve exposed, the leaflets are resected, and the annulus is débrided of calcium. The surgeon must leave a thin rim of valve tissue and not excise the annulus completely. Resection of the valve is initiated at the commissure between the right and noncoronary sinuses. The commissure is excised from the aortic wall, and the right coronary cusp is excised (Fig. 9.3). The commissure between the left and right coronary cusps is excised, and the left coronary cusp is removed. Resection is completed with excision of the noncoronary cusp, performed toward the commissure between the left and noncoronary cusps (Fig. 9.4). When calcification is encountered, careful débridement is required to avoid detaching the aorta from the ventricle. A rongeur can be used to crush the calcium into smaller pieces to facilitate removal. All debris must be accounted for; this will minimize the possibility of stroke and coronary ostial occlusion of embolization. Extensive and vigorous irrigation must be performed after valve excision. A small gauze cloth may be placed into the left ventricle to prevent calcified particulate matter from entering the cavity, especially if the valve is severely calcified. Retrograde cardioplegia is given during irrigation to prevent debris from entering the coronary ostia.
· The annulus is measured, and the appropriate-sized valve is selected for the replacement. If the annulus is too small, various aortic root enlargement techniques can be used (see Chapter 11).
· Several suturing techniques have been used, but the most common technique uses horizontal pledgeted sutures with pledgets on the aortic or ventricular aspect of the annulus, depending on the type of valve being inserted.
· We use an interrupted suture technique that affords maximum strength of the prosthetic attachment and has a low incidence of perivalvular leak. We place sutures from below the annulus, exiting slightly above it into the aorta. Double-needle, pledgeted 2-0 Dacron sutures are used, with little space between them. The sutures are alternating green and white to simplify identification of the suture pairs. The pledgets are placed below the annulus in the LV outflow tract. This secures the prosthesis by compressing the annulus between the sutures and prosthesis (Fig. 9.5).
· Sutures are placed in the right coronary annulus toward the commissure between the right and noncoronary sinuses. In a similar fashion, the left coronary annulus is sutured toward the noncoronary sinus. Finally, the noncoronary sutures are placed (Fig. 9.6). Deep sutures along the posterior annulus, under the left main artery, should be avoided, given that the left main artery runs for a short distance along the posterior aspect of the aorta. Deep sutures in the muscle below the right coronary leaflet may damage the conduction system—in particular the left bundle and bundle of His, and should once again be avoided (see Fig. 9.1).
· The sutures are then passed through the sewing ring of the prosthesis, which is tied down in the supraannular position (Fig. 9.7). Supraannular valves allow for a larger orifice area and tend to seat well in the annulus. We prefer to tie down the commissure sutures first, followed by the left, right, and noncoronary sinuses.
· The use of sutureless prosthetic heart valves, initially developed in the 1960s, has been abandoned, due to multiple complications, such as paravalvular leaks and valve-related thromboembolic events.19 The rapid development of transcatheter technology, however, has fueled a reemergence of the sutureless strategy in an effort to accelerate the surgical procedure and potentially reduce adverse outcomes.20 Depending on the manufacturer, these valves may be contraindicated in bicuspid aortic valves, along with irregular or heavily calcified valves.
· The implantation of sutureless valves varies in technique. As with traditional sutured valves, the leaflets must be excised. The degree to which the annulus is débrided depends on the particular valve that is chosen. From one to three guiding sutures are used to ensure proper orientation of the valve relative to the annulus.
· Valves are deployed by releasing self-expanding Nitinol stents or balloon inflation of the valve, once positioned in the native annulus. The inflow portion of the valves are wrapped in cloth or pericardial tissue to promote adaptation of the prosthesis to the native annulus and prevent paravalvular leaks.
· Once the prosthesis has been secured into place, the aortotomy is closed. Pledgeted, double- needle polypropylene sutures are placed at the lateral aspects of the aortotomy and tied down. A horizontal mattress stitch is used from the lateral aortotomy toward the middle. A second continuous stitch is placed as a second layer for the closure (Fig. 9.8). When a friable or thin aorta is encountered, consideration should be given to using felt strips for closure.
· After release of the cross-clamp, transesophageal echocardiography (TEE) is used to assess the position of the prosthesis and evaluate for the possibility of perivalvular leak. Intraventricular air volume can also be determined. If a significant quantity of air remains in the ventricle, this can be aspirated using a needle in the ventricular apex. Right atrial and right ventricular pacing wires are placed. After recovery of a suitable heart rhythm, the patient is weaned from cardiopulmonary bypass, and TEE is used to monitor ventricular function. Cannulae are removed, heparin is reversed with protamine, and the incision is closed.
Step 4. Postoperative Care
· The postoperative management for a patient having undergone AVR is routine and standard for most postcardiac surgical patients.
· However, several points should be addressed. A patient with AS has a hypertrophied left ventricle and thus will likely be very sensitive to the preload state. In addition, atrial fibrillation is often not well tolerated in patients with a stiff, hypertrophic left ventricle. Although a Swan-Ganz catheter may not always be required, it may help assess the degree of volume loading and should be considered in complex cases.
· Wide fluctuations in blood pressure are not uncommon. Any sudden increase in bleeding from the chest tubes or mediastinal tubes should alert the surgeon to the possibility of aortotomy suture line bleeding.
· In patients in whom a mechanical valve has been placed, warfarin is started on the first or second postoperative day. If the international normalized ratio (INR) has not increased by the fourth day, we recommend intravenous heparin until the patient has achieved a therapeutic INR. The pacing wires are removed when clinically appropriate and prior to achieving an INR higher than 2.
Step 5. Pearls and Pitfalls
· Solitary AVR is usually a straightforward procedure. However, attention to several points can improve the outcome. Because the aortic valve is often calcified, the surgeon should take care not to lose calcified debris in the ventricle or down the coronary arteries. A gauze pad can be placed in the ventricle during débridement to prevent embolization, and the ventricle should be copiously irrigated with cold saline after débridement. In addition, retrograde cardioplegia should be administered during irrigation.
· When implanting any prosthetic valve, the surgeon needs to ensure that the coronary arteries are not occluded by the sewing ring, pledgets, or sutures. In case of a regional wall motion abnormality after bypass, it may be necessary to rearrest the heart and inspect the coronary ostia or to bypass the vessel supplying the dysfunctional region.
· In the presence of a small aortic root, it is not advised to force a valve into the root. This may result in a paravalvular leak or, worse, aortic or ventricular disruption. This is especially true in older frail patients with a calcified annulus. If the surgeon is concerned with the possibility of a patient-prosthesis mismatch (predicted aortic valve area index < 0.8 cm2/m2), he or she should consider enlarging the aortic root annulus (see Chapter 11).
· TEE has become a standard part of the procedure. It allows the surgeon and anesthesiologist to assess the adequacy of replacement in terms of possible paravalvular leak, abnormal leaflet motion, or regional or global myocardial dysfunction. In our opinion, it should be used in every case of valve replacement or repair unless contraindicated.
1. Connolly HM, Oh JK, Orszulak TA, et al. Aortic valve replacement for aortic stenosis with severe left ventricular dysfunction: prognostic indicators. Circulation. 1997;95:2395–2400.
2. Smith N, McAnulty JH, Rahimtoola SH. Severe aortic stenosis with impaired left ventricular function and clinical heart failure: results of valve replacement. Circulation. 1978;58:255–264.
3. Schwartz F, Baumann P, Manthey J, et al. The effect of aortic valve replacement on survival. Circulation. 1982;66:1105–1110.
4. Murphy ES, Lawson RM, Starr A, Rahimtoola SH. Severe aortic stenosis in patients 60 years of age or older: left ventricular function and 10-year survival after valve replacement. Circulation. 1981;64:II184–II188.
5. Lund O. Preoperative risk evaluation and stratification of long-term survival after valve replacement for aortic stenosis: reasons for earlier operative intervention. Circulation. 1990;82:124–139.
6. Kouchoukos NT, Davila-Roman VG, Spray TL, et al. Replacement or the aortic root with a pulmonary autograft in children and young adults with aortic-valve disease. N Engl J Med. 1994;330:1–6.
7. Lund O, Larsen KE. Cardiac pathology after isolated valve replacement for aortic stenosis in relation to preoperative patient status: early and late autopsy findings. Scand J Thorac Cardiovasc Surg. 1989;23:263–270.
8. Bonow RO, Nikas D, Elefteriades JA. Valve replacement for regurgitant lesions of the aortic or mitral valve in advanced left ventricular dysfunction. Cardiol Clin. 1995;13:73–83.
9. Ross J Jr. Afterload mismatch in aortic and mitral valve disease: implications for surgical therapy. J Am Coll Cardiol. 1985;5:811–826.
10. Nishimura RA, McGoon MD, Schaff HV, Giuliani ER. Chronic aortic regurgitation: Indications for operation—1988. Mayo Clin Proc. 1988;63:270–280.
11. Bonow RO. Asymptomatic aortic regurgitation: indications for operation. J Card Surg. 1994;9:170–173.
12. Rahimtoola SH. Valve replacement should not be performed in all asymptomatic patients with severe aortic incompetence. J Thorac Cardiovasc Surg. 1980;79:163–172.
13. Carabello BA. The changing unnatural history of valvular regurgitation. Ann Thorac Surg. 1992;53:191–199.
14. Gaasch WH, Sundaram M, Meyer TE. Managing asymptomatic patients with chronic aortic regurgitation. Chest. 1997;111:1702–1709.
15. Turina J, Turina M, Rothlin M, Krayenbuehl HP. Improved late survival in patients with chronic aortic regurgitation by earlier operation. Circulation. 1984;70:I147–I152.
16. Bonow RO, Lakatos E, Maron BJ, Epstein SE. Serial long-term assessment of the natural history of asymptomatic patients with chronic aortic regurgitation and normal left ventricular systolic function. Circulation. 1991;84:1625–1635.
17. Klodas E, Enriquez-Sarano M, Tajik AJ, et al. Aortic regurgitation complicated by extreme left ventricular dilation: long-term outcome after surgical correction. J Am Coll Cardiol. 1996;27:670–677.
18. Byrne JG, Aranki SF, Cohn LH. Aortic valve operations under deep hypothermic circulatory arrest for the porcelain aorta: “no-touch” technique. Ann Thorac Surg. 1998;65:1313–1315.
19. Magovern GJ, Cromie HW. Sutureless prosthetic heart valves. J Thorac Cardiovasc Surg. 1963;46:726–736.
20. Carrell T, Englberger L, Stalder M. Recent developments for surgical aortic valve replacement: the concept of sutureless valve technology. http://rossscience.org/ARTICLE/OJCAR-4-1.php. p 2013.