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.
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.
References
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.
