Calcific aortic stenosis implies stenosis secondary to heavy dystrophic calcification of a congenitally abnormal valve ( Fig. 12.1 A and B). Calcification is rarely present before age 20; thereafter, it slowly progresses and results in important stenosis, most often in the fifth and sixth decades of life, earlier in unicommissural than bicuspid valves and earlier in men than women. The calcification presents as a bulky cauliflower-like mass within the cusps, maximal at sites of commissural fusion or congenital buttress formation, often extending into the anulus (left ventricular [LV]-aortic junction) and adjacent aorta. Retrograde extension of calcification into the region beneath the right noncoronary cusp commissure adjacent to the membranous septum may lead to complete heart block. The valvar orifice is slit-like, often eccentrically located and oriented in a sagittal (most often) or transverse plane, and fixed, which often results in trivial or mild aortic regurgitation. (For description of critical congenital aortic stenosis, see “ Morphology ” in Chapter 50 .)

Morphology of aortic valve stenosis. (A) Calcific aortic stenosis (congenital bicuspid valve). Valve is bicuspid due to fusion of one of the commissures. Calcification is bulky within the cusps. (B) Calcific aortic stenosis (congenital unicuspid valve). Valve has only one open commissure. Calcification is not severe in this example. (C) Rheumatic aortic stenosis. This morphology is characterized by diffuse fibrosis in leaflets of a tricuspid valve. Cusp edges are thick and rolled. Commissural fusion is variable but is severe in this example. Calcification is mild. (D) Degenerative aortic stenosis. Valve is tricuspid and without commissural fusion. Calcification occurs in diffuse nodular or eggshell deposits, which stiffen the valve and prevent opening. Calcification may involve sinuses of Valsalva or ascending aorta. Degenerative aortic stenosis usually occurs in patients over age 65.

Bicuspid aortic valve is the most common congenital heart anomaly, reported in 0.5% to 2% of the general population. ^, The valve has two cusps, most often of unequal size, the larger one containing a central raphe. The raphe results from commissural fusion (Sievers type 1). The most common pattern involves fusion of the right and left cusps and is associated with coarctation of the aorta. Rarely, the cusps are symmetric without residual commissure or raphe (Sievers type O). Even less common is a unicuspid valve with two raphes (Sievers type 2), usually with a well-developed commissure between the left and noncoronary sinuses.

Among patients with a bicuspid aortic valve, structural abnormalities exist at the cellular level independent of hemodynamic effects. The thoracic aorta typically shows reduced fibrillin-1, and increased matrix metalloproteinases are associated with smooth muscle cell detachment, matrix disruption, and cell death. The genetics of bicuspid aortic valve are complex and likely involve multiple pathways. Mutations in the signaling and transcriptional regulator NOTCH1 and in the ACTA2 gene (which encodes vascular smooth muscle cell B-actin) are linked with bicuspid aortic valve and familial thoracic aortic aneurysms. Numerous cardiac malformations are associated with bicuspid aortic valve and include coarctation, Shone syndrome, William syndrome, Turner syndrome, and hypoplastic left heart syndrome. ^, Abnormalities of the aorta (aortopathy) are the most frequent cardiac anomalies (with a male predominance of 3:1). Three phenotypes have been identified to which several classification monikers have been applied including “root,” “ascending,” and “extended” phenotypes. Although ascending aortic dilation is most common, aortic root and arch involvement are also frequent.

Controversy exists regarding the contribution of genetic mutations versus flow characteristics in the genesis of the aortopathy. Using magnetic resonance imaging (MRI), Hope and colleagues demonstrated two distinct flow patterns specific to the two most common cusp fusion types and related these to location of thinning and dilation of the ascending aorta. Asymmetric distribution of wall stress in patients with a bicuspid aortic valve (likely superimposed on genetically conferred aortic wall weakness) has been linked with asymmetric aortic smooth muscle cell apoptosis that could be flow-mediated.

Degenerative disease is often present in stenotic aortic valves of patients older than 65 years of age, and its prevalence increases with age. In a series of patients whose mean age was older than 70, prevalence of degenerative aortic valve stenosis exceeded 70%. The valve is tricuspid, without commissural fusion, and the cusps are held in a closed position by deposits of diffuse nodular or eggshell calcification ( Fig. 12.1 D). These deposits are not bulky and may also involve the sinuses of Valsalva and ascending aorta. Although degenerative (senile or senescent) aortic stenosis is presumed to be arteriosclerosis, Hoagland and colleagues found no correlation between aortic stenosis in adults over age 50 and systemic hypertension, elevated serum cholesterol, smoking, or diabetes. A more recent study of 5201 subjects older than 65 years, however, found that clinical factors associated with aortic sclerosis and stenosis are similar to risk factors for arteriosclerosis. Aortic valve sclerosis was present in 26% and aortic valve stenosis in 2% of the entire study cohort. In patients over 75 years of age, the prevalence of aortic sclerosis was 37%, and stenosis was 2.6%. Smoking increased the risk by 35% and hypertension by 20%. Other factors associated with increased risk of aortic valve disease were high lipoproteins, elevated low-density cholesterol levels, and diabetes mellitus. Older age was directly associated with risk, with a twofold increase in risk for each 10-year increase in age. Mitral anular calcification is common in elderly patients with calcific aortic stenosis. Presumably, both are degenerative in origin.

Rheumatic aortic stenosis is characterized primarily by diffuse, prominent fibrous cusp thickening of a tricuspid valve ( Fig. 12.1 C), with fusion to a variable extent of one or two commissures (rarely all three). The orifice is approximately central and irregular in shape. Calcification other than a mild form is rarely present except in elderly patients but is bulkiest at sites of commissural fusion. Rheumatic aortic stenosis is seldom, if ever, isolated, although this may appear to be the case at the patient’s first operation. In surgical series of apparently isolated aortic stenosis, prevalence of rheumatic etiology is low compared with that when patients with important mitral valve stenosis are included.

About half of patients with so-called rheumatic aortic stenosis fail to report a history of rheumatic fever, suggesting other unrecognized inflammatory processes as the cause. However, with the decline in incidence of rheumatic fever in the United States and other developed countries, rheumatic aortic stenosis decreased from a prevalence of 30% to 18% by the 1980s (and senile degenerative disease increased from 30% to 46%).

Basic anatomy of the aortic root is detailed in Chapter 1 . This section provides additional details about aortic root anatomy and relationships that are relevant to aortic root reconstruction and valve-sparing aortic root replacement (discussed later in this chapter). The aortic root is that part of the aorta bounded proximally by the bases of the aortic valve cusps and distally by the sinutubular junction. McAlpine conceptualizes a continuous membrane covering the ostium or opening of the left ventricle (called the aortoventricular membrane ) that contains the anulus of the mitral valve and the aortic anulus and adjacent fibrous components. The left anterior fibrous trigone is a membrane between the left and right cusps and the ostium of the left ventricle. The remaining structures related to the aortic root result from thickening of the aortoventricular membrane ( Fig. 12.2 ), and these are the right anterior fibrous trigone, the ventricular and atrial segments of the membranous septum, intervalvar trigone, right fibrous trigone, and fila coronaria (the portion of the aortoventricular membrane between the ostium of the left ventricle and the left atrial attachment, which comprises about 75% of the mitral anulus). The region where the aortic valve cusps are in fibrous continuity with the anterior leaflet of the mitral valve (aortomitral anulus) is thickened at each end to form a left and right fibrous trigone. The right fibrous trigone is in continuity with the membranous portion of the septum, and these two structures form the central fibrous body. The left anterior fibrous trigone, right anterior fibrous trigone, and intervalvar trigone are also termed intercusp triangles . The membranous septum is divided into the ventricular membranous septum and atrial membranous septum by attachment of the tricuspid valve septal leaflet to the aortoventricular membrane ( Fig. 12.3 ). Attachment of the right ventricle (RV) to the aortoventricular membrane is in close relationship to the left and right anterior fibrous trigones ( Fig. 12.4 ).

Structures attaching to or resulting from thickening of the ventriculoarterial membrane (subaortic curtain) as viewed from within the left ventricle looking up at the ventriculoarterial membrane. Lines of attachment of left atrium, right atrium, and right ventricle are indicated. Division of membranous septum into atrial membranous septum and ventricular membranous septum is by the tricuspid valve. Right anterior fibrous trigone, left anterior fibrous trigone, and intervalvar trigone are indicated. The fila coronaria are the portions of the atrioventricular membrane between the ostium of the left ventricle and the left atrial attachment. L, Left noncoronary sinus; LA, left atrium; N, noncoronary sinus; R, right noncoronary sinus; RA, right atrium; RV, right ventricle; TV, tricuspid valve.

(From McAlpine. )

Components of the ventriculoarterial membrane from within left ventricle, with aortic valve opened through the right aortic sinus. L, Left noncoronary sinus; LA, left atrium; LAF, left anterior fibrous trigone; LF, left fibrous trigone; N, noncoronary sinus; R, right noncoronary sinus; RA, right atrium; RV, right ventricle; TV, tricuspid valve.

(From McAlpine. )

Attachment of right ventricle and tricuspid valve anulus to the ventriculoarterial membrane. Right ventricular outflow tract has a very close relationship and fibrous attachment to the left anterior trigone (which is of particular importance to the operation of aortic valve–sparing root replacement). There is a further attachment of the posterolateral wall of the right ventricle together with the septal leaflet of the tricuspid valve to the ventriculoarterial membrane. The dashed line indicates demarcation between right and left ventricles.

(From McAlpine. )

The aortic root forms the outflow tract from the left ventricle and contains the aortic valve cusps, sinuses of Valsalva, and intercusp triangles (trigones). Morphology of the aortic valve cusps reflects their exposure to the mechanical stress of diastolic pressure. They have three distinct layers. The outflow surface is the fibrosa , comprising bundles and sheets of collagen aligned in the circumferential direction. The cusp has a coaptional portion (where the collagen bundles are discontinuous) and a noncoaptional surface or cusp belly (where the collagen bundles are continuous). The ventricular surface of the cusp is composed of the ventricularis , which is another fibrous layer. It is a mixture of both collagen and elastin (although the elastin is not as important as the collagen from a biomechanical standpoint). The fibers are arranged randomly, and therefore, when the ventricularis is under load, the fibers realign in the direction of the applied load and only then resist further extension. The spongiosa layer between the fibrosa and ventricularis is composed principally of glycosaminoglycans, which are responsible for energy dissipation and lubrication of the movements between fibrosa and ventricularis. The biomechanical properties of the fibrosa and ventricularis allow radial extension of the cusp to form a large coaptional area.

The sinuses of Valsalva are the bulging portions of the aortic root from which the coronary arteries arise. They accommodate the open cusps of the aortic valve and generate vortices that are important for aortic cusp closure. The base of the aortic cusp attachment forms a coronet-like structure ( Fig. 12.5 ). The tissue between the attachment of the aortic valve cusps to the aortic wall is the intercusp triangle , a layer composed of circularly oriented collagen fibers. The base of two of the intercusp triangles is LV muscle, and the intercusp triangle beneath the commissure of the left and right cusps is fibrous (left anterior fibrous trigone). Attachment of the base of the aortic root is approximately 55% fibrous and 45% muscular. The intercusp triangles are exposed to ventricular hemodynamics and may function, in part, to allow each sinus to act independently. An important surgical point regarding the ventricular-aortic junction is the site of attachment of prosthetic valves, which are largely circular structures. Prosthetic valves are actually attached to the anatomic ventricular-aortic junction and do not follow the cusp attachment, although this is usually regarded as the “anulus.”

Diagram of the aortic root. Inset, Note coronet-like arrangement of valvar attachments.

(From Sutton. )

A spectrum of aortic pathology may result in aortic regurgitation due to alterations in the geometry of the sinutubular junction, sinuses, and the ventricular-aortic junction. Ascending aortic aneurysms and aortic root disease may be distinct processes, or they may coexist as a blending of morphologic manifestations.

Many different pathologies may result in ascending aortic aneurysms (see Chapter 23 ). These include long-standing hypertension, arteriosclerosis, aneurysms associated with bicuspid aortic valves, and extreme forms of poststenotic dilation of a stenotic aortic valve. Ascending aortic aneurysms may also result from inflammatory processes causing aortitis, including rheumatoid arthritis, ankylosing spondylitis, and Reiter syndrome. Ascending aortic aneurysms and aortic root disease may arise from clearly defined genetic syndromes, including Marfan syndrome, Loeys-Dietz syndrome, Ehlers-Danlos syndrome, and filamin A mutations. Most patients with thoracic aorta disease and aortic dissections do not have a clearly defined genetic disorder, but many have an inherited predisposition to the process.

Marfan syndrome , one of the most common connective tissue disorders, is an autosomal dominant condition affecting about 1 in 3000 to 5000 people. Most patients with the typical Marfan phenotype have mutations involving the FBN1 gene that codes for fibrillin-1, an extracellular matrix glycoprotein that contributes to structural integrity of connective tissue. In a minority of cases, an FBN1 mutation is not found. Fibrillin-1 is an important component of both elastic and nonelastic connective tissue. In about 10% of Marfan phenotypes, mutations have been noted in transforming growth factor (TGF)-β receptor genes. The commonly accepted criteria for diagnosis of Marfan syndrome involving genetic studies, family history, and major and minor clinical manifestations have been codified as the Ghent Criteria. These features include presence of both aortic root aneurysm and ectopia lentis, the presence of one of these with a bona fide FBN1 mutation, or a combination of major and minor clinical features or family history. Histologic features of the ascending aorta media in Marfan patients include fragmentation of elastic lamellae, loss of smooth muscle cells, fibrosis, and cystic medial necrosis (a misleading term coined to describe the lacunar appearance of medial degeneration when, in fact, cystic changes and necrosis are absent).

Other connective tissue disorders that predispose to aortic aneurysmal disease and dissection include Loeys-Dietz syndrome and the vascular type of Ehlers-Danlos syndrome. Loeys-Dietz syndrome is an autosomal dominant aortic syndrome resulting from mutations in genes for the cytokine (TGF)-β receptor (TGFBR) type I or II. Arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate characterize the disease phenotype. Skeletal features are similar to those of Marfan syndrome. The aortic disease in this syndrome is particularly aggressive, and 98% of patients develop aortic root aneurysms that have a high propensity for dissection. ^, Mean age of death with this syndrome is 26 years. In children affected with Loeys-Dietz syndrome, prominent craniofacial features are associated with more severe aortic disease. Because these patients are prone to aneurysm development in other locations, yearly MRI or computed tomography (CT) is advisable from the pelvis to the brain.

The vascular form (type IV) of Ehlers-Danlos syndrome is a rare autosomal dominant disease caused by a defect in type III collagen, encoded by the COL3A1 gene. Prominent clinical features include easy bruising, thin skin, characteristic facial features, and tendency for rupture of arteries, uterus, or intestines. The role of prophylactic aortic replacement surgery to prevent aortic rupture or dissection is less clear than for Marfan or Loeys-Dietz syndromes. Of importance, these patients typically have extreme tissue fragility, so if aortic aneurysms or aortic regurgitation require cardiac surgery, reinforcement of suture lines with felt pledgets or strips is recommended.

Anuloaortic ectasia is a term that has largely fallen out of use but refers to anular dilation resulting in aortic regurgitation even though the cusps are normal. It is frequently associated with aortic dilation, which may be secondary to medial degeneration and may be associated with Marfan syndrome. Even in the absence of Marfan syndrome, anuloaortic ectasia appears to be a genetic disease. It may be associated with dilation of the aortic wall at the sinutubular junction separating the commissures, preventing coaptation of the free edges of the leaflets during diastole. As the dilation of the aorta progresses, so does central aortic valve regurgitation. The LV-aortic junction usually does not increase in size, even in patients with large aneurysms. Accordingly, the size of the aortic valve prosthesis used in these patients (if indicated) is generally similar to that used for replacement in patients with rheumatic or other disease.

The aneurysmal process may involve the entire ascending aorta, often ending just before the level at which the brachiocephalic artery originates, although the remainder of the arch may show cystic medial degeneration. The aneurysms are thin-walled with a smooth lining. Dissection may begin within the aneurysms, extending proximally and distally or rarely remaining localized. In patients with Marfan syndrome, dissection may be limited to the ascending aorta in about half the patients and extends into the transverse and descending aorta in the remainder. Frequently, dissection is unexpectedly found at operation. With proximal extension of this dissection, the commissural attachment of the valve becomes separated from the outer aortic wall such that the valve prolapses centrally, and regurgitation may abruptly increase (see Chapter 23 ).

As previously noted, ascending aortic aneurysms also produce valvar regurgitation because of distraction of the commissures, preventing coaptation of the free edges of the cusps. In syphilitic ascending aortic aneurysm, aortic regurgitation is exacerbated by valvulitis that produces thickening and retraction of the cusp edge.

In some patients with rheumatoid arthritis, ankylosing spondylitis, or Reiter disease, an aortitis may lead to aneurysmal dilation of the ascending aorta and aortic valvar regurgitation. The aortitis is characterized by dense adventitial inflammatory fibrosis involving the sinuses of Valsalva and proximal aorta, especially adjacent to the commissures. The process may extend below the base of the aortic valve to form a characteristic subvalvar ridge and may involve the base of the anterior mitral leaflet or even the adjacent ventricular septum, causing conduction disturbances. Particularly in rheumatoid arthritis, the cusps may be thickened and shortened and show rheumatoid nodules histologically.

Rheumatic aortic regurgitation results from a different response of the valve to the rheumatic process than occurs when stenosis develops. Commissural fusion is minimal or absent, and the cusps are only slightly thickened. Minor calcification is present in about 10% of affected valves. The major pathologic process is cicatricial shortening of the cusps between their free edge and their anular attachment, with rolling of the free edge. As time passes, the aortic root widens in response to the regurgitation, further increasing central valvar regurgitation.

Native valve endocarditis (see also Chapter 14 ), which may occur on structurally normal, congenitally, or rheumatically deformed valves, is a common cause of aortic regurgitation. The regurgitation may result from a destroyed commissure and consequent cusp prolapse or a perforation in the belly of the cusp. An infected pannus may appear below the cusps, or extensive destruction of the aortic root may occur, with a periaortic root abscess sometimes extending into the mitral anulus and anterior mitral leaflet. Mitral regurgitation may also develop because of perforation of the anterior leaflet by a “drop lesion” caused by the infected regurgitant stream from the diseased aortic valve.

A congenitally bicuspid or unicuspid valve can produce regurgitation from prolapse of the free edge of a redundant cusp. In such patients, the regurgitation may be aggravated by infective endocarditis or an improper valvotomy (see Chapter 50 ). Lack of support of the aortic anulus in association with ventricular septal defect may result in aortic valve prolapse and regurgitation.

Occasionally, aortic regurgitation may be caused by prolapse of redundant aortic cusps that are mildly thickened and myxomatous. The aortic root may be normal or dilated, usually with cystic medial necrosis, and mitral valve prolapse may also occur. ^,

A number of physician-related interventions may cause aortic valve regurgitation. Perforation of the aortic valve cusps may result from diagnostic or balloon dilation catheters or from mechanical circulatory support devices that require positioning across the aortic valve. Even with newer methods and lower doses of mediastinal irradiation, occasional cases of mediastinal fibrosis occur, with injury to the pericardium, cardiac valves, coronary arteries, and myocardium. Cardiac valve disease has also been associated with migraine medications (ergotamine, methysergide) and appetite suppressants (fenfluramine, with or without phentermine) ( Fig. 12.6 ).

Iatrogenic aortic valve disease. Aortic valve regurgitation caused by physician intervention. (A) Aortic valve affected by fenfluramine/phentermine (Fen/Phen). One cusp is contracted due to a fibrotic plaque. The other two cusps are normal. (B) Echocardiogram of Fen/Phen iatrogenic aortic valve disease. A regurgitant jet indicates moderately severe aortic valve regurgitation before repair. Repair consisted of débridement of fibrotic plaques from the valve cusps and narrowing of the sinutubular junction by a prosthetic band. After repair, there is trivial aortic valve regurgitation.

Other causes of aortic valve regurgitation include spontaneous rupture of the residual cord above a fenestration or rupture caused by severe closed-chest trauma (see Chapter 16 ). ^, In patients with long-standing hypertension, regurgitation may result from typical myxoid degeneration of the valve. Some instances of regurgitation are probably related to arthropathies with minimal joint involvement or to hypertension, psoriasis, giant cell aortitis, or Takayasu disease. Occasionally, the etiology of regurgitation is not apparent.

Grant reported that 35% of unoperated patients with usual symptoms of aortic stenosis are alive at 10 years. Wood stated that 46% of such patients were alive 1 to 7 years later. Frank and Ross reported that of 12 unoperated patients with severe aortic stenosis, only 18% were alive 5 years later. Based on their data, Ross and Braunwald concluded that average survival after onset of angina or syncope is 3 years and after onset of heart failure about 1.5 years. ACC/AHA guidelines suggest that after onset of symptoms, average survival is less than 2 to 3 years, with a high risk of sudden death. ^, Thus, development of symptoms identifies a critical point in the natural history of aortic stenosis. Once a patient crosses the threshold from asymptomatic to symptomatic state, the risk of mortality promptly increases. O’Keefe and colleagues followed 50 symptomatic patients with severe aortic stenosis in whom operation was declined or deferred. Average age of these patients was 77 (60-89) years. Survival was 55%, 37%, and 25% at 1, 2, and 3 years, respectively, compared with a matched general population of 93%, 85%, and 77%. Death was from cardiac causes in all cases except one. Of 179 patients aged 83 ± 8.3 years deemed inoperable in the PARTNER IB cohort, 1-year survival was 49%.

Although it is impossible to rigorously assemble such disparate data, a likely survival curve for adult patients with severe, unoperated aortic stenosis is estimated in Fig. 12.8 . Deaths within the first 1 or 2 years are likely to be sudden, presumably associated with ventricular fibrillation (15%–20% of all deaths in aortic stenosis are sudden ) or, after a few hours or days of acute pulmonary edema, from sudden LV failure. Most unoperated patients die in the latter mode within about 5 years of diagnosis. Beyond 5 years of follow-up, some die of gradually worsening cardiac failure, with low cardiac output and gradually worsening symptoms of pulmonary venous hypertension. Moderate pulmonary artery hypertension develops in some patients who exhibit these findings; in a few, typical symptoms and signs of RV failure become prominent.

Nonrigorously derived survival curves for patients with surgically untreated severe aortic stenosis (solid line) and severe aortic regurgitation (dashed line) . Time zero is the time of developing an important hemodynamic effect. Survival of patients with aortic stenosis reported by Wood, Frank and Ross, and Grant is shown by filled circles .

Asymptomatic patients with severe aortic stenosis usually develop symptoms within a few years of diagnosis. Otto and colleagues showed that about one-fourth of initially asymptomatic patients with aortic valve stenosis had developed symptoms, half by 3 years, and three-fourths by 4 years. When the Doppler outflow velocities were initially 4.0 m · s ⁻¹ or greater, progression was more rapid, with three-fourths of patients symptomatic by 2 years. Thus, even in initially asymptomatic patients with aortic stenosis, progression to symptoms may be rapid, and patients should be monitored closely for progressive disease. Sudden death is uncommon in asymptomatic patients with aortic stenosis, occurring in less than 1% per year. ^, However, as noted by Freed and colleagues, failure to identify subtle symptoms of severe aortic stenosis is common, and the subsequent mortality without surgery may exceed 10% in the ensuing 1 to 1.5 years.

The left ventricle hypertrophies progressively in the presence of important aortic stenosis, which usually develops over decades. The increase in wall thickness is usually enough to counter the high intraventricular systolic pressure and maintain normal ventricular volume. ^, In this circumstance, LV wall stress (afterload) remains within normal range, and EF remains preserved (given the inverse relationship between systolic wall stress and EF). However, when the hypertrophic response is not adequate for progressively higher intracavitary pressures, the increased afterload can cause a decrease in EF, which is generally reversible with valve replacement. ^,

Myocardial hypertrophy in aortic valve stenosis is caused by new myofibrils added in parallel to myocytes. No new myocytes are added, but existing myocytes become thicker, not longer, compared with normal myocytes. The hypertrophy of myocardial cells (increased myocardial cell diameter) is a determinant of both increased systolic load stress and decreased LV diastolic function found in aortic stenosis, and is also related to reduction in EF. Myocardial fibrosis exerts little effect.

Schwartz and colleagues found good systolic function and only hypertrophic myocardial cells when LV mass was less than 200 g · m ⁻² . ^, When it was 200 to 300 g · m ⁻² , degenerative changes were present but mild. When LV mass was greater than 300 g · m ⁻² , systolic function was greatly depressed, and multiple degenerative changes in ultrastructure were present (mitochondrial changes, disruption of sarcomeric units, nonoriented growth of fiber components, disappearance of organelles). Maron and colleagues also described these degenerative changes in detail. Krayenbuehl and colleagues found degenerative changes in the form of increased interstitial nonmuscular tissue in association with myocardial cellular hypertrophy. These changes are probably the morphologic basis for loss of inotropic (contractile) strength and irreversibility.

Thus, during the compensated phase, thickening of the LV wall keeps LV afterload (systolic wall stress) more or less normal, preserving LV systolic function. LV compliance and diastolic function are gradually impaired, to a degree primarily related to extent of LV hypertrophy. At a more advanced stage, hypertrophy and wall thickness may increase less than LV systolic pressure (afterload mismatch ); the resulting increase in afterload impairs LV systolic function. The degree of LV hypertrophy and decrease in contractility that ultimately develop are more often the cause of declining cardiac function. As indices of systolic function (EF, end-systolic volume, LV fractional shortening, velocity of circumferential shortening) decline, cardiac output decreases gradually or acutely, and LV diastolic function decreases with a consequent increase in LV end-diastolic pressure. By this time the condition is advanced, and chronic heart failure is present.

The atrial contribution to ventricular filling is of great importance with a thickened, noncompliant ventricle. As long as sinus rhythm is maintained, left atrial and pulmonary venous pressure can remain near normal. However, loss of atrial contraction with the onset of atrial fibrillation can induce rapid clinical decompensation.

The hypertrophied ventricle may have reduced coronary perfusion per gram of muscle with diminished coronary vasodilator reserve. Added myocardial oxygen demands with exercise or tachycardia may induce subendocardial ischemia and angina in the absence of coronary artery disease. ^,

Occasionally, complete heart block develops in patients with extensive calcification of the stenotic aortic valve. It may be the result of gradually increasing pressure on the bundle of His by calcific deposits beneath the commissural area between the noncoronary and right coronary cusps. However, complete heart block sometimes occurs without calcific pressure on the bundle of His. Pressure in the left ventricle is hypothesized to play a role. Rarely, relief of aortic stenosis relieves the heart block.

Even when aortic regurgitation becomes severe, there may be a long latent period (3-10 years), during which LV enlargement is only mild, symptoms are absent or mild, and the prognosis is good as long as the findings remain unchanged. Bonow and colleagues followed patients with chronic aortic regurgitation and normal EF. They found that 81% were alive and without need of aortic valve replacement 5 years later. Less than 6% per year required aortic valve replacement because of symptoms or LV dysfunction at rest, less than 3.5% per year developed asymptomatic LV systolic dysfunction, and less than 0.2% per year died suddenly. Vasodilator therapy using nifedipine may benefit such patients and delay surgical intervention. When important symptoms develop, however, prognosis becomes severely limited (see Fig. 12.8 ).

The probability of death increases with development of specific risk factors. Symptoms of cardiac failure, development of ventricular premature beats, marked cardiomegaly (cardiothoracic ratio >0.6), and ECG evidence of severe LV hypertrophy all increased the risk of death in a group of 180 surgically untreated patients with isolated severe aortic regurgitation of rheumatic etiology. When severe aortic regurgitation develops acutely, as from infective endocarditis, the natural history is much less favorable. Only 10% to 30% survive more than 1 year after onset. ^{, ,}

Cardiac size gradually increases in the presence of important aortic regurgitation. Quantitative angiography has shown that increased LV end-diastolic volume is directly related to the magnitude of aortic regurgitant flow.

Bonow and colleagues found a higher-risk subgroup within asymptomatic patients with normal LV systolic function. Progressive enlargement (dilation) of the left ventricle or reduction in resting EF identified by serial echocardiography heralds onset of symptoms. Patients at risk for sudden death are those with extreme LV dilation or an LV cavity dimension of 75 mm or more at end-diastole and 55 mm or more at end-systole (normal values are ≤55 mm and ≤35 mm, respectively). As LV size and end-diastolic volume steadily increase, eventually, there is loss of LV reserve, and LV end-diastolic pressure then rises rapidly.

As the left ventricle enlarges, LV hypertrophy begins to develop. In addition, the left ventricle undergoes an increase in mass and wall thickness, and its shape and ultrastructure change. The myocardial cell hypertrophy and increase in interstitial nonmuscular tissue found in the pressure-overloaded left ventricle of aortic stenosis are similar in the volume-overloaded left ventricle of aortic regurgitation. Concomitant with hypertrophy, LV compliance decreases, compromising diastolic function. Finally, LV end-diastolic and left atrial pressures become elevated, with further increases during exercise.

At some point, LV stroke work fails to respond to increased wall stress (e.g., afterload increase by infusion of angiotensin). As LV systolic function decreases, LV end-systolic dimension steadily increases, and even in asymptomatic patients, the rate of increase is about 7 mm per year.

Despite these changes and because of the complex interaction between aortic regurgitation and decreasing systemic vascular resistance, left ventricular ejection fraction (LVEF) response to exercise is favorable for a considerable time. Eventually, however, it declines, and systolic function may even decrease during stress. Symptoms then worsen, and the decline in LV function accelerates.

After the usual preparations and median sternotomy, cardiopulmonary bypass (CPB) is established at 28°C to 34°C as per surgeon preference using a single two-stage venous cannula. A cardioplegia infusion catheter is positioned in the ascending aorta, and a coronary sinus perfusion catheter may be passed through a purse-string stitch in the right atrium and positioned in the coronary sinus if there is aortic regurgitation. One arm of a multi-arm assembly on the cardioplegic infusion tubing may be connected to the antegrade cannula in the ascending aorta and another to the coronary sinus retrograde perfusion catheter with other arms fitted to ostial cannulae to be used for direct cardioplegic infusion into the coronary ostia (see “Technique of Retrograde Infusion” in Chapter 3 ).

If cooling below 32°C, the heart may fibrillate, in which case the ascending aorta should be promptly occluded if aortic regurgitation is significant to prevent LV distention. The operation may be performed with or without an LV vent introduced through the right superior pulmonary vein. If the vent catheter is introduced before aortic occlusion, one must fill the heart so that there is positive pressure in the left atrium to prevent air entry. Following aortic clamping, antegrade cold blood cardioplegia may be infused into the aortic root if no significant aortic regurgitation exists. Even the slightest leak at the aortic valve will cause ventricular filling, although a properly functioning LV vent may prevent ventricular distention. Cold cardioplegia may be infused retrograde into the coronary sinus to achieve electromechanical arrest when there is significant aortic regurgitation. Cardioplegic arrest may be accomplished by exclusive perfusion of the coronary sinus, although right ventricular protection may not be optimal. The aortic root may be vented when coronary sinus perfusion is performed. Alternatively, in the presence of aortic regurgitation, topical and systemic cooling of the vented left ventricle may intentionally induce ventricular fibrillation, after which the aorta is promptly clamped, an aortotomy made, and direct coronary artery cardioplegia administered.

Once CPB has been initiated, the plane between the aorta and pulmonary artery is dissected to optimize visualization of the aorta and aortic valve and to facilitate closure of the aortotomy. An important technical step is to identify the surface anatomy of the right coronary artery as it originates from the right sinus of Valsalva. An initial aortotomy is made about 15 mm distal from the origin of the right coronary artery. Its precise location is important not only for surgical exposure but also because of space for intraaortic positioning of an allograft, autograft, or prosthetic valve; ease and security of closure; avoiding damage to the right coronary artery or its ostium; and facilitating aortic root enlargement if necessary. Exposure for this incision is facilitated by the first assistant’s retraction of the fat pad along the right atrioventricular groove over the aortic root. The pulmonary trunk may also need to be partially dissected from the aorta to avoid incising it. The initial incision is made directly anteriorly with scissors, facilitated by the collapsed state of the aorta. Once this small incision is made, the inside of the aortic root is visualized, and a decision made as to whether an allograft valve, a pulmonary autograft valve, or a prosthesis will be used or repair performed (see “Nonreplacement Aortic Valve Operations in Adults” under Special Situations and Controversies later in this chapter).

The incision is extended. The surgeon has a choice depending on the operation to be performed:

• •

  Extend the incision transversely ( Fig. 12.9 A). This has the advantage of providing good exposure of the aortic root without distorting it. The sinutubular junction is not disturbed. Exposure at the level of the aortic valve and below into the left ventricular outflow tract (LVOT) is usually very good.

  

  Initial steps for aortic valve replacement. (A) Initial transverse incision into ascending aorta (dashed line) is 15 mm above right coronary artery. Lengthened just a little, it suffices for evaluating the aortic valve and deciding on procedure to be used. Lengthened further, it is sufficient for aortic valve replacement. (B) Incision is extended into middle of noncoronary sinus of Valsalva, providing excellent exposure of aortic valve for its replacement with prosthetic device. (C) Transverse incision may be extended to divide aorta above sinutubular junction. This permits working within the intact aortic root for correct positioning of aortic valve allografts or stentless xenografts below the coronary arteries (subcoronary technique).

  

  

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  Extend the incision into the posterior commissure between the left and noncoronary cusps if posterior enlargement (Manougian procedure) of the aortic root is required.

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  Extend the incision obliquely ( Fig. 12.9 B) into the noncoronary sinus to a point near the aortic anulus to provide maximal exposure at the level of the aortic valve and below into the LVOT. This incision, which divides the sinutubular junction, can be extended into the anterior leaflet of the mitral valve for posterior aortic root enlargement (Nicks procedure).

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  Extend the incision to divide the aorta completely ( Fig. 12.9 C). This incision provides optimal exposure of the aortic root because the proximal aortic structures can be easily moved and displaced inferiorly and anteriorly so that the surgeon may visualize the intact aortic root and look directly into it. This incision is best for placing aortic allografts and stentless porcine bioprostheses inside the aortic root, as well as for aortic valve replacement with a pulmonary autograft or other procedures requiring replacement of the complete aortic root. It also provides excellent exposure for routine prosthetic valve implantation.

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  Traction stitches are placed just above the aortic valve commissures for optimal exposure of the aortic root structures, regardless of type of incision.

The aortic valve is removed ( Fig. 12.10 A). Unless the aortic valve disease is noncalcific, a short strip of narrow packing gauze can be inserted through the valve orifice into the left ventricle (and some foolproof system is used to ensure its removal) to trap all calcific fragments that may escape during valvectomy. Neat, complete removal of the valve, particularly when heavily calcified, without damage to the LV-aortic junction, ventricular septum, or aortic wall, is one of the operation’s critical aspects. Usually, an area exists in about the midportion of the right coronary cusp where an initial scissors cut can be made from the free edge to the point of cusp attachment. This incision allows entry of a knife blade to incise precisely along the attachment of the right coronary cusp toward the commissure between left and right coronary cusps. This commissure may also be calcified, but the incision can usually be carried between it and the aortic wall, often with scissors. The incision is then carried along the attachment of the left coronary cusp, stopping at a point about two-thirds of the distance to the left coronary–noncoronary cusp commissure because, beyond that point, there is a tendency to carry the incision into the aortic wall or LV-aortic junction.

Excision of aortic valve and débridement. (A) A scissors cut is made in aortic valve cusp, extending to, but not into , aortic wall. Valve excision is along hinge line of aortic valve cusp. Careful excision of valve usually includes removing most calcium deposits along with the valve. (B) Residual calcium deposits are debrided from aortic anulus and sinus aorta. Sellman or other forceps and bone rongeurs are instruments commonly used to accomplish this.

Returning to the right coronary cusp, the incision is extended toward the right coronary-noncoronary cusp commissure. In this area and in this commissure, the calcification is often especially abundant, sometimes extending onto the underlying ventricular septum or, especially at the commissure, onto the aortic wall or underlying membranous septum. Thus, in dissecting this area, great care must be taken in deciding whether to cut through the calcific cusp attachment to the aortic wall or to go around some of the calcific material and leave it for later piece-by-piece removal. To the extent possible, one-piece removal is preferable, but perforation of the septum, LV-aortic junction, or aortic wall should not become a risk.

When calcium deposits completely replace the aortic valve, or when the deposits extend into the sinus aorta or anterior leaflet of the mitral valve, it is useful to mobilize the calcified tissues by the endarterectomy technique. Using a scalpel, a shallow incision is made in the aortic intima alongside the calcific deposit. This allows insertion of an endarterectomy spatula (Freer septum elevator) to lift the intact hard deposit away from the soft underlying aortic or mitral valve tissues without fragmenting the calcified material. The incision is carried down along the attachment of the noncoronary cusp, stopping about two-thirds of the distance to the commissure between the noncoronary and left coronary cusps. The latter commissural area, which is at particular risk of junctional or aortic wall perforation during valvectomy, can then be approached with excellent visibility from both sides; the incision is carried through this area with firm upward traction on the valve.

After the valve is excised, the bed is examined, and any loose calcific particles removed. Any remaining fragments are grasped with forceps or small rongeur and gently enucleated with a twisting motion ( Fig. 12.10 B).

The downstream area of aorta is irrigated and examined for any loose calcific fragments, and the valve bed is wiped with gauze and irrigated with cold saline solution to remove any tiny fragments. The LV vent is turned off so that it will not suck fragments into the inaccessible depths of the ventricle, and the gauze strip is carefully removed from the LV cavity, most likely having trapped a few small calcific fragments. The LV cavity is then vigorously irrigated and aspirated with high suction and inspected for fragments. Generally, no fragments are found. With the preventive measures against calcific embolization complete, the LV vent is again activated.

Insertion of a prosthetic aortic valve is the most common operation for replacing the aortic valve. The anulus is sized, and an appropriate-size prosthesis selected. There is no advantage in choosing an oversized prosthesis that will erode the aortic anulus. Instead, if the aortic anulus is too small to accommodate a prosthesis that will provide adequate hemodynamic performance, a supraanular device may be chosen or the anulus enlarged (see “ Managing the Small Aortic Root ” under Special Situations and Controversies later in this chapter).

Interrupted suture technique.

The valve may be implanted using simple stitches, figure of eight or horizontal mattress stitches, the latter with pledges on the aortic side (everting intraanular) or on the ventricular side (noneverting, supraanular) technique. Most often, mattress sutures are fitted with a compressed PTFE pledget placed centrally and needles at each end. Regardless of technique, alternating suture colors (green, white) simplifies sorting so that sutures may be held together as a group for each aortic sinus. Suture placement begins at the commissure between the left and right coronary cusps and continues clockwise to the right-noncoronary commissure ( Fig. 12.11 A). Time can be saved by passing the suture through the sewing ring of the prosthesis after completing each anular pass. This is easier for a trileaflet than bicuspid valve, although, with experience, it can be accomplished in this setting as well. Planning a consistent number of sutures in each cusp (for mattress or figure of eight stitches, 4 stitches in each cusp for small valves such as 19, 21, or 23 mm for a total of 12 stitches, and 5 stitches in each cusp for a total of 15 stitches for larger valves) facilitates this technique. The prosthesis is held away from the aortic anulus until all stitches have been placed.

Aortic valve replacement with mechanical prosthesis or stent-mounted bioprosthesis, interrupted suture technique. (A) Polytetrafluoroethylene felt pledget–reinforced 2-0 braided polyester suture is placed as interrupted horizontal mattress stitches passed from aortic side through aortic anulus. Needles are then passed through sewing cuff of replacement device. Suturing begins at commissure between left and right sinus of Valsalva and proceeds clockwise in right coronary sinus to commissure between right and noncoronary sinus. Alternating color of suture aids suture sorting. (B) Suturing continues in left coronary sinus of Valsalva in a counterclockwise fashion to commissure between left and noncoronary sinus. (C) Sutures surrounding anterior commissure should not penetrate tissues of membranous septum, to protect the His bundle from injury. Suturing is completed in noncoronary sinus of Valsalva. (D) Prosthesis is passed over sutures into position on aortic anulus. Sutures are sorted and tied to fix prosthesis to aortic anulus. (E) Some bioprostheses are designed to be implanted above aortic anulus (supraanular). When these devices are used, horizontal mattress stitches are passed from ventricular side of anulus to aortic surface and then through sewing cuff of bioprosthesis.

The anulus of the left coronary sinus of Valsalva is then approximated to the sewing ring of the aortic valve prosthesis, working counterclockwise from the commissure between the left and right coronary cusps ( Fig. 12.11 B). Finally, the anulus of the noncoronary sinus of Valsalva is approximated to the valve prosthesis, working clockwise from the commissure between the right and noncoronary cusp toward the commissure between the left and noncoronary cusp ( Fig. 12.11 C). Needles are passed through the anulus in a backhand manner. Alternatively, one can continue to place sutures in a counterclockwise fashion. The three groups of sutures are then strongly retracted so that the prosthesis may slide over the suture loops into the aortic anulus. The position of the occluder mechanism may be adjusted before the valve holder is removed.

Sutures are sorted and tied down in order, working first in the noncoronary sinus in a counterclockwise approach. The first suture in the left coronary sinus closest to the commissure between the left and right coronary cusps is tied to secure seating of the prosthesis directly across the anulus from those sutures already tied in the noncoronary sinus. The sutures of the left coronary sinus are tied down in a counterclockwise fashion. Sutures are tied in the right sinus, working clockwise to complete the procedure ( Fig. 12.11 D). Alternatively, one may choose to tie down the sutures at the nadir of each sinus, beginning in the left, then right, and finally, the non-coronary sinus. For valve prostheses that have any part of the device projecting below the sewing ring, such as the hinge guards of a mechanical valve prosthesis, the order of tying should be altered so that the prosthesis is first secured adjacent to the portions of the device below the anulus.

For supraanular placement, which is particularly important in the small aortic anulus ( Fig. 12.11 E), pledgets are placed below the anulus in the LVOT by passing a double-needle suture with a center pledget as a mattress stitch from below the anulus and up through the prosthesis. A larger prosthesis is thereby secured above the anulus as the anulus is compressed between the pledget and device.

Continuous suture technique.

Continuous suture technique provides the advantage of tight approximation of the prosthesis to the aortic valve anulus, because the suture loops can slip through the tissues so that tension is equalized with heart motion. Inserting a slightly larger prosthesis may also be possible because an interrupted mattress suture technique may bunch tissues together.

The aortic anulus is divided into three segments by the commissures. During valve replacement, the anulus is further subdivided into six subsegments at the midpoint on the anulus between the commissures. Polypropylene suture (2-0) is used, with needles at each end and a compressed PTFE pledget in the center of the suture. An initial mattress stitch is placed at the center of the sinus of Valsalva through the anulus of the aortic valve and brought through the sewing ring of the prosthesis ( Fig. 12.12 A). The prosthetic valve is held away from the anulus and positioned and retracted for added exposure. Exactly three stitches are placed between the initial pledgeted stitch and the commissure on each side of the sinus. The final stitch at each end is secured to the wound drapes by a hemostat. A loop of size 0 suture is placed around the polypropylene suture as the first suture loop is completed through the prosthesis in each subsegment. This suture loop is held by a hemostat to be used to adjust tension on the suture line.

Aortic valve replacement with mechanical prosthesis or stent-mounted bioprosthesis, continuous suture technique. (A) Polytetrafluoroethylene felt pledget–reinforced 2-0 polypropylene suture is placed through aortic anulus as a horizontal mattress stitch at midpoint of right coronary sinus. Stitch is brought through sewing cuff of prosthesis. Exactly three suture loops are placed through aortic anulus and sewing cuff between initial stitch and commissure. Tension loop is placed around first suture loop. After suturing right sinus, prosthesis is attached to left coronary sinus and finally to noncoronary sinus. (B) Prosthesis is approximated to anulus of aortic valve by pulling up suture loops. Tension loops are pulled up to tightly approximate sewing cuff to deepest point in sinus of Valsalva. Suture ends at commissures are then pulled up to seat the valve in aortic root. Sutures are joined at commissures.

Sutures in the right coronary anulus are placed from the center toward the commissures in the first and second subsegments. The initial stitch in the left coronary sinus passes through the sewing ring of the prosthesis opposite the last stitch of the second subsegment. Working from the center to the commissures in the left coronary sinus, the third and fourth subsegments are approximated to the prosthesis, and then the fifth and sixth subsegments are completed in the noncoronary sinus.

Traction is placed on the six size-0 silk loop sutures to pull the prosthesis into the anulus of the aortic valve ( Fig. 12.12 B). The occluder of the prosthesis is opened, and the area below the prosthesis is checked to ensure that no loose suture loops exist in the LVOT beneath the prosthesis.

The tension suture loops are removed sequentially, and the ends of the polypropylene suture pulled up tightly to approximate the sewing ring of the prosthesis to the anulus. A final check of this approximation should be made with special attention to placement of the pledget, which should be above the anulus at the point of maximal stress deep in the center of the sinus of Valsalva. The suture ends are then joined by a knot at the three commissures (see Fig. 12.12 B).

Replacing the aortic valve with a transplanted human aortic valve became more feasible and available to surgeons because of improved commercial cryopreservation techniques and is of value in the setting of complex aortic root endocarditis.

Subcoronary technique.

This technique is seldom employed in favor of root replacement but may still be of value in certain circumstances. Since the graft is to be sewn in “freehand” using the natural aorta for support with this technique, a clear understanding of the anatomy and spatial relationships of the aortic root is essential. Important deformity of the aortic sinuses should be appreciated and corrected, or the procedure abandoned in favor of conventional valve replacement or aortic root replacement techniques.

A transverse aortotomy is initially made. After assessing aortic valve morphology and anatomy of the aortic root, the incision is extended to transect the aorta (see Fig. 12.9 C). The aortic valve is excised, and anulus debrided using usual techniques. The diameter of the aortic root at the level of the ventricular-aortic junction (anulus) is determined using standard sizing devices. This dimension must be accurately measured and clearly visualized. The aortic valve allograft to be placed inside the aortic root will consume space simply because of the thickness of its wall. Therefore, it must be 1 to 2 mm smaller in internal diameter than the measured aortic anulus. This will allow some redundant aortic valve cusp to provide a larger-than-normal coaptation surface to accommodate the expected tissue shrinkage for several weeks after implantation.

The aortic allograft is removed from the liquid nitrogen freezer valve bank and thawed by protocol. The septal muscle is excised, with a finger placed inside the aorta to stabilize the graft, gauge the thickness of the trimmed graft, and remove endothelial cells that are antigenic. Excess aorta is trimmed from the valve cusps, leaving a 3- to 4-mm rim of aorta beyond attachment of the cusps. Most of the sinus aorta is removed from the right and left coronary sinuses, leaving the noncoronary sinus intact ( Fig. 12.13 A). This technique was described by Ross and colleagues in London and has been used successfully for many years.

Aortic valve replacement with aortic valve allograft, subcoronary technique. (A) Aortic allograft is chosen that is no more than 2 mm smaller in internal diameter than LVOT at aortic anulus. Cryopreserved aortic allograft is taken through the standard controlled thawing process. Its septal myocardium is thinned out and anterior leaflet of mitral valve removed along with tissues below aortic valve to create a level plane. Allograft aorta is removed from right and left coronary sinus of Valsalva, leaving 3 to 4 mm of aorta beyond hinge point of valve. Noncoronary sinus remains intact, maintaining relationships of commissures on each side of sinus. (B) Patient’s aorta is divided above sinutubular junction so that valve replacement may proceed within the intact aortic root. Traction stitches are placed above each commissure. Allograft is inverted through its anulus into patient’s LVOT. Allograft is attached to aortic anulus and below commissures in a generally level plane using continuous stitches of 3-0 polypropylene suture. (C) Allograft is pulled back into aorta. Sinus aorta of allograft is attached to patient’s sinus aorta below the coronary ostia. Sutures proceed progressively up commissures to accurately re-create relations of aortic valve within aortic root. Suturing begins at lowest point of sinus of Valsalva and proceeds to top of each commissure. Separate sutures are used for each sinus and are joined at top of commissures. Intact noncoronary sinus of graft is sewn to patient’s aorta by continuous suture.

The allograft is implanted in anatomic position. Three stitches are used to attach it to the outflow tract. The first suture is 3-0 or 4-0 polypropylene, placed using two small (17-mm) strong half-circle needles. This suture is chosen for high needle strength and low tissue drag. The suture is placed through the patient’s aortic outflow tract below the medial commissure between the right and left coronary sinuses and through the septal myocardium below the corresponding commissure in the graft; the stitch is placed below the anulus of the aortic valve. The other two stitches are simply stay sutures placed to assist in aligning the allograft to the patient’s aortic root. These sutures will be removed because the primary suture line includes their position. They are placed beneath the appropriate commissure of the allograft and directly below the anterior and posterior commissures of the patient’s aorta.

The allograft valve is lowered into position in the patient’s aortic root. Commissures of the allograft are inverted through its anulus into the patient’s left ventricle so as to expose the subvalvar edge of the allograft. A knot is placed in the primary suture, and the stay sutures are tightened to align the allograft with the LVOT. Stitches are placed between the allograft and the LVOT at or below the level of the anulus, attempting to make a level suture line ( Fig. 12.13 B). Because the aortic anulus is not circular but crescent-shaped, the stitches are well below the fibrous anulus in the subcommissural region and through this fibrous tissue of the anulus at the midpoint of the aortic sinus (see Chapter 1 ). The stitches below the left coronary sinus are placed first. The suture line is taken to a point below the posterior commissure. Using the opposite needle, the stitches between the allograft and LVOT are placed below the right coronary sinus and completed below the noncoronary sinus (see Fig. 12.13 B). Alternative suture techniques are equally effective, such as using three separate polypropylene sutures to facilitate placing multiple suture bites without “snugging” the suture line to improve exposure, after which the sutures are tightened with a blunt nerve hook prior to tying. In the small aortic root, simple sutures of 4-0 polypropylene are also effective.

The commissures of the allograft are pulled out of the left ventricle so that the allograft assumes its normal position and configuration. The allograft commissures are attached to the patient’s sinus aorta using continuous 4-0 or 5-0 polypropylene sutures. Separate sutures are used for each aortic sinus. The first stitch is taken deep in the sinus aorta at mid position in the sinus slightly above the aortic anulus and then passed through the allograft. Suturing proceeds along the aortic sinus toward the commissure so as to place the allograft flat against the patient’s aortic wall. The final stitch is placed at the top of the commissure, leaving the suture to be secured later ( Fig. 12.13 C). Suturing proceeds in each aortic sinus until the allograft is completely attached. Either the right or left coronary sinus is completed first, sewing from the center point of the sinus to each of the commissures using opposite ends of the suture. The repair is completed in the noncoronary sinus by shortening the allograft aorta to approximate the height of the patient’s intact noncoronary sinus. The two edges of the aorta are oversewn by continuous suture so that the intact noncoronary sinus of the allograft is completely enclosed within the aorta. Optionally, the space between the allograft noncoronary sinus and the underlying native aortic wall can be partially obliterated with mattress sutures that are tied outside the native aorta. The ends of the patient’s aorta are then anastomosed by continuous suture.

Intraoperative echocardiography is used to confirm aortic valve competence.

Root-enlarging technique.

An aortic allograft may be used for valve replacement as part of a root-enlarging operation. A transverse incision is made in the patient’s aorta. The incision is extended to the posterior aspect of the aorta and into the posterior commissure between the left and noncoronary sinuses. Incision into the triangular space of the commissure between the fibrous attachment of the native aortic valve opens the aortic root where there is little fibrous support so that the edges of the aortotomy will separate widely. The incision is taken to the upper edge of the anterior leaflet of the mitral valve, but it does not need to enter the leaflet tissue to provide the desired separation of the edges of the incision. The increased diameter of the patient’s aortic root is measured and an appropriately sized aortic allograft chosen. The allograft is trimmed, leaving the noncoronary sinus intact. The sinus aorta is removed from the left and right sinuses, leaving a few millimeters attached to the fibrous support of the cusps. The allograft is attached to the rim of the aortic-mitral anulus (without entering the actual anterior leaflet of the mitral valve) and superior aspect of the left atrium with interrupted 3-0 or 4-0 polypropylene sutures. The stitches are placed in the corresponding mitral valve and left atrium of the allograft’s noncoronary sinus. A PTFE felt strip is fashioned to slightly more than the length of the unsupported area of the separated aortotomy. The sutures of the noncoronary sinus are then tied down over the felt strip so as to incorporate it and fill in any potential defects in the suture line. The commissures of the valve are inverted into the LVOT, and the rest of the repair is completed according to the approach previously described under “Subcoronary Technique.” The allograft’s intact noncoronary sinus is used to close the aortotomy and widen the aortic root.

When greater enlargement of the LVOT is required, or when there is infective endocarditis with extension of anular abscess into the anterior leaflet of the mitral valve, the incision in the aorta is extended across the mitral valve anulus into the middle of the valve’s anterior leaflet. Anular abscesses are thoroughly debrided and much of the anterior leaflet of the mitral valve removed ( Fig. 12.14 A). The anterior leaflet of the mitral valve is left attached to the aortic allograft and used to widen the LVOT or repair defects in the patient’s mitral valve ( Fig. 12.14 B). The defect in the roof of the left atrium is closed with a patch taken from the aorta of the allograft or with bovine pericardium.

Aortic valve replacement with allograft, aortic root enlarging technique, or repair of anular abscess. (A) Aortotomy is extended through posterior commissure into abscess of patient’s mitral valve anterior leaflet. Abscess is debrided or simply incised if procedure is used to widen LVOT. (B) Anterior leaflet of mitral valve is left attached to allograft and used to widen LVOT or repair defects caused by endocarditis. Anterior leaflet repair is done with interrupted stitches for greatest security. Defect in left atrium is closed with a patch of aorta from the allograft.

Aortic root replacement technique.

An aortic allograft may be used to replace the patient’s aortic root completely when gross deformity is caused by infection or congenital anomaly, or it may be used to enlarge the root. Many surgeons use this technique routinely because aortic valve competence is virtually assured due to retention of the valve relationships within the intact aortic root of the allograft.

An initial transverse aortotomy is made ( Fig. 12.15 A). After decision to proceed with aortic root replacement, the patient’s aorta is transected ( Fig. 12.15 B). The sinus aorta is removed except for a rim surrounding the ostia of the coronary arteries. The aortic valve is removed and an appropriately sized aortic allograft selected. The allograft is used intact and in a natural anatomic orientation, with only the excess of septal myocardium and the anterior leaflet of the mitral valve removed. Size match is not nearly as important as it is for freehand subcoronary valve replacement, but if the aortic anulus is more than 3 mm larger in diameter than the largest available aortic allograft, the patient’s aortic root should be narrowed to approximate the size of the allograft. This can be done conveniently by placing a pledgeted mattress stitch through the aortic anulus alongside the commissures so that when tied, the intercusp triangle below the commissure is obliterated (see “ Method for Reducing Diameter of Dilated Aortic Anulus ” later in this chapter).

The allograft is attached to the LVOT at the aortic anulus and below the commissures by simple interrupted stitches of 3-0 or 4-0 polypropylene ( Fig. 12.15 C). Some, but not all surgeons, add a hemostatic PTFE felt collar. The felt is approximately 5 mm wide and long enough to encircle the allograft. The allograft is slipped over the sutures into the desired position in the LVOT. The sutures are then tied down, incorporating the felt strip within the suture loops ( Fig. 12.15 D). This is less desirable in the setting of infection.

Aortic valve replacement, aortic root replacement technique. (A) Transverse aortotomy is made. (B) Traction stitches are placed in aorta above each commissure, and aortic valve is excised. When decision is made to proceed with complete replacement of aortic root, aortotomy is extended to divide aorta. Aorta is removed from sinuses of Valsalva, except for generous buttons around coronary artery ostia. (C) Aortic allograft is minimally trimmed, removing anterior leaflet of mitral valve. Allograft root is attached to anulus of patient’s aortic valve with interrupted stitches of 3-0 or 4-0 polypropylene suture. Simple stitches are used. (D) Suture loops are tied down over a narrow strip of polytetrafluoroethylene felt or pericardium to support and fix diameter of aortic anulus and seal spaces between stitches. (E) Left coronary artery button is anastomosed to opening in allograft created by excising left coronary artery of graft. Continuous stitches of 4-0 or 5-0 polypropylene are used, depending on thickness of tissues. (F) Opening is made in allograft at position of right coronary artery unless patient’s aortic root was greatly dilated. Dilation of aortic root displaces right coronary artery; in this case, it is advisable to complete the aortic anastomosis so that aorta may be filled under pressure to properly locate position for anastomosis of right coronary artery. (G) End-to-end anastomosis of allograft to patient’s aorta completes the repair.

An alternative hemostatic method is to incorporate a double-suture-line technique in which the first suture line uses three separate polypropylene continuous sutures (one for each sinus), placing the sutures as in the interrupted technique. They are gently tightened with a nerve hook and tied. A second suture line incorporates the cut edge of the aortic wall adjacent to the anulus and the adventitia of the allograft immediately above the prior suture line.

The coronary ostia on the allograft are removed to create openings 5 to 10 mm in diameter ( Fig. 12.15 E and F). The coronary arteries are anastomosed to the allograft by continuous 4-0 or 5-0 polypropylene suture using a small needle (exact size depends on thickness of the tissues). The left coronary anastomosis is created first ( Fig. 12.15 E), followed by the right coronary anastomosis ( Fig. 12.15 F). Repair is completed by end-to-end anastomosis of the distal end of the allograft to the patient’s aorta ( Fig. 12.15 G). Continuous stitches of 3-0 or 4-0 polypropylene are used.

Porcine xenograft stentless aortic valves are available as an entire untrimmed aortic root (Medtronic, Inc, Minneapolis, MN; Freestyle Aortic Root Bioprosthesis) ( Fig. 12.16 A).

Aortic valve replacement, porcine xenograft stentless bioprosthesis. (A) St. Jude Medical Toronto SPV bioprosthesis is presented with sinus aorta removed from all three sinuses of Valsalva. Device is covered with polyester fabric. Medtronic Freestyle porcine xenograft bioprosthesis is presented with intact aortic root with less fabric. There is an inflow sewing ring, and fabric covers portions of septal myocardium on aortic root. Aorta is removed by the surgeon from right and left coronary sinuses of Valsalva, leaving noncoronary sinus intact. (B) Inflow sewing cuff of bioprosthesis (Freestyle) is attached to aortic valve anulus with continuous stitches of 3-0 polypropylene suture. Tension loops are placed around every third suture loop to make it easier to tighten suture and approximate bioprosthesis to aortic anulus. Alternatively, simple interrupted stitches of 2-0 or 3-0 braided polyester are used. (C) Placement of stitches to attach device to aortic anulus. A generally level plane is achieved by sewing through anulus, except in intercusp triangles, where stitches are placed below hinge point of aortic valve. Stitches should not be placed into membranous septum below anterior commissure, to protect conduction system from injury. (D) Sinus aorta of graft is attached to sinus aorta of patient below right coronary artery. Continuous stitches of 4-0 polypropylene suture are used. Suturing continues around coronary ostium to smoothly attach xenograft to patient and to achieve correct positioning of commissures. Because it is fixed tissue, xenograft will direct suture placement so as not to distort itself (i.e., patient’s aorta is made to conform to xenograft, rather than distorting graft to conform to shape of patient’s sinus of Valsalva). (E) Suturing continues below left coronary artery and up edges of xenograft to attach adjacent commissures of xenograft to patient’s aorta. Noncoronary sinus aorta of xenograft is trimmed to match height of patient’s noncoronary sinus aorta so that xenograft and patient’s aorta may be attached by simple continuous suture. (F) Complete root replacement technique may be employed when Medtronic Freestyle device is used to repair aortic root disease. Inflow sewing cuff of xenograft is attached to patient’s aortic anulus by continuous or simple interrupted suture technique. A narrow strip of polytetrafluoroethylene felt may be placed within suture loops for greater hemostasis. Left coronary artery of xenograft is removed and will always be the proper site for anastomosis of patient’s left coronary artery to xenograft. Because porcine coronary arteries are closer together than 120 degrees, it is often necessary to position the opening for right coronary artery anastomosis farther to the right than the location of the porcine right coronary artery. SPV, Stentless porcine valve.

The aortic valve may be replaced with the patient’s own pulmonary valve (pulmonary autograft), and a pulmonary allograft may be used to replace the pulmonary valve. This operation was devised by Ross and carries his name. The operation has the advantage of placing autogenous tissue in the high-pressure aortic position that theoretically should last indefinitely, assuming the procedure is technically correct, and the autograft does not dilate in the high-pressure arterial circulation. It is of particular value in the growing child (See “ Selection of Technique and Choice of Device for Isolated Aortic Valve Replacement” later in this chapter). The allograft tissue is placed in the low-pressure pulmonary position, where if it should fail in a regurgitant manner, regurgitation may be well tolerated for a long time.

CPB is established using two cannulae for venous drainage. A right-angle cannula is placed directly into the superior vena cava at the pericardial reflection. The other is placed in the inferior vena cava through the right atrium at the diaphragm (see Chapter 2 ). Alternatively, a single two-stage venous uptake cannula may be used, placing the second-stage opening low in the right atrium near the inferior vena cava orifice. The vacuum-assisted venous return provides more safety and reserve when the single-cannula technique is used, reducing the risk and consequences of the airlock, which may occur in a gravity drainage system when the RV is opened (see “ Vacuum-Assisted Venous Return ” in Chapter 2 ). Oxygenated blood is returned to the ascending aorta.

Pulmonary autograft technique.

The aortic root is explored through the usual transverse incision. Once it is determined to proceed with the pulmonary autograft operation, the ascending aorta is divided, the aortic valve removed, and the entire sinus aorta excised except for a generous rim around the coronary ostia ( Fig. 12.17 A). Traction stitches on the aorta above the coronary arteries are helpful. Only the fibrous connection of the aortic cusps remains for attachment of the pulmonary autograft. Traction stitches are placed above each commissure. Diameter of the aortic anulus is measured using Hegar dilator sizers.

Aortic valve replacement with pulmonary autograft (Ross procedure), aortic root replacement technique. (A) Ascending aorta is divided, aortic valve is removed, and all aorta from sinuses of Valsalva is excised except for generous buttons around coronary artery ostia. Traction stitches are placed above each commissure. (B) Pulmonary trunk is divided at bifurcation. Pulmonary valve is inspected to ensure normal morphology. (C) Dissection between medial commissure of aortic valve and pulmonary trunk enters infundibular septum. Plane between infundibular septum and RVOT is identified and dissection carried as far behind pulmonary trunk as is convenient. (D) RVOT is opened anteriorly 5 mm below pulmonary valve. (E) Incision of RVOT is extended posteriorly to extent of previous dissection (C). (F) Shallow incision is made below pulmonary valve posteriorly in RVOT, joining extent of RV incisions. Angle of scalpel is changed so that ventricular myocardium may be shaved off infundibular septum without injuring underlying first septal branch of left anterior descending coronary artery. (G) Pulmonary autograft trunk is transferred to aortic position. Simple interrupted stitches of 3-0 polypropylene are used to attach pulmonary autograft to aortic anulus (see Fig. 12.15 B). (H) Narrow strip of polytetrafluoroethylene felt or pericardium is placed within suture loops. Pulmonary autograft is partially inverted into LVOT . Sutures are tied to secure pulmonary autograft to anulus of aortic valve, making sure that there is direct tissue approximation and keeping support strip to the outside. (I) An opening is made in posterior sinus of Valsalva of pulmonary trunk and a narrow strip of tissue removed from one side to create a site for anastomosis of left coronary artery. (J) Left coronary artery is anastomosed to pulmonary trunk using continuous stitches of 5-0 polypropylene. (K) Pulmonary trunk is anastomosed in end-to-end fashion to ascending aorta. Aortic occlusion clamp is removed temporarily to fill pulmonary autograft under pressure so that proper position for right coronary artery anastomosis can be located. A small opening is made into graft, and right coronary artery is anastomosed to it. (L) A cryopreserved pulmonary allograft of appropriate size, having previously been selected and thawed, is anastomosed in end-to-end fashion to pulmonary artery bifurcation. Exposure for this anastomosis may sometimes be better if it is performed before aortic anastomosis. Proximal end of pulmonary allograft is anastomosed to RVOT using continuous stitches of 3-0 polypropylene. Stitches are placed through only partial thickness of infundibular septum posteriorly over location of first septal branch of left anterior descending coronary artery. (M) Completed repair: aortic valve replacement with pulmonary autograft, pulmonary trunk replacement with pulmonary allograft.

The pulmonary trunk is separated from the aorta up to its bifurcation. It is divided at the bifurcation, taking care not to shorten the right pulmonary artery ( Fig. 12.17 B). The pulmonary valve is inspected from above. If it is normal, operation may proceed. If it is abnormal, the pulmonary artery is reanastomosed and an aortic allograft used to replace the aortic root.

Dissection between the medial commissure of the aorta and the pulmonary trunk comes down onto the muscle of the right ventricular outflow tract (RVOT; Fig. 12.17 C). Thorough dissection between the aorta and pulmonary trunk, especially low onto the RV in the plane between the RVOT and the infundibular septum, makes removing the pulmonary trunk much easier.

The anterior intercusp triangle below the anterior commissure is identified as a reference point for opening the RVOT. A small right-angle clamp is placed precisely in the anterior intercusp triangle and pushed through the anterior wall of the RV. The small opening is carefully enlarged. The pulmonary trunk is separated from the RV, looking inside frequently to maintain appropriate length of the ventricle below the pulmonary valve ( Fig. 12.17 D). Incision of the RVOT continues on the right side and posterior to the extent of previous dissection ( Fig. 12.17 E).

The critical and unique part of the Ross operation is separating the pulmonary trunk from the RVOT above the infundibular septum. When done correctly, this part of the procedure makes the entire operation safe. Anatomy of the subpulmonary infundibulum is described in “Right Ventricle” under Cardiac Chambers and Major Vessels in Chapter 1 . Injury to the underlying first septal branch of the left anterior descending coronary artery during dissection of the pulmonary trunk is a major source of morbidity in this operation. A shallow incision of the endocardial surface is made to join both ends of the partly excised pulmonary trunk ( Fig. 12.17 F). The incision extends completely across the remaining undivided RVOT. The angle of the scalpel is immediately changed to shave off the ventricular myocardium almost parallel to the endocardial surface. This shaves off the pulmonary trunk without injuring the underlying first septal branch. This part of the operation should be performed deliberately and under precise control. The septal excision eventually separates the pulmonary trunk completely, leaving the left main coronary artery and the first septal branch behind and protected by a generous layer of tissue. The septal artery is occasionally seen in the myocardium.

The separated pulmonary trunk is placed in the pericardial sac for immediate use. The trunk is not removed from the operating field to prevent its misplacement or inadvertent mixture with the allograft. At this point, it is convenient to measure the dimensions of the pulmonary anulus using standard prosthetic valve sizers and to choose a pulmonary allograft for preparation for later use.

The pulmonary autograft is attached to the unmodified LVOT using interrupted stitches of 3-0 polypropylene ( Fig. 12.17 G). Size discrepancy between the pulmonary autograft anulus and aortic anulus should not exceed 2 mm. A larger discrepancy indicates the need to adjust the anulus of the aorta to match that of the pulmonary autograft (see “ Method for Reducing Diameter of Dilated Aortic Anulus ” later in this chapter). The autograft is marked below each of the commissures for orientation. The anterior commissure of the autograft is oriented to approximate the commissure between the right and noncoronary sinuses. Suturing proceeds below each sinus, separating the stitches into three groups. Stitches are placed through the strong fibrous tissue of the aortic anulus, keeping the plane of repair as level as possible. A strip of PTFE felt about 5 mm wide may be used to fix the diameter of the proximal suture line and to ensure hemostasis between the sutures ( Fig. 12.17 H). A strip of autogenous pericardium may also be used. A “supported” repair is favored to prevent dilation of the pulmonary autograft at the proximal suture line. Some surgeons prefer a continuous suture line using absorbable stitches without prosthetic material, especially for children in whom growth of the pulmonary autograft is desired. However, the accuracy of carefully spaced individual stitches and fixation support of the anulus seem best in adult patients. The felt or pericardial strip is placed within the suture loops so that it is incorporated as the sutures are tied down. The pulmonary autograft is partially inverted into the LVOT as the sutures are tied to ensure that tissue approximation is accurate and that the support ring is to the outside rather than interposed between the tissues of the autograft and the aortic anulus.

An opening is made into the left coronary sinus of the autograft using a scalpel ( Fig. 12.17 I). Only minimal sinus tissue is excised because the delicate pulmonary artery dilates and separates readily. The sinutubular junction of the autograft is preserved to maintain proper relationships between the commissures and cusps.

The left coronary anastomosis proceeds, working on the outside of the pulmonary autograft ( Fig. 12.17 J). Continuous stitches of 5-0 polypropylene are used. As a practical matter, it is best to perform the right coronary anastomosis after completing the aortic anastomosis so that the pulmonary trunk can be distended by temporarily removing the aortic clamp ( Fig. 12.17 K). The right coronary anastomosis typically fits high in the right sinus or even above the sinutubular junction on the anterior wall of the pulmonary trunk. It may also be advisable to anastomose the pulmonary allograft to the bifurcation of the pulmonary trunk before the aortic anastomosis if the medial aspect of the pulmonary anastomosis might be obscured by the overlying aorta ( Fig. 12.17 L). Often, the diameter of the aorta is larger than that of the pulmonary trunk, but the pulmonary trunk is usually sufficiently long enough that a bevel can be created to take up any size discrepancy. With gross aortic enlargement or aneurysm, the entire ascending aorta may be removed and the pulmonary trunk extended with a prosthetic graft (see “ Method for Extending Pulmonary Autograft ” later in this chapter).

Method for lengthening pulmonary allograft.

The pulmonary allograft may be tailored to achieve greater length, reducing the chance that the graft will be too tight between the RVOT and pulmonary artery bifurcation. The entire left pulmonary artery may be retained on the graft. The right pulmonary artery is removed and closed by direct suture using 5-0 polypropylene to lengthen the graft ( Fig. 12.18 A). The left pulmonary artery is cut back to the bifurcation to create a large circumference for anastomosis. Making the pulmonary allograft long or even slightly redundant may be important in maintaining proper allograft length because myocardium below the pulmonary allograft valve is resorbed and replaced with contracting scar.

Methods for adjusting Ross operation in specific situations. (A) Method for lengthening pulmonary allograft to prevent tension on graft between right ventricular outflow tract and bifurcation of pulmonary artery as right ventricular myocardium on allograft is reabsorbed and replaced with scar tissue. Left pulmonary artery is retained with pulmonary trunk; it may be cut back (broken line) to pulmonary bifurcation to create a large opening. Right pulmonary artery is removed and its origin closed by continuous suture. (B) Method for reducing diameter of dilated aortic anulus for proper size match with pulmonary autograft. Pledget-reinforced horizontal mattress stitches are placed through the fibrous tissue adjacent to intercusp triangles posteriorly and medially to obliterate triangular space, thereby reducing anular diameter. (C) Method for extending pulmonary autograft when there is aneurysm or dilation of ascending aorta. Aneurysmal aorta is removed. Pulmonary autograft is lengthened by attaching a tubular polyester graft of exactly the same diameter as the pulmonary trunk just above valve commissures. (D) Method of fixing sinutubular junction of pulmonary autograft to prevent dilation. A segment of tubular polyester vascular prosthesis 10% smaller than measured diameter of pulmonary valve is placed around outside of autograft at level of sinutubular junction. A few interrupted stitches are placed to attach graft to pulmonary trunk to prevent migration. (E) Echocardiogram of pulmonary valve before aortic valve replacement with pulmonary autograft shows typical trivial central valve regurgitant jet. After pulmonary trunk is transferred to aortic position and subjected to systemic arterial pressure, there is moderate (2+) valve regurgitation. Narrowing the sinutubular junction with an external band restores valve to preoperative state of trivial regurgitation.

The early steps of the en bloc operation differ somewhat from those of simple aortic valve replacement. The arterial cannula may need to be placed in the common femoral artery or axillary artery (see “ Cardiopulmonary Bypass Established by Peripheral Cannulation ” in Chapter 2 ). When the ascending aortic aneurysm stops short of the brachiocephalic artery origin, the proximal transverse arch can be cannulated in the usual manner.

A limited dissection is done, separating the right and contiguous portion of the pulmonary trunk from the back of the aorta and the aneurysm. This approach affords safe placement of the aortic occlusion clamp just proximal to the brachiocephalic artery. The procedure involves clean surgical separation of the right and contiguous portion of the pulmonary trunk from the back of the aorta and from the aneurysm, if possible.

If circulatory arrest for open distal anastomosis is not required, CPB may be established at 28°C to 34°C. The aorta is occluded just proximal to the brachiocephalic artery. The ascending aorta is opened transversely in its midportion, stay sutures are applied, and cardioplegia is given.

The patient’s aortic root is disconnected from the LVOT and left atrium–mitral valve complex. The sinus aorta surrounding the coronary arteries is retained. The remaining sinus aorta is excised, leaving only fibrous aortic valve attachments, which are normal and uninvolved with the disease process being treated. The ascending aorta is divided by extension of the transverse aortotomy.

When the ascending aorta is replaced along with the valve, sizing of the allograft valve is less critical than in the case of isolated aortic valve replacement. The length of the retained ascending aorta and arch are considered when choosing the graft to accommodate replacement of the ascending aorta to the extent required (see Fig. 12.14 ). The distal allograft aorta is tailored to fit the native aorta, most often by creating a bevel to match the cut edges in length. The distal anastomosis is performed directly or under circulatory arrest with the patient’s body temperature at 18°C.

In young patients, it may be desirable to use a pulmonary autograft as part of the en bloc operation. The pulmonary autograft is used as an intact pulmonary trunk to replace the aortic root, as described earlier for isolated aortic valve replacement (see Fig. 12.18 C). The abnormal dilated or aneurysmal ascending aorta is excised. A crimped polyester tubular graft, collagen-coated and of the same diameter as the distal end of the pulmonary autograft, is selected for replacing the ascending aorta. This graft is anastomosed to the distal end of the pulmonary trunk. The graft is shortened and beveled appropriately for end-to-end anastomosis to the distal ascending aorta.

Replacing the aortic valve and ascending aorta as an en bloc procedure is most often done with a composite prosthesis containing a mechanical or bioprosthetic cardiac valve enclosed within a slightly larger (typically by 5 mm) tubular polyester graft. This operation is frequently referred to as the Bentall procedure. These grafts have a collagen or gel coating that makes them impervious to blood.

The patient is placed on CPB using a single venous two-stage cannula, with oxygenated blood returned to a cannula in the mid arch, axillary artery, or femoral artery, depending on the extent of aortic resection required. Axillary artery cannulation facilitates delivery of selective antegrade perfusion. The ascending aorta is occluded by a vascular clamp, and a vent catheter is placed through the right superior pulmonary vein and left atrium and into the left ventricle. A vertical incision is made in the ascending aorta aneurysm. Cold cardioplegic solution is administered to the coronary sinus by a retrograde coronary perfusion cannula. Traction stitches are placed above each aortic valve commissure to expose the aortic root ( Fig. 12.19 A). The aortic valve is excised, and coronary artery ostial buttons are mobilized, retaining a generous button of sinus aorta for the freestanding root replacement technique, which has replaced the inclusion root as originally described by Bentall and DeBono. A limited dissection of the coronary artery is sufficient to ensure that excision of the coronary artery is complete and that the coronary button will move easily up to the composite prosthesis without kinking or creating undue tension on the artery. The remaining sinus aorta is removed.

Replacement of aortic root and ascending aorta (en bloc) with composite prosthetic valve conduit. (A) Aortic valve is excised. Aorta is removed from sinuses of Valsalva except for generous buttons around coronary ostia. Abnormal ascending aorta is removed. (B) Composite prosthetic valve conduit is attached to anulus of aortic valve with pledget-reinforced horizontal mattress stitches of 2-0 braided polyester. Continuous suture technique may also be used. (C) Sutures are tied to tightly approximate prosthesis to aortic anulus. (D) An opening is made into graft posteriorly. Left coronary artery is anastomosed to graft using continuous stitches of 3-0 or 4-0 polypropylene. (E) An opening is made into graft anteriorly. Right coronary artery is anastomosed to graft. (F) Generally, coronary arteries may be anastomosed to the graft directly, without special treatment. Dissection of aorta around coronary ostium may require repair with polytetrafluoroethylene (PTFE) felt “washers” placed on endothelial and adventitial surfaces to sandwich the aortic tissue. Biological glue may also be applied. When coronary ostia are widely displaced, a short segment of tubular polyester or PTFE graft may be placed between aortic graft and coronary ostium. A short segment of saphenous vein may be used as an interposition graft. (G) When coronary ostia are destroyed by dissection or involved with arteriosclerotic disease, a saphenous vein bypass graft may be placed from aortic graft to affected coronary artery (in this case, left anterior descending). Coronary ostium is then closed by oversewing it with continuous suture. (H) End-to-end anastomosis of graft to aorta is constructed using continuous suture technique. A short segment of graft is cut and placed around anastomosis to reinforce suture line for hemostasis. (I) Completed repair: replacement of aortic root and ascending aorta. Hemostasis collar is shown covering graft-to-aorta anastomosis. (J) Cabrol modification when coronary ostia are tightly bound to aortic anulus such that composite graft sewing cuff may impinge on coronary ostia. A prosthetic valve is placed within a tubular polyester graft so that there is a short length of graft extending below valve. Graft and prosthetic valve are attached by continuous suture. The thin tubular graft is attached to aortic anulus without obstructing coronary arteries. Ten-millimeter tubular polyester grafts are used to extend coronary arteries to composite aortic graft above location of prosthetic valve. (K) When coronary arteries are carried laterally by aneurysm of aortic root, extensions from coronary arteries to aortic graft are created, following paths shown by broken lines. Then 10-mm tubular polyester grafts are anastomosed to coronary arteries and brought up to aortic graft, where end-to-side anastomoses are created. Interposition graft prevents tension on coronary artery anastomoses, thereby reducing chance of hemorrhage.

The diameter of the anulus is calibrated, and an appropriately sized composite prosthesis, including the prosthetic aortic valve and attached crimped polyester tubular prosthesis, is selected. Stitches are placed through the anulus of the aortic valve and brought up through the sewing ring of the prosthesis using mattress stitches of 2-0 braided polyester with PTFE felt pledgets ( Fig. 12.19 B). Suture placement is started in the right coronary sinus, working clockwise, as for typical aortic valve replacement. Repair of the left coronary sinus follows, working counterclockwise. The repair is completed in the noncoronary sinus, working clockwise.

Sutures are tied down to approximate the sewing ring of the prosthetic valve firmly to the aortic anulus ( Fig. 12.19 C). A running suture technique is an acceptable method, provided the anulus is strong and able to support the repair.

A decision is then made regarding the method of reimplanting the coronary arteries to the graft. A direct anastomosis of the coronary ostia to the graft is usually made ( Fig. 12.19 D and E). When aortic dissection involves the coronary ostia, it may be necessary to reapproximate the dissected layers of aorta primarily or, in some cases, between PTFE felt washers ( Fig. 12.19 F). In unusual circumstances when the coronary ostia are displaced far laterally by a large-diameter aneurysm, it may be advisable to interpose a second graft between the coronary ostia and aortic graft to prevent tension on the coronary anastomosis, which is the most frequent point of hemorrhage after repair. Irreparable coronary ostial obstruction may require a saphenous vein bypass graft between the aortic graft and the affected coronary artery ( Fig. 12.19 G). The primary ostium of the affected coronary artery is closed by suture.

The graft may be shortened appropriately to facilitate anastomosis of the coronary arteries to its side. Openings are made into the side of the graft exactly opposite the coronary artery ostia using scissors or battery-operated cautery. An adequate amount of graft should be left between the sewing ring of the prosthesis and the new coronary artery opening. The left coronary anastomosis is made first (see Fig. 12.19 D). The coronary ostium is approximated to the side of the graft by continuous stitches of 5-0, 4-0, or 3-0 polypropylene, depending on thickness of the aortic tissues. All the suture loops around the inferior rim of the coronary ostium are placed before pulling them up so that this difficult area may be accurately approximated to the graft (see Fig. 12.19 D). Stitches are placed in cartwheel fashion around the coronary artery ostium, with deep bites into the aorta.

The right coronary anastomosis is performed after completing the left coronary anastomosis (see Fig. 12.19 E), although some surgeons perform this anastomosis following completion of the distal anastomosis to facilitate proper placement of the button. Both coronary ostia are approximated to the side of the graft in a similar manner.

The distal end of the graft is then shortened to approximate the distal end of the aorta, and the aorta is completely divided to allow direct end-to-end anastomosis. A short segment of graft may be cut and placed as a collar over the main portion of the graft. The anastomosis is constructed using continuous stitches of 3-0 or 4-0 polypropylene, depending on the thickness and strength of the aorta. It is convenient to bring the first stitch from the outside of the aorta so that the stitching may continue from the inside surface of the graft. Several suture loops may be placed posteriorly before pulling the graft tightly against the aorta, to ensure accurate closure of the posterior wall of the anastomosis ( Fig. 12.19 H).

The anastomosis is continued anteriorly and is completed by including all layers of the aorta in the graft. The graft collar is used to cover the completed anastomosis for hemostasis ( Fig. 12.19 I).

Modifications are required when coronary artery ostia are either close to the anulus or widely separated laterally by an aortic aneurysm. When coronary artery ostia are bound tightly to the aortic anulus, usually by prior operation or valve replacement, it is impossible to create an accurate anastomosis to the tubular portion of a composite graft because the valve sewing ring may impinge on the coronary ostia. In this situation, a composite valve prosthesis is constructed by placing a prosthetic valve within a tubular polyester graft so that there is a short length of tubular graft extending below and a longer length of graft extending above the sewing ring of the valve ( Fig. 12.19 J). The graft and sewing ring of the prosthetic valve are attached by continuous suture. The extension of the tubular graft below the prosthetic valve is attached to the aortic anulus, displacing the level of the prosthetic valve cephalad above the bound-down coronary ostia. Obstruction of the coronary ostia from contiguous placement of the thick sewing ring of the prosthetic valve is avoided. Extension grafts of 8- or 10-mm diameter from the aortic graft above the prosthetic valve to the coronary ostia complete the repair.

When the coronary artery ostia have been carried laterally and superiorly from the usual location relative to the aortic anulus by aneurysm or dilation of the aortic root, it may also be necessary to create an extension from the composite prosthesis to the coronary arteries again using 8- or 10-mm tubular polyester grafts ( Fig. 12.19 K).

After induction of anesthesia, intraoperative transesophageal echocardiography (TEE) is used to measure aortic root dimensions at the sinutubular junction and ventricular-aortic junction. Operations are performed on CPB using a single two-stage cannula for venous uptake, with oxygenated blood returned to a cannula placed high in the ascending aorta or arch or in the axillary or femoral artery. Hypothermic circulatory arrest is used when the aneurysm extends beyond the ascending aorta.

The aorta is divided above the sinutubular junction, and the aortic valve thoroughly examined. Normal aortic valve cusps suggest the possibility of a valve-sparing operation. Diameters of the sinutubular junction and ventricular-aortic junction are measured using Hegar dilators or accurate valve sizers. Alterations of aortic root dimensions are noted and will guide the steps taken to restore dimensions to normal.

Aortic anulus normal, normal sinuses of valsalva, sinutubular junction enlarged.

A normal aortic anulus with enlarged sinutubular junction is found in patients with aortic ectasia and aneurysm of the ascending aorta not involving the aortic sinuses. The coronary arteries are not displaced from their usual location in relation to the anulus. In this instance, a vascular graft of the same diameter as the aortic anulus is selected. A 4- to 5-mm segment of the graft is prepared for placement on the outside of the aorta at the sinutubular junction ( Fig. 12.21 ). The thickness of the aortic wall, when compressed within the graft, will reduce the inside diameter of the aorta to restore the normal dimension, which is 15% less than the diameter of the aortic anulus. Using this short segment of graft is easier and more accurate than attempting to attach a longer graft directly to the sinutubular junction.

Repair of aortic valve regurgitation caused by dilation or aneurysm of ascending aorta when aortic anulus is normal and sinutubular junction is enlarged without aneurysmal enlargement of sinuses of Valsalva and without displacement of coronary ostia. A 4- to 5-mm segment of graft the same diameter as anulus is placed as a band on outside of aorta at sinutubular junction to reduce inside diameter by 10%. Ascending aortic aneurysm is resected and replaced with graft of same size.

In the remodeling procedure, the aortic sinuses are removed. The aortic anulus is reduced to a diameter appropriate for the patient’s body size ( Fig. 12.22 ), generally 25 mm for the average adult male, 27 mm for a large male, and 23 mm for an adult female. A vascular graft 10% to 15% smaller than that diameter is selected; thus, for a 25-mm anulus, a 22-mm graft is chosen. Two 4- to 5-mm segments (rings) of the graft are prepared to adjust the anulus diameter. The remaining graft is tailored by making three incisions, trimming the flaps for sinus reconstruction, and replacing the ascending aorta. To achieve an LVOT 25 mm in diameter at the ventricular-aortic junction, the circumference of the aorta must be reduced to 78 mm (25 · π = 78). This reduction is accomplished by anuloplasty, using the short segments of graft to size the anulus accurately and to support the repair.

Remodeling method for restoring aortic root dimensions in an aortic valve–sparing operation when aortic anulus and sinutubular junction are enlarged, as in anuloaortic ectasia with Marfan syndrome. A vascular graft 10% to 15% smaller than desired diameter of aortic anulus is used to provide 4- to 5-mm strips of fabric that will support a reduction anuloplasty of five-sixths of circumference of left ventricular outflow tract (avoiding conduction system) just below aortic valve. Graft adjusts diameter at sinutubular junction. Sinuses of Valsalva are reconstructed as described in text.

Anuloplasty mattress stitches are placed in the LVOT at a level plane just below the hinge point of the aortic valve. The stitches are placed beginning below the nadir or midpoint of the right coronary cusp of the aortic valve and working counterclockwise to the commissure between the noncoronary and right coronary cusps. This places the stitches on five-sixths of the circumference, avoiding stitches in the one-sixth of the ventricular septum that contains the conduction system. A strip of fabric that covers five-sixths of the circumference and achieves a diameter of 25 mm will be 65 mm in length (78 · ⁵⁄₆ = 65). It is convenient that a 22-mm crimped tubular polyester graft provides a strip of fabric 75 mm in length when the 4- to 5-mm segment is cut, opened, and stretched to length. From the strip of the graft, 10 mm of length is removed. The anuloplasty stitches are placed through the fabric strip and passed through the LVOT to the outside. Thickness of tissue through which the needles pass is about 3 mm. Thus, the outside diameter to be supported will be about 28 mm in diameter. The length of fabric needed to support this diameter is, conveniently, about 75 mm (28 · π · ⁵⁄₆ = 73). The anuloplasty stitches are passed through the outside fabric strip. A 25-mm-diameter Hegar dilator is placed in the LVOT while the sutures are tied down. This narrows the LVOT to a calculated diameter while distributing the tension equally over five-sixths of its circumference.

The sinus aorta is reconstructed to the flap graft. Diameter of the sinutubular junction is accurately restored by the diameter of the graft chosen for the repair. Relationships just described should hold for the various graft sizes that might be chosen for reconstructing the aortic root. Intraoperative TEE is performed with the heart contracting and ejecting at normal pressure to determine adequacy of the repair.

The reimplantation technique involves excising all three sinuses, leaving a rim of 4 to 5 mm of aortic wall and buttons of aorta around the coronary ostia ( Fig. 12.23 A). An appropriately sized polyester graft (see later text for sizing details) is selected, and marks are made on one end of it corresponding to position of the commissures. Multiple interrupted pledgeted horizontal mattress sutures of 2-0 polyester are passed from inside the LVOT immediately below the nadir of the aortic valve following a horizontal plane except in the region of the left anterior fibrous trigone (dense adherence of fibrous trigone to pulmonary trunk) and near the conduction system at the commissure between right and noncoronary sinuses ( Fig. 12.23 B). (In these two commissural areas, the sutures follow the hinge point line of the valve cusps.) These horizontal mattress sutures are then placed through the base of the polyester graft (placed slightly higher in the two commissural areas noted). Position of the commissures within the graft is then determined (the orientation being critical to competence of the aortic valve), and the aortic wall above each commissure is sutured to the graft with 4-0 polypropylene mattress sutures. The remainder of the suturing of the native aortic valve to the inside of the graft is similar to a subcoronary allograft procedure described earlier under “Allograft Aortic Valve.” The suture line starts at the lowest point of each scallop and continues to the top of each commissure. The valve is inspected for adequate cusp coaptation. If the free edge of one or more cusps is elongated and tending to prolapse, the free margin can be shortened by using 6-0 PTFE suture to imbricate the central portion of the cusp (nodulus of Aranti).

Reimplantation procedure. (A) Ascending aorta and sinuses of Valsalva are excised and coronary ostial buttons created. Base of aortic root is mobilized to a level just below aortic anulus circumferentially except at the commissure between right and left sinuses, where left anterior fibrous trigone creates dense adhesions between aortic root and pulmonary trunk. (B) Pledgeted sutures are passed from left ventricular outflow tract (just below aortic valve hinge points) out through aortic wall and through graft. Lower sutures are placed in a circular fashion, except in area of left anterior fibrous trigone and near membranous septum (at commissure between right and noncoronary sinuses), where they are placed close to the valve hinge point line. (C) Aortic valve is reimplanted into polyester graft. It is secured at two levels below cusps by horizontal mattress sutures and above cusps by suturing remnants of arterial wall to graft. Coronary arteries are reimplanted into graft. To create larger sinuses and still narrow the graft just above sinutubular junction, a second graft that approximates the aortic anulus diameter can be anastomosed to the upper ascending aorta (or arch), and a graft-to-graft anastomosis can be constructed that narrows the lower graft just above sinutubular junction (the “Stanford modification”).

(From Demers. )

The coronary artery reimplantation steps are the same as described for the total root replacement operation ( Fig. 12.23 C). The distal aortic anastomoses can be performed either with the same graft or with a separate smaller graft (see text that follows on creating pseudosinuses).

Two important technical considerations in the reimplantation procedure deserve special comment: commissure resuspension height and graft sizing with the construction of pseudosinuses.

Alternative techniques generally focus on simplifying the operation by retaining aortic tissue and providing an external wrap to prevent further aortic enlargement. The advantage is a simpler procedure with fewer suture lines to bleed, which must be weighed against the potential for dissection in the retained aorta. The Florida sleeve repair ^, is a valve-sparing operation in which the ventricular-arterial junction, sinuses of Valsalva, and sinutubular junction are supported by a polyester conduit as a sleeve. In a technique reported by Laks and colleagues, aortic root aneurysms associated with bicuspid aortic valve regurgitation are treated with a combination of pericardial cusp extension, lining the sinuses of Valsalva with autologous pericardium (with holes punched to accommodate the coronary orifices), and wrapping the ascending aorta with polyester. More recently, the PEARS procedure has been developed in which a custom-printed sleeve is created based on perioperative axial imaging.