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Anderson CA, Rizzo RJ, Cohn LH. Ascending Aortic Aneurysms.
In: Cohn LH, Edmunds LH Jr, eds. Cardiac Surgery in the Adult. New York: McGraw-Hill, 2003:11231148.

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Chapter 46

Ascending Aortic Aneurysms

Curtis A. Anderson/ Robert J. Rizzo/ Lawrence H. Cohn

HISTORY
????Early Descriptions and Surgical Interventions
????Evolution of Modern Surgical Techniques
INCIDENCE AND RISK FACTORS
ETIOLOGY AND PATHOPHYSIOLOGY
????General
????Idiopathic Cystic Medial Degeneration
????Genetic Disorders
????????MARFAN SYNDROME
????????EHLERS-DANLOS SYNDROME
????????FAMILIAL ANEURYSMS
????Atherosclerosis
????Aneurysms Associated with Aortic Dissection
????Aneurysms Associated with Aortic Valve Disease
????Infection
????????BACTERIAL (MYCOTIC) ANEURYSMS
????????SYPHILITIC ANEURYSMS
????Arteritis
????Trauma
????Pseudoaneurysms
NATURAL HISTORY
????General
????Size
????The Influence of Etiology on Natural History
????????MARFAN SYNDROME
????????FAMILIAL ANEURYSMS
????????AORTIC DISSECTION
????????SYPHILITIC ANEURYSMS
CLINICAL PRESENTATION
????Signs and Symptoms
????Physical Examination
DIAGNOSTIC STUDIES
????Electrocardiogram
????Chest Radiography
????Echocardiography
????Aortography
????Computed Tomography
????Magnetic Resonance Imaging
INDICATIONS FOR OPERATION
????Symptoms
????Size/Growth Rate
????The Influence of Etiology
PREOPERATIVE PREPARATION
CHOICE OF PROCEDURE
????Ascending Aortic Aneurysms
????Annuloaortic Ectasia
????????COMPOSITE VALVE-GRAFT CONDUIT
????????AORTIC ALLOGRAFT
????????PULMONARY AUTOGRAFTS (ROSS PROCEDURE)
????????VALVE-SPARING PROCEDURES
????????ALTERNATIVE PROCEDURES
????Management of Associated Conditions
????????CORONARY ARTERY DISEASE
????????MITRAL VALVE DISEASE
OPERATIVE TECHNIQUE
????General
????????MONITORING AND ANESTHESIA
????????INCISION
????????PERFUSION
????????MYOCARDIAL PROTECTION
????????CHOICE OF GRAFT
????Specific Operative Techniques
????????REPLACEMENT OF THE ASCENDING AORTA
????????REPLACEMENT OF THE ASCENDING AORTA AND AORTIC ROOT WITH A COMPOSITE VALVE-GRAFT CONDUIT
????????REPLACEMENT OF THE ASCENDING AORTA AND AORTIC ROOT WITH AN ALLOGRAFT OR AUTOGRAFT
????????OPEN TECHNIQUE FOR DISTAL ANASTOMOSIS
????????CABROL TECHNIQUE FOR REESTABLISHING CORONARY FLOW
????????REOPERATION ON THE ASCENDING AORTA AND AORTIC ROOT
????Management of Complications
????????BLEEDING
????????STROKE
????????PULMONARY DYSFUNCTION
????????POSTOPERATIVE CORONARY INSUFFICIENCY
RESULTS OF OPERATION
????Perioperative Morbidity
????Perioperative Mortality
????Risk Factors for Hospital Mortality
????Late Mortality
????Reoperation
????Thromboembolism
????Prosthetic Valve Endocarditis
????Results of Operation in Patients with Marfan Syndrome
LONG-TERM SURVEILLANCE AFTER ASCENDING AORTIC OPERATIONS
THE INFECTED AORTIC GRAFT
????Incidence
????Risk Factors
????Diagnosis
????Treatment
REFERENCES

?? HISTORY
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Early Descriptions and Surgical Interventions

Galen is credited as the first to describe arterial aneurysms. This was based on his observation of false aneurysms in gladiators injured during battle in the 2nd century A.D.1 Antyllus, during the same time period, made the distinction between traumatic aneurysms and those of a degenerative etiology. Antyllus was also the first to attempt surgical treatment of aneurysms with proximal and distal ligation,2 but his techniques were not broadly applied at the time. Ambroise Par? in the late 1700s proposed that syphilis played a causative role in some aortic aneurysms, but this was not generally accepted until many years later when Dohle described the histology of syphilitic aortitis.1

The earliest surgical treatment of aneurysms consisted of interruption of arterial flow via either ligation or the stimulation of thrombosis. These procedures met with variable success depending upon the position of the aneurysm and the extent of collateral circulation.2 Arterial ligation was popularized in the 1800s by John Hunter, who demonstrated safe and reproducible means of ligating certain peripheral arteries.3 Innovative measures used to cause thrombosis of aneurysms included the insertion of long segments of wire4 with the application of an electric current,5 and wrapping of aneurysms with cellophane or other irritating materials.6,7

In 1888, Rudolph Matas introduced a very different approach. In an operation he referred to as obliterative endoaneurysmorraphy,8,9 stitches placed from within the aneurysm sac obliterated the arterial openings. This provided more secure closure of large aneurysms that would have been difficult to ligate externally. Recognizing the importance of maintaining arterial continuity for certain aneurysms, he subsequently devised techniques of restorative or reconstructive endoaneurysmorraphy10 in which diseased segments of the aneurysm wall were resected and the remaining vessel wall was reconstructed to reestablish flow. The number of aneurysms to which these techniques could be applied, however, was very limited. The broad application of surgical treatment for major arterial aneurysms would have to await the development of satisfactory conduits and the techniques to insert them.

Evolution of Modern Surgical Techniques

Replacement of the ascending aorta, which had to await the development and refinement of cardiopulmonary bypass technology, was first performed by Cooley and DeBakey using an aortic allograft in 1956.11 Mueller et al combined allograft insertion with aortic valve repair in 1960 in a patient with Marfan syndrome.12 As the need for conduits grew, attention was shifted to the development of a suitable artificial conduit. The first fabric to be utilized was Vinyon N cloth by Blakemore and Voorhees.13 Dacron was subsequently introduced by DeBakey,2 who discovered it in a Houston department store, and it soon became the artificial conduit of choice for aortic replacement.

Replacement of the supracoronary ascending aorta with a synthetic graft and separate mechanical aortic valve replacement was performed by Starr et al in 1963.14 Wheat et al15 in 1964 resected the ascending aorta and entire aortic root except for small tongues of aortic tissue surrounding the coronary arteries. They then performed a mechanical valve insertion and fashioned the proximal tube graft to accommodate the coronary arteries, which were left in situ. The first use of a composite valve-graft conduit to replace the aortic root and ascending aorta was by Bentall and De Bono in 1968.16 The coronaries were left intact in the aortic wall and the surrounding aortic tissue was sewn to orifices that were created in the tube graft. The remaining aorta was wrapped tightly around the tube graft, creating an inclusion cylinder arrangement. In 1981 Cabrol used an 8- to 10-mm Dacron graft to facilitate the restoration of coronary blood flow following aortic root replacement.17 Variations of these pioneering procedures using modern low-profile mechanical valves and hemostatic collagen- or gelatin-impregnated woven Dacron grafts are commonly performed today.


?? INCIDENCE AND RISK FACTORS
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Aortic aneurysms are the 13th leading cause of mortality in the United States.18 The incidence of thoracic aortic aneurysms is estimated to be 5.9 cases per 100,000 person-years,19 and replacement of the ascending aorta accounts for the majority of thoracic aortic procedures.20 The mean age at the time of diagnosis ranges from 59 to 69 years.21 Men are typically diagnosed at a younger age and there is a 2:1 to 4:1 male predominance.21

Traditional risk factors have included smoking, hypertension, atherosclerosis, and well-defined genetic disorders such as Marfan syndrome and Ehlers-Danlos syndrome.19,2225 Subtler forms of inherited metabolic disorders are being elucidated,26 and perhaps play a role in more instances than was previously suspected. Syphilis, at one time the predominant etiology of ascending aortic aneurysms, has become very uncommon with the development of effective antibiotics. Bicuspid and unicuspid aortic valves are associated with ascending aortic aneurysms and dissections beyond that which can be attributed to simple hemodynamic disturbance, suggesting an underlying abnormality of the aortic wall.27


?? ETIOLOGY AND PATHOPHYSIOLOGY
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General

Most of the elasticity and tensile strength of the aorta is derived from its medial layer, which consists of approximately 45 to 55 lamellar units of elastin, collagen, smooth muscle cells, and ground substance. In the ascending aorta, the elastin content is high, consistent with its compliant nature, and diminishes as one proceeds distally into the descending thoracic and abdominal aorta. The media also becomes thinner distally, and in the abdominal aorta the total number of lamellae is reduced by approximately one half.28

The aortic wall is a biologically active environment. Smooth muscle cells synthesize and degrade elastin, collagen, and proteoglycans.29 In the media of a typical ascending aortic aneurysm there is fragmentation of elastic fibers, and loss of smooth muscle cells30 or alteration in smooth muscle cell function.29 The resulting pathologic entity is referred to as cystic medial degeneration or cystic medial necrosis. In advanced forms there is a dramatic loss of elastic fibers and smooth muscle cells with the accumulation of a basophilic amorphous material giving the media a true cystic appearance.30 Subtler degrees of elastic fiber fragmentation are normal, and the diameter of the ascending aorta typically increases with age.31 Smoking has been associated with increased concentrations of elastolytic enzymes within the aortic wall, possibly hastening this process.31,32 The role of atherosclerosis is controversial.

During systole, the ascending aorta expands, converting a portion of the kinetic energy of left ventricular contraction into potential energy in the aortic wall. During diastole the aorta recoils, converting this potential energy once again into the kinetic energy of forward flow.33 This coupling of the left ventricle and aorta ensures efficient forward flow during both phases of the cardiac cycle. With weakening of the aortic wall and loss of elasticity, dilation ensues. Dilation results in increased wall tension relative to intra-aortic pressure according to the law of Laplace. This amplifies the injurious forces on the aortic wall produced by hypertension and results in progressive dilation. These pathologic changes in the aortic wall can result in inefficient ventricular-aortic coupling, aortic valve incompetence, and the potential for rupture or dissection.

Idiopathic Cystic Medial Degeneration

Elastic fiber fragmentation is a normal process of aging,31 but is accelerated in some individuals for poorly understood reasons. This results in premature weakening of the aortic wall, aneurysmal dilation, and the potential for rupture or dissection. Many cases that are now considered idiopathic may in the future be described as subtle disorders of metabolism that accelerate aortic wall degeneration in response to common risk factors.

Genetic Disorders

MARFAN SYNDROME

Marfan syndrome is an autosomal dominant connective tissue disorder, with potentially life-threatening cardiovascular manifestations.34 The estimated frequency is 1 per 10,000 births.35 This disorder has been traced to the fibrillin gene of chromosome15,3640 with more than 70 different defects identified thus far.41 It is believed that one third of cases are secondary to spontaneous mutations.42 Fibrillin is one of the major structural components of the elastic fiber.43 The resulting abnormal elastic fibers are prone to disruption and result in histologic findings consistent with cystic medial degeneration at an early age.30 Seventy-five to eighty-five percent of patients with Marfan syndrome have dilation of the aortic sinuses and annulus in addition to the ascending aorta. This morphology, referred to as annuloaortic ectasia, is the classic presentation of Marfan syndrome, but can occur in the absence of a known connective tissue disorder. Because of the frequent aortic root involvement, aortic insufficiency is common.44 One third of patients with Marfan syndrome also have mitral regurgitation.44

EHLERS-DANLOS SYNDROME

Ehlers-Danlos syndrome is an inherited disorder of connective tissue with multiple subtypes. Type IV Ehlers-Danlos may be associated with life-threatening cardiovascular manifestations.45 Spontaneous arterial rupture is the most common cause of death and usually involves the mesenteric vessels.45 Less commonly, patients develop abdominal or thoracic aortic aneurysms or dissections.46,47 Surgical treatment is challenging because of the friable nature of the vascular tissue.

FAMILIAL ANEURYSMS

Certain families, without phenotypic expression of Marfan syndrome, exhibit strong histories of ascending aortic aneurysm formation and dissection transmitted in an autosomal dominant fashion. In a recent study of 15 such families, 9 demonstrated evidence of linkage to the 5q locus, although the specific gene and product have not been identified.26 None of the 15 families demonstrated linkage to the fibrillin gene. Further investigation will likely reveal other examples of more subtle inherited or spontaneously occurring disorders of metabolism that result in accelerated deterioration of the aortic wall.

Atherosclerosis

Atherosclerosis is less commonly seen in ascending aortic aneurysms than in descending thoracic or abdominal aortic aneurysms. It has long been theorized that the development of invasive atheromas results in destruction of elastic fibers and smooth muscle cells in the media, resulting in weakening and dilation.19 This process was proposed as the primary etiology of descending thoracic and abdominal aortic aneurysms, and the second most common cause of ascending aortic aneurysms.19,48 These theories are now challenged by the concept that atherosclerosis is a concomitant process that infiltrates a diseased media with altered barriers.49 This would explain the divergent course of the atherosclerotic abdominal aorta towards obstructive versus aneurysmal disease.

Aneurysms Associated with Aortic Dissection

Patients who survive acute dissection of the ascending aorta often have or will develop an associated aneurysm. The rate of expansion is higher than other types of ascending aortic aneurysms as the barrier to dilation and rupture is only the outer one third of the media and the adventitia.19,50 Aortic dissection is discussed in Chapter 45.

Aneurysms Associated with Aortic Valve Disease

Bicuspid and unicuspid aortic valves are associated with ascending aortic aneurysm formation. Although initially thought to be secondary to poststenotic dilation, a primary structural abnormality of the aortic wall appears contributory. Aortic enlargement occurs at an accelerated pace in congenitally stenosed valves compared to trileaflet valves with equivalent degrees of stenosis.27,51 Aortic dissection occurs in patients with bicuspid aortic valves at a rate 10-fold the normal population, a trend that is not found in other forms of aortic stenosis.22 This strongly implies an inherent weakness in the aortic wall.

Infection

BACTERIAL (MYCOTIC) ANEURYSMS

True primary bacterial infection of the ascending aortic wall resulting in aneurysm formation is rare. This is believed to occur either after an episode of bacterial endocarditis or from an aortic jet lesion causing endothelial trauma.52 The most common organisms include, in order of decreasing frequency, Staphylococcus aureus, Staphylococcus epidermidis, Salmonella, and Streptococcus.53 Infection of laminar clot within a previously formed aneurysm may also occur after transient bacteremia.53

SYPHILITIC ANEURYSMS

Syphilitic aortitis, caused by the spirochete Treponema pallidum, was once the most common cause of ascending aortic aneurysms. It has now become a rarity in developed countries because of effective antibiotic therapy. In this disease an obliterative endarteritis of the vasa-vasorum results in ischemic injury to the aortic media with subsequent destruction of elastic and muscular elements.30 The media is replaced by a thickened fibrous tissue, which begins to dilate. This process most commonly involves the ascending aorta and arch,54 but may involve the root as well. If the regions of the coronary ostia are involved, significant coronary obstruction may occur.1 Antibiotic therapy does not reverse the vascular pathology.

Arteritis

Takayasu's arteritis most commonly involves the aortic arch and its major branches, but may involve any or all segments of the aorta. Takayasu's usually produces obstructive lesions, but may have a dilative component in 15% of cases.55 Giant cell arteritis (temporal arteritis) may lead to weakening of the aortic wall and eventual aneurysm formation or dissection.56,57 In one population-based study temporal arteritis was associated with a greater than 17-fold increase in the risk of developing a thoracic aneurysm.58

Trauma

Chronic traumatic aneurysms of the ascending aorta are rare. Although the ascending aorta is the site of rupture in 20% of blunt aortic injuries, survival beyond the initial injury is unusual, with the patient usually succumbing to acute cardiac tamponade.59 This subject is covered in Chapter 51.

Pseudoaneurysms

The wall of a pseudoaneurysm is composed primarily of adventitia, thrombus, and surrounding structures.30 Postoperative pseudoaneurysms may occur at an aortic suture line or at the site of aortic cannulation. Causes include technical error, acute dissection, native tissue degeneration, or deterioration of the graft or suture material.60,61 The use of modern monofilament suture and low-porosity collagen- or gelatin-impregnated Dacron grafts,62 as well as the abandonment of the inclusion cylinder technique,63,64 have lessened the incidence of this complication. Less commonly, pseudoaneurysms of the ascending aorta occur after trauma or infection.


?? NATURAL HISTORY
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General

The appropriate application of surgical treatment depends upon an understanding of the relative risks of surgery versus the natural history of the disease. The natural history of untreated aneurysms of the thoracic aorta often concludes with patient death because of rupture or dissection. Figure 46-1 shows the estimated actuarial survival curve for 72 patients who were diagnosed with thoracic aneurysms from 1951 to 1980 and were followed nonoperatively. Seventy-four percent of the patients experienced rupture, and 94% of these patients died.19 The potential for complications of rupture or dissection is primarily dependent upon size and the underlying etiology of the aneurysm.



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FIGURE 46-1 Actuarial survival estimates of 72 patients followed nonoperatively with thoracic aneurysms and dissections. (Reproduced with permission from Bickerstaff LK, Pairolero PC, Hollier LH, et al: Thoracic aortic aneurysms: a population-based study. Surgery 1982; 92:1103.)

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Size

Based on the law of Laplace, wall tension increases as the diameter of an aneurysm increases. It is therefore intuitive that larger aneurysms have a greater risk of rupture. This was first established for abdominal aortic aneurysms by Szilagyi et al in 1966.65 Subsequent natural history studies have confirmed this finding and have found also that larger aneurysms have a higher rate of expansion.66,67 Coady et al68 have written extensively on the natural history of thoracic aortic aneurysms. The incidence of acute dissection or rupture according to size in their cohort of patients is shown in Figure 46-2. Logistic regression analysis revealed a 4.3-fold increased risk of rupture or dissection in an aneurysm 6.0 to 6.9 cm in diameter compared to an aneurysm 4.0 to 4.9 cm in diameter. Growth rates varied from 0.08 cm per year for aneurysms less than 4.0 cm to 0.16 cm per year for aneurysms greater than 8.0 cm in diameter. Mean growth rates as great as 0.42 cm per year have been reported in other series.69,70 Dapunt et al 50 also noted an increased rate of growth in smokers and patients with a history of hypertension.



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FIGURE 46-2 The incidence of acute dissection or rupture of thoracic aneurysms according to size. The height of the column corresponds to the total number of patients and the black area to the proportion of patients who suffered complications of dissection or rupture. (Reproduced with permission from Coady MA, Rizzo JA, Elefteriades JA: Developing surgical intervention criteria for thoracic aortic aneurysms. Cardiol Clin 1999; 17:827.)

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The Influence of Etiology on Natural History

MARFAN SYNDROME

Although size criteria are perhaps most important, the underlying etiology must be considered. Patients with Marfan syndrome have accelerated aneurysm growth and tend to rupture or dissect at smaller sizes.71 This is particularly true for those with a family history of early complications.71 The average age of death for untreated patients with Marfan syndrome is 32 years72 with complications of the aortic root being responsible for 60% to 80% of these deaths.44,72

FAMILIAL ANEURYSMS

The inheritance of aneurysmal disease without an associated phenotypic syndrome such as Marfan syndrome was first noted for abdominal aortic aneurysms.73,74 In 1997 familial aggregation of thoracic aneurysms was noted by Biddinger et al.75 Coady et al76 estimated that 19% of their study population fit criteria for familial aneurysms by pedigree analysis. The primary mode of inheritance was autosomal dominant, but X-linked and recessive patterns were also evident in some cases. This subgroup had an annual growth rate almost double the growth rate for the entire population.

AORTIC DISSECTION

In chronic dissections, the barrier to rupture is the outer third of the media and the adventitia. Dissections are therefore associated with an accelerated rate of expansion and rupture. Comparisons between dissecting and nondissecting thoracic aneurysms of similar size have revealed as much as a 6-fold greater growth rate for dissections.21

SYPHILITIC ANEURYSMS

The average time from the diagnosis of advanced syphilis to cardiovascular symptoms is 10 to 20 years.1 The average survival from the onset of cardiac symptoms is only six to eight months.1 Saccular aneurysms, which are common in this disease, may have a more rapid rate of expansion and greater risk of rupture.77 Dissection is less likely because of the scarring that occurs within the media.30 Modern studies of growth rates and size at the time of rupture are not feasible because of the rarity of this condition


?? CLINICAL PRESENTATION
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Signs and Symptoms

Many ascending aortic aneurysms are asymptomatic when diagnosed, being incidentally noted on chest x-ray or other imaging study.24 Echocardiographic evaluation of aortic insufficiency is also a frequent mode of diagnosis. Between 25% and 75% of patients, however, present with chest pain that results in the diagnosis of an aneurysm.24,78,79 Pain from the ascending aorta is usually localized to the anterior chest. The pain may be acute in onset signifying impending rupture, or a chronic gnawing pain from compression of the overlying sternum. Occasionally signs of superior vena caval or airway compression are present.79 Less commonly, aneurysms of the ascending aorta or aortic root can rupture into the right atrium or the superior vena cava, presenting with high output cardiac failure or into the lungs with ensuing hemoptysis. Hoarseness resulting from stretch injury of the left recurrent laryngeal nerve suggests involvement of the distal aortic arch or proximal descending thoracic aorta. In contrast, dissection of the ascending aorta presents with severe "tearing" pain in 75% of patients.23,24

Physical Examination

In the case of rupture, the patient will present in extremis. In a patient without rupture, the examination is often unremarkable. If the sinotubular ridge or aortic root is dilated, a widened pulse pressure or diastolic murmur signifying aortic insufficiency may be noted. If dilation is isolated to the ascending aorta, however, the aneurysm can reach large dimensions without producing physical findings. A thorough vascular exam should be carried out to look for any concomitant peripheral vascular disease, carotid disease, or sequelae of distal embolization. Abdominal aortic aneurysms are present in 10% to 20% of patients with atherosclerotic involvement of an ascending aortic aneurysm,23,80 and this should also be sought on physical examination. In rare cases, aneurysms may cause compression necrosis of the overlying sternum and ribs. Syphilitic aneurysms have been noted to erode through the chest wall and rupture externally.1


?? DIAGNOSTIC STUDIES
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Electrocardiogram

With significant aortic insufficiency, left ventricular hypertrophy or strain is evident. Patients with generalized atherosclerosis may show evidence of concomitant coronary artery disease, or previous myocardial injury.

Chest Radiography

Many asymptomatic ascending aortic aneurysms are first detected on chest x-ray. The enlarged ascending aorta produces a convex contour of the right superior mediastinum (Fig. 46-3A). In the lateral view, there is loss of the retrosternal air space (Fig. 46-3B). Aneurysms confined to the aortic root can be obscured by the cardiac silhouette and may not be evident on chest radiograph.81



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FIGURE 46-3 PA and lateral chest radiograph of a patient with an ascending aortic aneurysm. The PA view (A) shows convexity of the right mediastinum, and the lateral view (B) shows loss of the normal retrosternal air space. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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Echocardiography

Ascending aortic aneurysms are the most common cause of isolated aortic insufficiency,82 and therefore aneurysms are frequently detected during evaluation of a regurgitant aortic valve. Transesophageal echocardiography (TEE) can accurately detect and differentiate between ascending aortic aneurysms, dissections, and intramural hematoma.83 Imaging of the distal ascending aorta is obscured by air in the tracheobronchial tree with up to 40% of its distal extent not well visualized.84 Transthoracic echocardiography is far less reliable.78

Aortography

Aortography provides precise delineation of the aortic lumen, and certain diseases have very characteristic arteriographic patterns. Annuloaortic ectasia has a "pear-shaped" morphology (Fig. 46-4) with prominent dilation of the aortic sinuses and less severe dilation of the ascending aorta tapering to normal caliber at the origin of the innominate artery. Pseudoaneurysms appear as saccular outpouchings with an irregular contour.85 Syphilitic aneurysms involving the aortic root are often associated with coronary ostial stenosis.30



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FIGURE 46-4 Aortic angiogram of patient with classic annuloaortic ectasia. The aortic root is dilated and the ascending aorta tapers to a normal caliber at the origin of the innominate artery giving the classic "pear-shaped" morphology. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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One of the beneficial aspects of aortography is accurate demonstration of the relationship of the aneurysm to the arch vessels. Aortography also detects aortic regurgitation and cephalad displacement of the coronary ostia. In patients over the age of 40 or with a pertinent history, the opportunity is afforded to check for coronary disease and left ventricular dysfunction. Disadvantages include contrast and radiation exposure, puncture site complications, underestimation of aneurysm size in the presence of laminar clot, and the likelihood of missing dissections.

Computed Tomography

Contrast-enhanced computed tomography (CT) provides rapid and precise evaluation of the ascending aorta (Fig. 46-5). CT scanning detects areas of calcification, and accurately identifies dissections and mural thrombus. When laminar clot is present, CT scanning provides a more accurate assessment of aneurysm size than aortography. However, because structures are visualized in an axial view only, the diameter of a tortuous aorta can be grossly overestimated. Three-dimensional reconstruction of CT scans may prove useful in determining the proximal and distal extent of aortic disease relative to the arch vessels, which can aid the surgeon in operative planning.78



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FIGURE 46-5 Computed tomographic scan of an 8-cm ascending aortic aneurysm. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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Magnetic Resonance Imaging

The benefits of magnetic resonance imaging (MRI) over CT scanning include visualization in the sagittal and coronal planes (Fig. 46-6), and the avoidance of contrast and radiation exposure. Cardiac imaging with MRI is evolving, and may provide evaluation of cardiac perfusion, myocardial function, and coronary and valve anatomy with a single modality in the future.8688 Currently, however, MRI is expensive, less readily available, and more time consuming than CT scanning.



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FIGURE 46-6 Magnetic resonance image of ascending aortic aneurysms demonstrating saggital (A) and coronal (B) views. The origin of the innominate and its relationship to the distal portion of the aneurysm can be appreciated on the saggital view. (Images provided courtesy of Kent E. Yucel, M.D.)

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?? INDICATIONS FOR OPERATION
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Symptoms

Emergent operation is indicated in the setting of acute ascending aortic dissection or rupture. Ascending aortic aneurysms rupture into the pericardial space and result in death from acute cardiac tamponade. Aortic dissections may rupture or may compromise coronary or cerebral circulation. Operative mortality is significant in this setting, but death is certain in the case of rupture and probable in the case of acute dissection if not surgically addressed.

Symptomatic aortic insufficiency or stenosis may be the primary indication for operation. When replacing or repairing a diseased valve a decision must be made regarding the moderately dilated aorta. Michel et al 89 reported that 25% of patients undergoing surgery for aortic insufficiency who had ascending aortic diameters greater than 4 cm required subsequent operation for aortic replacement. Prenger et al 90 reported a 27% incidence of aortic dissection following aortic valve replacement in patients with aortic diameters greater than 5 cm. Based on these findings it is recommended that aortic diameters of 4 to 5 cm be dealt with at the time of aortic valve surgery. Further incentive for earlier surgery is the improved possibility of native valve preservation.

Size/Growth Rate

Because the diameter of an aneurysm strongly correlates with the risk of rupture or dissection, size has long been used as the criteria for elective surgical intervention. Although size criteria for the abdominal aorta have been well established and generally agreed upon, less of a consensus has emerged for the thoracic aorta. Variable growth rates and propensities for rupture in different regions of the thoracic aorta and with different underlying pathologies are perhaps to blame. The average size of rupture of the thoracic aorta reported in the literature is highly variable.50,91,92 Coady et al68 report rupture or dissection at a median size of 5.9 cm in the ascending aorta (Fig. 46-7 and 7.2 cm in the descending aorta. Because intervention at these diameters would have by definition resulted in rupture or dissection in 50% of patients, preemptive surgical therapy at 5.5 cm and 6.5 cm, respectively, for ascending and descending aneurysms seems appropriate.



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FIGURE 46-7 Logistic regression analysis of initial aneurysm size for risk of rupture or dissection. The probability of rupture or dissection is 25% higher in patients who present with aneurysms 6.0 cm or larger versus a comparison group with aneurysms 4.0 to 4.9 cm in diameter. Six centimeters appears to be a "hinge point" beyond which the risk of complications greatly increases. (Reproduced with permission from Coady MA, Rizzo JA, Hammond GL, Kopf GS, Elefteriades JA: Surgical intervention criteria for thoracic aortic aneurysms: a study of growth rates and complications. Ann Thorac Surg 1999; 67:1922.)

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As opposed to absolute size criteria, some surgeons prefer the use of ratios of measured to expected size. The expected size is based on the body surface area and age of the patient. The ratio indicating intervention is adjusted based on the underlying etiology. Ergin et al93 advocate a ratio of 1.5 for the average patient with an asymptomatic incidentally discovered ascending aortic aneurysm. This leads to intervention at a size of only 4.8 to 5.0 cm in an adult less than 40 years of age with a body surface area of 2 m2. Because the ascending aorta normally increases in size with age, the diameter for intervention would be higher in a patient more than 40 years old.

The rate of expansion is also an important consideration. Reported mean growth rates of thoracic aneurysms vary from 0.10 to 0.42 cm per year.50,69,70,9496 The rate of expansion is usually greater in the descending aorta and in conditions with a weakened aortic wall, such as Marfan syndrome or chronic dissection.68 Growth at a rate of greater than 1.0 cm per year is certainly an accepted indication for surgical intervention,50 but more often the rate of dilation is used by the surgeon as supplementary information that helps to guide the timing of surgery rather than serve as an absolute indication.

The Influence of Etiology

Patients with Marfan syndrome or with familial aneurysms, particularly when there is a history of early dissection or rupture, should undergo earlier intervention. Gott et al 97,98 recommend intervention in patients with Marfan syndrome at an ascending aortic diameter of 5.0 to 6.0 cm. Coady et al99 recommend intervention at 5.0 cm. Ergin et al93 recommend a measured to expected size ratio of 1.3. Patients with chronic dissection should be considered to have similar intervention criteria as those with Marfan syndrome. Patients with bicuspid and unicuspid aortic valves are probably at intermediate risk, and Ergin et al93 recommend intervention at a ratio of 1.4 in these patients. Pseudoaneurysms are at a high risk of rupture and should be treated when discovered.


?? PREOPERATIVE PREPARATION
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A careful preoperative evaluation of the patient is important to minimize the risks of surgery. Nearly one third of patients undergoing surgery for thoracic aortic disease have chronic obstructive pulmonary disease.80 Patients with suspect pulmonary function should have spirometery and room air arterial blood gases. Smoking cessation, antibiotic treatment of chronic bronchitis, and chest physiotherapy may prove beneficial in elective situations. Normal renal function should be ensured with the appropriate blood work, and abnormal results should prompt further investigation. Because unaddressed severe carotid disease is a risk factor for stroke during ascending aortic operations,100 patients over the age of 65 should have duplex imaging of their carotids. Younger patients with peripheral vascular disease, extensive coronary artery disease, carotid bruits, or history suspicious for cerebral ischemia should be investigated as well.101 Abdominal aortic aneurysms occur in 10% to 20% of patients with ascending aortic aneurysms.23,80 Patients with "atherosclerotic aneurysms" that extend into the aortic arch have a greater than 50% probability of having distal thoracic or abdominal aortic aneurysms.80 CT or MRI of the abdominal aorta is indicated if disease is suspected.


?? CHOICE OF PROCEDURE
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The specific procedure that is performed depends on the distal extent of aortic involvement, condition of the aortic root and the aortic valve, underlying pathology, life expectancy of the patient, desired anticoagulation status, and surgeon preference. Specific procedures and their indications are listed in Table 46-1.


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TABLE 46-1 Specific procedures and indications

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Ascending Aortic Aneurysms

Ascending aortic aneurysms with normal sinuses and aortic annulus require only replacement of the ascending aorta from the sinotubular ridge to the origin of the innominate artery with a Dacron tube graft. If the aortic valve is diseased, this can be replaced separately. The sinuses in patients with Marfan syndrome should not be preserved because of the frequent need for reoperation (Fig. 46-8).102,103



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FIGURE 46-8 Actuarial estimate of freedom from late aortic root aneurysm for patients with and without Marfan syndrome who have undergone ascending aortic operations (p<.0001>Reproduced with permission from Yun KL, Miller DC: Ascending aortic aneurysm and aortic valve disease: what is the most optimal surgical technique? Semin Thorac Cardiovasc Surg 1997; 9:233.)

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Annuloaortic Ectasia

COMPOSITE VALVE-GRAFT CONDUIT

Patients who have significant dilation of the aortic root in addition to an aneurysm of the ascending aorta or patients with Marfan syndrome should undergo replacement of the ascending aorta and root. This is usually done with a composite graft consisting of a mechanical valve inserted into a collagen- or gelatin-impregnated Dacron graft that comes preassembled. The coronary arteries are reimplanted as buttons.

AORTIC ALLOGRAFT

The ascending aorta and root can be replaced with an aortic allograft with coronary reimplantation.104 Accepted indications include patients with endocarditis, women anticipating pregnancy, young adults with active lifestyles, or patients with any other contraindications to anticoagulation.105

PULMONARY AUTOGRAFTS (ROSS PROCEDURE)

A pulmonary autograft can be used to replace the aortic root and proximal ascending aorta. More distal replacement of the ascending aorta requires addition of a Dacron graft. The Ross procedure is most commonly performed for congenital surgery because of the proposed growth potential of the autograft. The use of the Ross procedure in adults with aneurysmal disease is more controversial. Potential indications include young adults with active lifestyles and life expectancies exceeding 15 to 20 years, women anticipating pregnancy, or patients with any contraindication to warfarin therapy.105 The Ross procedure is contraindicated in patients with Marfan syndrome or inherited weakness of the aortic wall that may affect durability of the autograft.105,106

VALVE-SPARING PROCEDURES

If the aortic valve leaflets are grossly normal and aortic insufficiency is secondary to dilation of the sinotubular ridge or aortic root, then the native valve can often be spared.107,108 Yacoub has been able to apply valve-sparing techniques in almost 80% of patients operated on for ascending aortic aneurysms.109 A variety of procedures are used to preserve the aortic valve. Reduction of the diameter of the sinotubular ridge via ascending aorta replacement110 may be all that is required to correct central insufficiency. If the aortic root is involved, it may be completely replaced by inserting the scalloped native valve into a Dacron graft,111 or dilated sinuses may be individually remodeled with tongues of the proximal Dacron graft.112 If significant annular dilation is present, an aortic annuloplasty can be performed with the external application of a strip of graft material.113 The application of valve-sparing procedures to patients with Marfan syndrome is controversial as the durability of the leaflets is in question.114 These procedures are discussed in detail in Chapter 31.

ALTERNATIVE PROCEDURES

In older patients who are high risk, or who have limited life expectancy, external wrapping of the aorta or separate valve and ascending aorta replacement may be appropriate without addressing the aortic root.93,103,115

Management of Associated Conditions

CORONARY ARTERY DISEASE

Twenty-five percent of patients undergoing surgery for ascending aortic aneurysms will have concomitant coronary artery disease.80 These patients should have appropriate bypass grafting performed at the time of ascending aneurysm surgery.

MITRAL VALVE DISEASE

Mitral valve disease is frequently encountered in patients with aortic aneurysms. This is particularly true for patients with Marfan syndrome, where the incidence approaches 30%.44 Patients who have evidence of moderate to severe mitral regurgitation should undergo mitral valve repair or replacement at the time of aortic replacement.61,116 Gilinov et al 117 reported results of mitral valve repair in patients with Marfan syndrome, many of whom also had simultaneous replacement of the aortic root. They observed an 88% actuarial rate of freedom from significant mitral regurgitation at 5 years.


?? OPERATIVE TECHNIQUE
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General

MONITORING AND ANESTHESIA

Venous access consists of two large-bore peripheral lines and a central line. We monitor filling pressures and cardiac output with a pulmonary artery catheter. A radial artery line provides blood pressure monitoring and determination of activated clotting times. Systemic temperature is monitored with nasopharyngeal and bladder probes. Transesophageal echocardiographic assessment of myocardial and valvular function is routine. Anesthesia is maintained with isoflurane and intravenous fentanyl.

INCISION

A median sternotomy is the preferred incision. Extension into the left 4th or 5th interspace facilitates exposure of the distal aortic arch or descending aorta when required.

PERFUSION

Cannulation is performed following heparinization (350 U/kg) and confirmation of an activated clotting time greater than 450 seconds. If the distal ascending aorta is not involved, this region or the proximal arch is cannulated. The aortic cannulation site must allow enough room proximally for the cross-clamp and a sufficient cuff of aortic tissue to sew to, while still allowing all diseased aorta to be resected. Epiaortic ultrasound assists in finding safe areas for clamping and cannulation. If the arch is involved and circulatory arrest will be required, the femoral artery or the aneurysm itself is cannulated. Before retrograde perfusion of the femoral artery is considered, however, TEE assessment of the descending aorta is performed. Venous cannulation is performed with a 21F or 24F two-stage cannula in the right atrial appendage. The superior and inferior vena cavae are cannulated separately if circulatory arrest or mitral valve intervention will be required. This allows for retrograde cerebral perfusion and a transeptal approach to the mitral valve.

The cardiopulmonary bypass circuit is primed with lactated Ringer's and 25 g of mannitol. No glucose is added to the prime to prevent exacerbation of neurological injury.118 The cannulas are attached, and low-flow cardiopulmonary bypass is initiated. A left ventricular vent is inserted via the right superior pulmonary vein and a balloon-tipped catheter is inserted into the coronary sinus for retrograde cardioplegia delivery. Cardiopulmonary bypass flow is increased to 2.2 to 2.5 L/min/m2 and moderate systemic hypothermia (28?C) and hemodilution (hematocrit 15%25%) are established.

MYOCARDIAL PROTECTION

Cold blood hyperkalemic cardioplegia (4?C) is given antegrade into the aortic root at a rate of 300 mL/min for 2 minutes and then retrograde at a rate of 200 mL/min for an additional 2 minutes. A cooling jacket may be used to facilitate this process. If the aortic valve is grossly incompetent, and prompt arrest is not achieved with retrograde cardioplegia, the aorta is opened and the coronary ostia are cannulated directly. During the procedure, retrograde cardioplegia is administered every 20 minutes.

CHOICE OF GRAFT

Woven double velour Dacron grafts impregnated with collagen or gelatin are relatively impervious to blood and have excellent handling characteristics. If root replacement is required, prefabricated composite grafts with mechanical valves are available. Bioprosthetic valves can be inserted into a Dacron graft if desired. The indications for pulmonary autograft or aortic allograft use have been previously discussed.

Specific Operative Techniques

REPLACEMENT OF THE ASCENDING AORTA

After cardiopulmonary bypass is established the aorta is clamped just proximal to the innominate artery, and the heart is arrested with cold blood cardioplegia. The aorta is transected below the clamp leaving a sufficient cuff for subsequent anastomosis (Fig. 46-9A). The proximal aorta is then transected just above the commissures. An appropriately sized Dacron graft is selected and sewn to the distal aorta with a continuous 3-0 or 4-0 polypropylene, incorporating a strip of felt (Fig. 46-9B). If required, the aortic valve is replaced at this time (Figs. 46-9C and 46-9D). The proximal anastomosis is performed in the same fashion after the graft is cut to the appropriate length (Figs. 46-9E and 46-9F). The graft is de-aired and the patient is weaned from cardiopulmonary bypass. After decannulation and protamine administration, suture line hemostasis is ensured.




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FIGURE 46-9 Illustration of simple aortic tube graft placement with separate replacement of the aortic valve. (A) The aorta is clamped proximal to the innominate artery (aortic perfusion cannula not shown) and the diseased aorta is resected down to just above the aortic valve commissures. (B) A Dacron graft is sewn to the distal aorta with a 3-0 or 4-0 polypropylene suture reinforced with a strip of Teflon felt. (C) If aortic valve replacement is indicated, the diseased valve is excised. (D) The valve is replaced with the valve of the surgeon's choice.

(E, F) The graft is sewn to the proximal aorta with 3-0 or 4-0 polypropylene reinforcing the aortic tissue with a strip of Teflon felt. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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REPLACEMENT OF THE ASCENDING AORTA AND AORTIC ROOT WITH A COMPOSITE VALVE-GRAFT CONDUIT

After establishing cardiopulmonary bypass, the aorta is clamped just proximal to the innominate artery and the heart is arrested with cold blood cardioplegia. The aorta is transected beneath the clamp ensuring an adequate cuff of aortic tissue. Proximally the aortic root is excised leaving only buttons of aortic tissue surrounding each of the coronary arteries (Fig. 46-10A). The coronaries are mobilized for 1 to 2 cm to prevent tension during reimplantation. A composite graft is selected based on the size of the aortic annulus. The sewing ring of the composite graft is sutured to the annulus with 2-0 pledgeted polyester mattress sutures placed immediately adjacent to each other (Fig 46-10B). The adjacent placement of sutures and the selection of a conduit that snugly fits within the annulus help to ensure hemostasis. Openings for coronary reimplantation are made in the appropriate position in the Dacron graft with an ophthalmic cautery (Fig. 46-10C). First the left and then the right coronary arteries are attached using 4-0 or 5-0 polypropylene suture in continuous fashion incorporating a thin strip of felt (Fig. 46-10D). The distal anastomosis is then performed with a continuous 3-0 or 4-0 polypropylene suture also incorporating a strip of felt. The graft is vented with a needle and the left atrium and ventricle are de-aired. After the patient is decannulated and protamine has been administered, suture line hemostasis is scrutinized.



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FIGURE 46-10 Illustration of insertion of a composite valve-graft conduit with coronary artery reimplantation. (A) A full-thickness button of aortic wall adjacent to each coronary ostium is fashioned. The aortic valve and sinuses are then excised. (B) Pledgeted 2-0 braided polyester sutures are placed in the supra-annular position and immediately adjacent to one another to ensure a watertight closure. The sutures are placed in the upper half of the sewing ring helping to seat the valve deep within the aortic annulus. Note that no knots or suture material are exposed to the bloodstream. (C) Ophthalmic cautery is used to create an orifice in the graft in the appropriate position for left coronary reimplantation. (D) The left coronary anastomosis is performed first with a continuous 4-0 or 5-0 polypropylene suture incorporating a thin strip of felt. The right coronary anastomosis is then performed in a similar fashion. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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REPLACEMENT OF THE ASCENDING AORTA AND AORTIC ROOT WITH AN ALLOGRAFT OR AUTOGRAFT

The muscular tissue at the base of the conduit is sutured to the aortic annulus with a continuous or interrupted 4-0 polypropylene or braided synthetic suture. The suture line is reinforced with a strip of Dacron or pericardium. Coronary ostia are created and coronary buttons are inserted with a continuous 4-0 or 5-0 polypropylene suture. Extension with a Dacron tube graft may be required to successfully replace the entire diseased aorta.

OPEN TECHNIQUE FOR DISTAL ANASTOMOSIS

The distal aortic anastomosis may need to be sewn under circulatory arrest as an "open technique" if clamping of the distal ascending aorta is not safe, or if partial or complete arch replacement is indicated. Clamping may be dangerous because of atherosclerotic disease or clot, or may not be possible because of the distal extent of the aneurysm. Cardiopulmonary bypass is initiated with femoral artery cannulation or direct cannulation of the ascending aneurysm depending on the indication for circulatory arrest. The typical cardiopulmonary bypass setup for a case requiring circulatory arrest is shown in Figure 46-11A. Central nervous system protection is enhanced by maintaining the blood glucose below 200 mg/dL, as well as by the administration of methylprednisolone (7mg/kg) and thiopental (715 mg/kg). Mannitol (0.30.4 g/kg) and furosemide (100 mg) are given for renal preservation. Once nasopharyngeal temperature reaches 15?C and the electroencephalogram has been isoelectric for 5 minutes, the patient is placed in Trendelenburg position and the circulation arrested. Approximately 25% of the patient's volume is drained into the venous reservoir. The superior vena cava is clamped to raise central venous pressure prior to opening the aorta to prevent air embolism.




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FIGURE 46-11 Schematic representation of the cardiopulmonary bypass circuit used for circulatory arrest when a portion or all of the aortic arch is to be replaced, or when it is unsafe to clamp the ascending aorta. (A) Cardiopulmonary bypass is established using two vena cava cannulas and a femoral artery cannula. A shunt connecting the venous and arterial lines is clamped. (B) The arterial and inferior vena caval lines are clamped and the shunt is opened allowing retrograde cerebral perfusion of cold oxygenated blood through the superior vena cava cannula. Air and atherosclerotic debris are evacuated from the brachiocephalic arteries (inset). A separate 8-mm Dacron graft is sewn to the side of the Dacron graft to allow antegrade reperfusion of the brain once the distal anastomosis is done.

(C) Cardiopulmonary bypass is reestablished in an antegrade fashion. The femoral arterial cannula is removed and the shunt is occluded. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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The aorta is divided distally in a region dictated by the distal extent of disease. If the aneurysm ends at the takeoff of the innominate artery, the aorta can be transected here and the graft sewn, leaving the arch intact. If the aneurysm extends to the proximal undersurface of the arch, the distal end of the graft is beveled to conform to the resected surface of the arch (Fig. 46-11B). If the arch in the region of the origin of the brachiocephalic vessels is involved, then the aorta is divided distal to the origin of the left subclavian artery. The distal anastomosis is performed with a running 3-0 polypropylene suture enforced with a felt strip. An elliptical portion of the graft is then excised which corresponds to a single island of aortic tissue that has been fashioned around the origin of the brachiocephalic vessels. This anastomosis is performed with felt-enforced running 3-0 polypropylene sutures as well. During this anastomosis, slow retrograde perfusion of the superior vena cava is performed to remove any air or particulate debris (Fig. 46-11B). Antegrade perfusion is then initiated via direct cannulation of the graft or insertion of a cannula into a previously placed 8-mm side graft (Fig. 46-11C). Femoral perfusion is not resumed in order to prevent cerebral embolization of distal aortic debris that may have occurred during previous manipulations.

The patient is rewarmed, and any additional procedures that are required such as coronary revascularization or mitral valve interventions are performed now that cerebral circulation has been restored. The proximal graft is sewn to the ascending aorta just above the sinotubular ridge or the aortic annulus in the case of composite graft placement. Thorough de-airing is performed and the patient is weaned from cardiopulmonary bypass. After protamine, suture lines are inspected closely.

CABROL TECHNIQUE FOR REESTABLISHING CORONARY FLOW

Avoidance of tension at the site of coronary reimplantation after aortic root replacement is essential to prevent postoperative bleeding and pseudoaneurysm formation. In the Cabrol technique, a single 8- to 10-mm Dacron graft is anastomosed end-to-end to the coronary arteries and then the mid segment of the coronary graft is anastomosed side-to-side to the aortic graft (Fig. 46-12). This technique is often required when the coronary ostia are low or when there is scarring from a previous operation preventing adequate mobilization. Tension on the left coronary anastomosis is more common, and a small Dacron interposition graft may be required on this side in isolation in certain cases.



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FIGURE 46-12 Classic Cabrol technique for coronary reimplantation. (A) An 8- to 10-mm Dacron tube graft is anastomosed end-to-end to the aortic tissue surrounding the left and right coronary ostia. (B) An opening is made in the mid portion of the coronary graft and in an appropriate position in the aortic graft and an anastomosis is formed. The modified Cabrol technique involves the formation of individual coronary buttons allowing the small caliber Dacron graft to be sewn to the full thickness of the aortic tissue surrounding the coronary ostia. (Reproduced with permission from Downing SW, Kouchokos NT: Ascending aortic aneurysm, in Edmunds LH Jr (ed): Cardiac Surgery in the Adult. New York, McGraw-Hill, 1997; p 1163.)

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REOPERATION ON THE ASCENDING AORTA AND AORTIC ROOT

Reoperative surgery on the ascending aorta and aortic root can be particularly challenging, but is becoming more frequent. Because of improved outcomes,61,64,100,119,120 the criteria for treatment of ascending aortic disease have been liberalized to include more elderly patients and more patients who have had previous cardiac surgery.121,122 Increasing use of allografts, pulmonary autografts, and valve-preserving techniques may also result in an increased need for subsequent reintervention as these patients age. Indications for reoperation include aortic insufficiency, development of aneurysms or dissections in remaining segments of the thoracic aorta, false aneurysms, prosthetic valve malfunction or infection, or degeneration of biologic prostheses.121

To maximize safety, preemptive femoral exposure or cannulation is required. In the case of large pseudoaneurysms or grafts tethered to the posterior sternal wall, significant blood loss may be unavoidable upon entry. In such situations it is necessary to go on "pump-sucker bypass" until structures are dissected out and bleeding is controlled. Fifty percent of patients undergoing reoperation have significant aortic insufficiency, making myocardial preservation more challenging. In such cases, the perfusate temperature must not be reduced until exposure is sufficient to allow either clamping of the aorta or venting in order to prevent fibrillation and distension of the left ventricle. Reimplantation of coronary buttons in the case of root replacement is often not possible without use of a modified Cabrol technique or an interposition graft.

Management of Complications

BLEEDING

Woven Dacron grafts impregnated with collagen or gelatin are relatively impervious to blood and have reduced blood loss following replacement of the ascending aorta. Anastomotic bleeding is lessened with the use of Teflon pledgets at the aortic and coronary anastomoses. When composite valve-graft insertion is indicated, choosing a valve size that snugly fits the annulus and placing mattress stitches immediately adjacent to each other are helpful. Tension must be avoided at the sites of coronary reimplantation, as this is a frequent site of bleeding. The modified Cabrol method or an interposition graft should be used when any tension is present. The inclusion technique of graft insertion is associated with an increased incidence of bleeding and pseudoaneurysm formation and has largely been abandoned.61,123,124 All coronary and aortic anastomoses should be sewn to the full thickness of the aorta, and wrapping of the graft with residual aorta is not indicated. After the administration of protamine, all anastomoses must be evaluated closely.

Suspected coagulopathy should be documented by laboratory tests and treated accordingly. In cases of refractory coagulopathy, the anastomosis can be wrapped tightly with a small segment of Dacron to reduce tension on the suture line and reduce needle hole bleeding. Homologous blood donation can be avoided in a significant number of patients with the use of blood conservation techniques such as cell savers, autologous blood donation, platelet pheresis, the reinfusion of chest tube drainage, and the use of antifibrinolytics.64

STROKE

Neurologic injury following proximal aortic surgery remains a significant cause of morbidity and mortality. Embolization of atherosclerotic debris or thrombus from the ascending aorta and arch produces focal neurologic deficits. Diffuse injury can be attributed to microemboli of air or cellular debris, insufficient or uneven cooling, and a prolonged circulatory arrest period. After circulatory arrest periods exceeding 40 minutes the incidence of stroke greatly increases.125 Profound hypothermia may itself be injurious to the central nervous system without associated circulatory arrest.125

Stroke due to embolization is diminished when the aorta is evaluated via epiaortic ultrasound or other imaging modality to detect atherosclerotic plaques and thrombus. This allows appropriate adjustments to be made in clamping and cannulation strategies.126 The utility of retrograde cerebral perfusion as an adjunct to hypothermic circulatory arrest is controversial, but some groups report an increase in the safe period of circulatory arrest.127129 Laboratory evidence suggests that the primary benefits of retrograde cerebral perfusion are flushing of embolic material and perhaps more homogeneous cooling, rather than effective nutrient delivery, which is far superior with antegrade circulation.130 Resumption of antegrade circulation through the graft once the distal aortic anastomosis is complete, rather than retrograde via the femoral vessels, after a period of circulatory arrest avoids embolization of distal aortic debris. Patients with severe carotid artery occlusive disease are at increased risk of stroke during ascending aortic procedures,100 and patients older than 65, those with peripheral vascular disease, or those with pertinent histories should be evaluated.

PULMONARY DYSFUNCTION

Cardiopulmonary bypass is known to cause alterations in pulmonary function as evidenced by changes in alveolar-arterial oxygen gradients, pulmonary vascular resistance, pulmonary compliance, and intrapulmonary shunting. Usually these changes are subclinical, but a full-blown adult respiratory distress-like syndrome is reported in 0.5% to 1.7% of patients following cardiopulmonary bypass.131 The specific cause is the subject of much investigation and debate, but it is generally accepted that exposure of blood elements to the foreign surface of the cardiopulmonary circuit results in the activation of inflammatory cells and the complement cascade resulting in pulmonary injury.131 The duration of cardiopulmonary bypass, urgency of the procedure, and general condition of the patient may roughly correlate with the occurrence and severity of pulmonary dysfunction, but it can be unpredictable.132

Treatment is supportive, with early diagnosis and treatment of any subsequent pulmonary infections. Preventative measures may include preoperative optimization of pulmonary function, minimization of pump time, judicious use of blood products, heparin-coated bypass circuits,133,134 and leukocyte depletion.135,136

POSTOPERATIVE CORONARY INSUFFICIENCY

Coronary insufficiency is uncommon in the postoperative period, but may occur following root replacement and coronary reimplantation. Ischemia may be due to kinking of a Dacron or saphenous vein interposition graft. Coronaries implanted under tension, or aortic suture lines, may bleed resulting in compression from an expanding hematoma. Suspicion of coronary insufficiency must be promptly evaluated with angiography and/or reoperation.


?? RESULTS OF OPERATION
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Perioperative Morbidity

The primary causes of significant morbidity in the early postoperative period are neurologic injury and bleeding. Stroke has been reported in 1.8% to 5.9% of patients in various series.64,80,120,137139 Antegrade reperfusion following completion of the distal aortic anastomosis64 and the use of retrograde cerebral perfusion127,128 may lower the risk of stroke in patients requiring circulatory arrest. Postoperative bleeding requiring reoperation ranges from 2.4% to 11.1%.61,64,120,137140 The use of the exclusion technique of graft insertion and blood impervious grafts has resulted in lower bleeding rates in more recent series. Ten to eighteen percent of patients require prolonged mechanical ventilation,64,139 and 18% to 25% require prolonged (more than 6 hours) inotropic support.61,139 Postoperative myocardial infarction, reported in up to 2.5%, may be related to technical problems with coronary reimplantation.64,120,137

Perioperative Mortality

Contemporary surgical series on ascending aortic disease using modern grafting techniques and methods of cerebral and myocardial protection report hospital mortality rates of 1.7% to 17.1%.41,64,93,119,120,140142 Comparison of outcomes is difficult, however, because of heterogeneity of patients. Some series do not include dissection,120 and the proportion of emergent operations, reoperations, and arch replacements is highly variable. The most common cause of early death is clearly cardiac failure. Other frequent causes of early death include stroke, bleeding, and pulmonary insufficiency.61,80,119,137139

Risk Factors for Hospital Mortality

Emergent operation after the onset of acute dissection or rupture is the clearest risk factor for early death.80,93,137 Risk of death following elective intervention is increased by increasing NYHA classification,119,137,143 increasing age,80,93,138,139,143 prolonged cardiopulmonary bypass time,61,137,138 dissection,119 previous cardiac surgery,80,139 and need for concomitant coronary revascularization.137,139 Major risk factors are shown in Table 46-2.


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TABLE 46-2 Independent predictors of early mortality

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Late Mortality

Reported actuarial survival, like early mortality, is variable and dependent upon the patient cohort. Survival rates are 81% to 95% at 1 year,80,137 73% to 92% at 5 years,80,93,119,137 60% to 73% at 8 to 10 years,93,119,139 and 48% to 67% at 12 to 14 years.61,119 Predictors of late mortality include elevated NYHA,61,139 requirement for arch reconstruction,139 Marfan syndrome,61 and extent of distal disease.80,137 The most common cause of late death is cardiac, but distal aortic disease accounted for 32% of late deaths in one series.80

Reoperation

Reoperations may be required because of pseudoaneurysm formation, valve thrombosis or endocarditis, progression of disease in the native valve or remaining aortic segments, or because of degeneration of a bioprosthesis. Reported mortality for reoperative ascending aortic surgery varies between 6% and 22%, but has been reported as low as 3% for elective reoperations122 and as high as 100% for emergent reoperations.144 Predictors of poor outcome have included emergent reoperation, requirement for arch replacement, preoperative functional class III/IV, and duration of cardiopulmonary bypass.121,122 Freedom from reoperation is 86% to 90% at 9 to 10 years.119,139 Predictors of late reoperation have included Marfan syndrome (Fig. 46-13), the inclusion cylinder technique (Fig. 46-14),61,145 and chronic dissection. Surveillance of patients who have undergone previous aortic surgery to minimize the need for urgent reoperations and appropriate resection of all diseased aortic tissue at the time of original operation will improve outcomes. In one series it was estimated that nearly 60% percent of redo aortic cases were required because of inadequate repair during previous operations.121



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FIGURE 46-13 Freedom from reoperation (Kaplan-Meier) of patients with Marfan syndrome (group A) versus those without fibrillinopathic etiologies (group B). (Reproduced with permission from Detter C, Mair H, Klein H, et al: Long-term prognosis of surgically-treated aortic aneurysms and dissections in patients with and without Marfan syndrome. Eur J Cardiothorac Surg 1998; 13:416.)

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FIGURE 46-14 Actuarial freedom from reoperation on the ascending aorta or aortic valve. Patients are divided into those who had inclusion versus exclusion grafting techniques. (Reproduced with permission from Kouchoukos NT, Wareing TH, Murphy SF, Perrillo JB: Sixteen-year experience with aortic root replacement: results of 172 operations. Ann Surg 1991; 214:308.)

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Thromboembolism

Major thromboembolic events following replacement of the aortic root with a composite graft are currently uncommon. Unlike simple aortic valve replacement, suture material and pledgets are excluded from the bloodstream. Freedom from thromboembolism was 82% to 83% at 10 to 12 years in two older series.61,138 The incidence in more recent series is considerably lower.64 Gott et al 119 reported an incidence of only 0.42 thromboembolic events per 100 patient years.

Prosthetic Valve Endocarditis

Prosthetic valve endocarditis is not reported in some series, but was the most common late complication occurring after root replacement reported by Gott et al.119 The actuarial freedom from endocarditis in 270 patients was 88% at 14 years.

Results of Operation in Patients with Marfan Syndrome

Gott et al 97 reviewed the experience of 10 surgical centers with regards to root replacement in 675 patients with Marfan syndrome from 1968 to 1996. The 30-day mortality was 3.3%, but was only 1.5% for elective repair. Emergency surgery resulted in a 30-day mortality of nearly 12%. The survival rate was 93% at 1 year, 84% at 5 years, 75% at 10 years, and 59% at 20 years. Complications related to the residual thoracic aorta and arrhythmias were the leading causes of death. The most frequent late complication was thromboembolism. Advanced NYHA at the time of original operation was the only predictor of late death. This very complete multicenter review demonstrates that root replacement in Marfan syndrome can be performed with a low mortality and good long-term survival. Kaplan-Meier survival analysis is shown in Figure 46-15.



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FIGURE 46-15 Kaplan-Meier survival analysis for 675 patients with Marfan syndrome from ten different surgical centers according to the urgency of the procedure. (Reproduced with permission from Gott VL, Greene PS, Alejo DE, et al: Replacement of the aortic root in patients with Marfan's syndrome. N Engl J Med 1999; 340:1307.)

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?? LONG-TERM SURVEILLANCE AFTER ASCENDING AORTIC OPERATIONS
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All patients who have undergone thoracic aortic surgery must have long-term follow-up. Residual aortic tissue is often not normal and patients are prone to subsequent development of dissections or aneurysms. Pseudoaneurysms are frequently asymptomatic in the early stages and may initially present as periprosthetic hematomas. A significant proportion of patients will require reoperation, and emergent operation is associated with a very high mortality. Periodic CT or MRI is ideal for assessing progression of disease in the residual aorta and for discovering the development of complications. Patients at increased risk of reoperation, such as those with Marfan syndrome, familial aneurysms, or dissections, require more vigilant follow-up.


?? THE INFECTED AORTIC GRAFT
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Incidence

Graft infections are reported in 0.9% to 1.9% of patients following surgery of the thoracic aorta146,147 and are associated with a mortality rate ranging from 25% to 75%.147,148 Most graft infections become evident in the first month after operation,148,149 but may occur years after graft insertion.150

Risk Factors

The risk of infection with any graft is increased with breaks in sterile technique and postoperative infectious complications. In one series 55% of patients had previous significant infectious complications including wound infection, line sepsis, pneumonia, empyema, or septicemia.150 The ascending aortic graft may be particularly vulnerable because of proximity to the wound and poor natural tissue coverage. The major infectious agents are Staphylococcus aureus, Staphylococcus epidermidis, and less commonly Pseudomonas.148150 Infections may also be polymicrobial, fungal, or indeterminate.

Diagnosis

The majority of patients present with clinical signs of infection such as fever, chills, and elevated white blood cell count.149151 CT or MRI may demonstrate fluid collections or air in the periprosthetic space, but these are nonspecific findings, particularly in the early postoperative period. Confirmation of infection may require CT-guided aspiration of suspicious fluid collections. Associated pseudoaneurysms are detected by aortography or transesophageal echocardiography. Nuclear imaging techniques are endorsed by some,152 but can be nonspecific for infection versus normal postoperative inflammation.150

Treatment

The traditional treatment of infected ascending aortic grafts, originally described by Hargrove and Edmunds in 1984,147 includes removal of the infected prosthetic material, aggressive tissue debridement, local irrigation, systemic antibiotic therapy, replacement of the infected conduit, and utilization of autologous tissue to surround the new conduit and obliterate deadspace. Most surgeons prefer replacement of the infected graft with a cryopreserved homograft, as it may be more resistant to subsequent infection.153155 The ideal autogenous tissue filler is the greater omentum because of its physical properties and its proposed ability to help combat infection.156 In some cases small pseudoaneurysms have been resected and the graft locally repaired,150 although this is controversial. Mortality rates remain substantial despite these aggressive measures.150


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