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Chronic Thoracic and Thoracoabdominal Aortic Disease
Definition
This chapter considers true aortic aneurysm, false aortic aneurysm, chronic aortic dissection, penetrating arteriosclerotic ulcer, intramural hematoma, and diffuse arteriosclerotic disease. Methods for protecting the brain during operations on the aortic arch are also discussed.
True aortic aneurysm is a permanent localized dilatation of the aorta, of a diameter 50% or greater than normal, contained by walls that although attenuated, have all layers of the normal wall. False aortic aneurysm is a localized dilatation whose wall consists of adventitia, some or all of the media, and compressed periaortic tissue. Chronic aortic dissection is a separation for more than 14 days of the outer from the inner layer of the media, caused by blood leaving the normal aortic channel through a point of exit (intimal tear). Penetrating arteriosclerotic ulcer is an arteriosclerotic lesion that penetrates the internal elastic lamina of the aortic wall. Intramural hematoma is an extravasation of blood into the aortic wall, commonly in the absence of an intimal disruption. Diffuse arteriosclerotic disease is sessile, mobile, or pedunculated atheroma involving lipid deposition in large areas of the intimal layer of the aorta.
Historical Note
An important contribution to modern aneurysm surgery was made by Rudolph Matas in New Orleans in 1902 when he described the basic maneuver of “getting inside the aneurysm” with minimal external dissection and after obtaining control of the artery above and below the aneurysm. Interestingly, this basic maneuver was ignored as aortic aneurysm surgery began to develop, and in early work with abdominal aortic aneurysms at the Mayo Clinic, the aneurysm was dissected away from surrounding tissues, often with a long and difficult operation and considerable hemorrhage from lumbar arteries. DeBakey and Cooley described this same tedious method in their classic paper of 1953. Javid and colleagues in 1962 and Creech in 1966 are generally credited with reintroducing the technique of working within the aneurysm. However, DeBakey and colleagues in Houston had reintroduced this concept into abdominal aortic aneurysm surgery by 1958. The inclusion technique of sewing the graft in place from within the aneurysm is an embodiment of this concept.
Throughout the first half of the 20th century, sporadic attempts were made to treat aortic aneurysms, almost all in the abdominal aorta. Treatment was by proximal partial or complete ligation of the aorta. Results were generally unsatisfactory. Various other palliative procedures had also been used unsuccessfully. In 1950, Estes at the Mayo Clinic published a classic paper that demonstrated the poor prognosis of patients with abdominal aortic aneurysms, only 50% of whom survived 3 years after diagnosis, with two thirds of the deaths attributable to aneurysmal rupture. In response to that study, the Mayo Clinic began a surgical approach to this condition in 1951, and in 1953 reported the results of aneurysm reinforcement and the tedious operation of aortoplasty and complete wrapping with fascia lata. In 1952, Schafer and Hardin in Kansas City reported resection and grafting with an aortic allograft of an abdominal aortic aneurysm, only to have the patient die of numerous complications 28 days after operation. In that same year, Dubost and colleagues, working in Paris, reported the first successful case of aortic resection for aneurysm and restoration of blood vessel continuity (in their case, an abdominal aortic aneurysm that was approached retroperitoneally and replaced by a preserved aortic allograft). In 1953, reports of similar successes came from DeBakey and Cooley in Houston and from the Mayo Clinic. Aortic allograft banks were subsequently established in some centers to provide aortic replacement grafts.
In 1944, Alexander and Byron successfully resected a thoracic aortic aneurysm secondary to coarctation, although without restoration of aortic continuity. Aortic allografts were developed in 1948 by Gross and colleagues in Boston to replace resected aortic segments. On May 24, 1948, they resected a coarctation in a 7-year-old boy, restoring aortic continuity with an aortic allograft. When the clamps were released, the distal vasculature dilated, and the patient became hypotensive and died. This led to a recommendation to slowly release the clamps following repair of aortic coarctation. They performed four more allograft replacements of the aorta for coarctation in 1948, five in 1949, and eight in 1950, including the first frozen and irradiated graft, which functioned for at least 30 years (Dr. Robert Replogle, personal communication, July 19, 2002). In 1950, Swan and colleagues also reported successful clinical use of allografts for treating complex coarctations, including those with aneurysms. Adopting this technique, Lam and Aram in 1951 reported resection and allograft replacement of a descending thoracic aortic aneurysm in an adult. Prophetically, paraparesis developed in their patient, who died 6 weeks after operation of empyema. About this time, Bahnson reported successful management of a saccular aneurysm of the descending thoracic aorta by lateral resection and aortorrhaphy. In 1953, DeBakey and Cooley reported the first successful application of resection and grafting to a descending thoracic aortic aneurysm.
Ascending aortic aneurysms were also approached surgically before the advent of cardiopulmonary bypass (CPB). In 1952, Cooley and DeBakey reported removal of sacciform ascending aortic aneurysms by lateral resection and aortorrhaphy, as did Bahnson and Johnston and colleagues in 1953. In 1956, Cooley and DeBakey reported the first successful modern operation for ascending aortic aneurysm, consisting of resecting the ascending aorta and grafting with an aortic allograft, with the aid of CPB. Wheat and colleagues then reported successful simultaneous but separate replacement of the ascending aorta and aortic valve with reimplantation of the coronary ostia into the graft. Bentall and De Bono in 1968 and Edwards and Kerr in 1970 reported accomplishing this replacement with a composite valve and polyester tube graft. Wheat and colleagues subsequently demonstrated long-term patency of their anastomoses between grafts and coronary ostia.
Aneurysms of the arch of the aorta presented a more difficult surgical challenge. By 1952, Cooley and DeBakey had removed some sacciform aneurysms in this portion of the aorta by lateral resection, as had Bahnson by 1953. The next year, DeBakey and Cooley reported successful resection of the distal aortic arch and replacement by a graft for an aneurysm that had resulted from acute traumatic aortic transection. The case is of interest in that the patient's temperature was reduced to 28°C by surface cooling before thoracotomy. The aorta was clamped proximal to the left subclavian artery (which was also individually clamped) for 1 hour, and paraplegia did not develop (see “Paraplegia” under Special Situations and Controversies in Chapter 24 for the significance of this finding). In 1955, Cooley and colleagues reported unsuccessful resection of an aneurysm of the entire aortic arch, using the cumbersome method of temporary shunts without CPB, as did Stranahan and colleagues in a 15-hour operation in 1955 and Creech and colleagues in 1956. In 1957, DeBakey and colleagues reported the first successful repair of an aortic arch aneurysm using CPB and allograft replacement.
Thoracoabdominal aneurysms also presented difficult surgical challenges, not only because of the magnitude of the operation but also the propensity of patients to develop renal and spinal cord dysfunction after repair. In 1952 during Bahnson's pioneering work with aneurysms of the aorta, he successfully repaired a saccular thoracoabdominal aneurysm by lateral resection and aortorrhaphy. Ellis and colleagues at the Mayo Clinic first reported repair of such an aneurysm involving a visceral artery (in their case, the renal artery) by resection and grafting in 1955. Etheredge and colleagues reported successful repair of a more complex thoracoabdominal aneurysm including the celiac axis and superior mesenteric artery in the same year. In 1956, DeBakey and colleagues reported successful repair of such an aneurysm involving all the visceral arteries (celiac, superior mesenteric, and both renals). Subsequently, they devised the technique of permanent aortic bypass with a synthetic graft and visceral arterial reattachment to appropriately located side-arm grafts, and in 1965 they reported 26% mortality among 42 patients. Crawford and colleagues modified and simplified the operation by applying the inclusion technique, reducing hospital mortality to 8% by 1978.
During this developmental phase, there was controversy about the lethality of thoracic aortic aneurysms. Some reports indicated that patients with thoracic aneurysms fared better than those with abdominal aneurysms. In 1964, Joyce and colleagues established that this was not the case.
A series of technical improvements evolved into many of the techniques currently used for surgical treatment of thoracic aortic aneurysms. Even after successful repair of aneurysms of the arch had been accomplished using CPB, methods remained complex, often involving separate cannulation of the brachiocephalic arteries. In 1964, Borst and colleagues reported repair of a traumatic aneurysm of the distal portion of the aortic arch through a left thoracotomy, using CPB to produce profound hypothermia and performing the repair during an interval of circulatory arrest.
In 1975, Griepp and colleagues established the value of profoundly hypothermic circulatory arrest for resecting and grafting of more proximal and more extensive aneurysms of the aortic arch.
Among the technical improvements was use of a single anastomosis between an oval opening in the graft and the aortic wall around all three brachiocephalic arteries in replacing aortic arch aneurysms, reported by Bloodwell and colleagues in 1968 and by Pearce and colleagues the following year. Later, Ott and colleagues reported tailoring the arch resection and graft so that a single distal anastomosis could be made. Crawford and Saleh applied the inclusion technique to arch aneurysms, working entirely within the aneurysm and wrapping the graft with aneurysm wall.
Technical improvements have also been made in the aortic replacement devices required for treating aortic aneurysms and dissections. Dubost and others in the early surgical period used preserved aortic allografts. Soon the search for synthetic aortic substitutes was revived despite the unsuccessful pioneering efforts of Carrel and others. The first satisfactory synthetic aortic substitute was a fabric tube made of polyvinyl chloride cloth, and the first clinical application of this device was reported by Blakemore and Voorhees in New York City in 1954. Shumacker and King in Indianapolis also used these fabric tubes for aortic replacement in the same year. For the next several years, surgeons autoclaved and used fabric grafts made on the sewing machines of wives and friends, with generally good results. Intensive study of prosthetic grafts was quickly undertaken by several groups, and in 1955, Deterling and Bhonslay reported that polyester was the best material then available for aortic replacement. Knitted and woven grafts of various types, mostly polyester, have been widely used since then. Subsequent development of polyester grafts impregnated with collagen, gelatin, or albumin has resulted in a substantial reduction in blood loss through the grafts (particularly in fully heparinized patients), a major cause of postoperative morbidity (see “Grafts for Use in Aortic Surgery” under Special Situations and Controversies in Chapter 24 .)
Stent-grafting of descending thoracic aortic aneurysms was introduced by Dake and colleagues at Stanford University in the early 1990s using custom-designed grafts. Since then, a number of commercially developed grafts have become available for clinical use.
Morphology and Morphogenesis
Classification
Diseases of the thoracic aorta that are amenable to surgical treatment are listed in Box 26-1 . Acute traumatic aortic transection and acute ascending and descending aortic dissection are discussed in Chapter 24, Chapter 25 .
Box 26-1
Diseases of Thoracic Aorta Amenable to Surgical Treatment
-
Aneurysm
-
Congenital or developmental
-
Marfan syndrome
-
Ehlers-Danlos syndrome
-
Loeys-Dietz syndrome
-
-
Degenerative
-
Cystic medial degeneration
-
Nonspecific (arteriosclerotic)
-
-
Chronic posttraumatic
-
Blunt trauma (acute aortic transection)
-
Penetrating trauma
-
-
Inflammatory
-
Takayasu arteritis
-
Behçet disease
-
Kawasaki disease
-
Giant cell arteritis
-
Ankylosing spondylitis
-
-
Infected
-
Bacterial
-
Fungal
-
Spirochetal
-
Viral
-
-
Mechanical
-
Poststenotic
-
Associated with arteriovenous fistula
-
-
Anastomotic
-
Postarteriotomy
-
-
-
False Aneurysm
-
Chronic Aortic Dissection
-
Type A (DeBakey types I and II), ascending aorta involved
-
Type B (DeBakey type III), descending aorta involved
-
-
Penetrating Arteriosclerotic Ulcer
-
Intramural Hematoma
-
Diffuse Arteriosclerotic Disease
Aneurysm
Aneurysm is the most common condition of the thoracic aorta that requires surgical treatment. This category includes congenital or developmental, degenerative, chronic traumatic, inflammatory, infectious, mechanical, and anastomotic aneurysms.
Congenital or Developmental
Marfan syndrome is an autosomal dominant disorder resulting from mutations in the FNB1 gene that lead to defective synthesis of the glycoprotein fibrillin (a component of elastic tissue in the medial layer of the aorta). The aorta becomes aneurysmal as a result of a reduced number of microfibrils in this layer. The dilated aortic segments are prone to rupture or dissection.
Loeys-Dietz syndrome is an autosomal dominant aortic aneurysm disorder with involvement of other systems. It results from mutations in either the transforming growth factor receptor type I or II (TGFBR1 or TGFBR2) genes. The majority of patients have aortic root aneurysms that result in aortic dissection. These patients also develop aneurysms of other vessels.
Ehlers-Danlos syndrome comprises a group of heterogeneous conditions characterized by various defects in the synthesis of type III collagen. Development of aneurysms is uncommon, but rupture or dissection of the aorta or other arteries (often abdominal) can occur as a catastrophic event. Tissue fragility and poor healing can complicate surgical treatment. Ehlers-Danlos type IV (vascular form) is generally sporadic, but when familial is usually an autosomal dominant disorder.
Other genetically mediated conditions associated with aneurysm development and aortic dissection include Turner syndrome, Beals syndrome (contractual arachnodactyly), Noonan syndrome, autosomal dominant polycystic kidney disease, and the nonvascular form of Ehlers-Danlos syndrome.
Degenerative
Cystic medial degeneration is the most frequent pathologic condition that results in aneurysms of the ascending aorta. Characteristic features are fragmentation and loss of elastic tissue and loss of smooth muscle cells. Inflammation and apoptosis may be components of this process as well. Enlargement is usually confined to the proximal portion of the ascending aorta. Dilatation of the sinuses of Valsalva and aortic anulus (anuloaortic ectasia) may result in aortic regurgitation. (See “Anuloaortic Ectasia” under Morphology in Chapter 12 for discussion of this entity in patients with aortic valve regurgitation.)
Degenerative aneurysms, often associated with arteriosclerosis of the aorta, are the most frequently occurring aneurysms of the thoracic and abdominal aorta and most commonly involve the descending thoracic or thoracoabdominal segments. Abnormal proteolysis, presence of elastolytic serum enzymes, and deficiencies of collagen and elastin have been implicated as factors contributing to development of these aneurysms. Although atheromatous changes are frequently present in and around such aneurysms, the causative role of arteriosclerosis in their development is not clearly established.
Chronic Posttraumatic
Aneurysms resulting from blunt trauma most frequently involve the proximal descending thoracic aorta and may present many years after the acute injury. When neither death nor operation follows the acute transection, disruption of at least part of the aortic circumference, usually at the level of the ligamentum arteriosum, results in extravasation of blood into the periaortic tissues (see Chapter 24 ). This blood may remain in communication with the aorta and form a pulsating hematoma that is contained by aortic adventitia or the mediastinal tissues. The resulting false aneurysm may enlarge and rupture from increased wall stress (Laplace law). Chronic posttraumatic aneurysms represent a small percentage of patients with aneurysms of the thoracic aorta.
Inflammatory
Patients with Takayasu arteritis, Behçet disease, Kawasaki disease, and giant cell arteritis may develop aneurysms of the thoracic aorta that require surgical treatment. Other inflammatory disorders, such as ankylosing spondylitis, psoriatic arthritis, polyarteritis nodosa, and Reiter syndrome, may result in dilatation of the aortic root and aortic valve regurgitation that require surgical intervention.
Infected
Primary infected (mycotic) aneurysms of the thoracic aorta are rare. A frequent cause is direct deposition of circulating bacteria in a diseased, arteriosclerotic, or traumatized aortic intima following an episode of endocarditis or infection of an aortic jet lesion. Infection of intraluminal clot in a preexisting degenerative aneurysm may occur after an episode of bacteremia or other infectious process. Organisms can also infect previously inserted prosthetic grafts, causing false aneurysms. Other risk factors for development of infected aneurysm include congenital cardiac or vascular defects, trauma, and impaired immunity. Staphylococcus aureus is the most frequent causative organism, followed by Staphylococcus epidermidis, Salmonella , and Streptococcus species. Infected aneurysms may be multifocal.
Mechanical
Aneurysmal changes can occur in the aorta distal to stenotic aortic valves and aortic coarctation and proximal to arteriovenous fistulae. Dilatation of the ascending aorta in patients with a bicuspid aortic valve and of the descending thoracic aorta in patients with aortic coarctation is more likely the result of structural abnormalities of the aortic wall rather than turbulent flow produced by the stenotic lesions.
Anastomotic
Aneurysms (usually of the false type) can develop at the site of aorta-to-aorta or aorta-to-graft anastomoses.
False Aneurysm
False aneurysms are most commonly associated with trauma, infection, and previous operations on the aorta.
Chronic Aortic Dissection
Morphologic features of acute aortic dissection, including classification, are discussed in Chapter 25 . When the false lumen persists after an acute aortic dissection, as it usually does, its outer wall, consisting of the outer layer of the media and the adventitia, has a tendency to weaken and enlarge. A saccular or fusiform aneurysm may result. Chronic aortic dissection with persisting false lumen is a common substrate for development of chronic thoracic or thoracoabdominal aneurysms.
Penetrating Arteriosclerotic Ulcer
Arteriosclerotic lesions involving the intimal layer of the aorta may ulcerate and penetrate the internal elastic lamina of the aortic wall ( Fig. 26-1 ). Penetrating arteriosclerotic ulcers occur most commonly in the descending thoracic aorta. They can result in separation of the layers of the media and formation of intramural hematoma. Saccular and fusiform aneurysms may develop, and dissection, rupture, and embolization can occur.
Intramural Hematoma
Intramural hematoma can occur in the absence of an intimal tear and may result in dissection ( Figs. 26-2 and 26-3 ). Rupture of an arteriosclerotic plaque and spontaneous rupture of vasa vasora have been postulated as mechanisms for development of the hematoma.
Diffuse Arteriosclerotic Disease
Sessile, mobile, or pedunculated atheroma is an important risk factor for stroke after operations that require cannulating and clamping the ascending aorta or aortic arch ( Fig. 26-4 ). Severe arteriosclerosis of the ascending aorta, aortic arch, and descending thoracic aorta is also an important cause of embolic stroke and embolization to the abdominal organs and lower extremities in patients who do not undergo cardiac or thoracic surgical procedures. In some situations, the latter condition is amenable to surgical treatment.
Prevalence
During the first half of the 20th century, thoracic aneurysms were far more common than abdominal aneurysms because of the predominance of syphilitic aneurysms. In 1952, the ratio of thoracic to abdominal aortic aneurysms was 2 : 1 in autopsy studies. By 1964, this ratio had declined to less than 1 : 1, primarily as a result of the decline in syphilitic aneurysms. In a study from England and Wales that examined mortality statistics, the number of deaths resulting from thoracic aneurysms increased 17% between 1974 and 1984. This increase was substantially less than that for abdominal aneurysms (53%).
Prevalence of thoracic and thoracoabdominal aortic aneurysms is difficult to determine because of underreporting of these aneurysms in mortality statistics. Between 1958 and 1985 in Malmo, Sweden, which has a stable urban population and an autopsy prevalence of 83%, thoracic aortic aneurysms were found in 489 per 100,000 autopsies in men and 437 per 100,000 autopsies in women. Prevalence of asymptomatic thoracic aneurysms was about 400 per 100,000 autopsies in 65-year-olds and about 670 per 100,000 autopsies in 80-year-olds. In a study by Bickerstaff and colleagues in Rochester, Minnesota, the prevalence of thoracic aneurysms between 1951 and 1980 was 5.9 per 100,000 population per year. In a subsequent study from the same institution, prevalence of thoracic aneurysms between 1980 and 1994 had increased to 10.4 per 100,000 population per year. A study of the entire population of Sweden by Olsson and colleagues from 1987 to 2002 found the prevalence of thoracic aortic disease (nonruptured or ruptured thoracic aneurysm, acute or chronic aortic dissection) to be 10.7 per 100,000 per year for men and 7.1 per 100,000 for women in 1987. By 2002, the prevalence had increased to 16.3 per 100,000 per year for men and 9.1 per 100,000 per year for women. The number of operations on the thoracic aorta increased sevenfold over this interval for men and 15-fold for women.
Penetrating arteriosclerotic ulcer and intramural aortic hematoma without an intimal tear are being diagnosed with increasing frequency, primarily because of aging of the population and more frequent use of imaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI). Among older patients who undergo cardiac surgical procedures, moderate or severe arteriosclerosis of the ascending aorta and aortic arch is present in approximately 15% to 20% of those older than 50 years and 33% of those 80 years of age or older.
Location
The true anatomic distribution of thoracic aortic aneurysms is not known with certainty. In 72 individuals with aneurysms, Bickerstaff and colleagues found that 37 (51%) involved the ascending aorta, 8 (11%) the aortic arch, and 27 (38%) the descending thoracic aorta. The cause was aortic dissection in 53%, degenerative disease in 29%, aortitis in 8%, cystic medial necrosis in 6%, and syphilis in 4%. Svensjo and colleagues found that thoracoabdominal aneurysms made up 5% of asymptomatic thoracic aneurysms.
Clinical Features and Diagnostic Criteria
Symptoms
Many patients with thoracic aortic aneurysms are asymptomatic at presentation, and the aneurysms are detected during testing for other disorders. Symptoms relating to the aneurysm usually develop later in the course of enlargement of the aorta and result from impingement of the aneurysm on adjacent structures. Patients with aneurysms involving the ascending aorta associated with dilatation of the aortic anulus frequently present with symptoms referable to the aortic regurgitation that develops as a result of progressive aortic enlargement. Patients with aneurysms of the aortic arch may present with pain in the neck and jaw. Hoarseness results from stretching of the left recurrent laryngeal nerve, stridor from compression of the trachea, dysphagia from impingement on the lumen of the esophagus, dyspnea from compression of the lung parenchyma, and plethora and edema from compression of the superior vena cava. Patients with aneurysms of the descending thoracic aorta may report pain in the interscapular area or left-sided pleuritic pain. Aneurysms of the thoracoabdominal aorta may be associated with back pain, abdominal pain, and pain in the left shoulder resulting from irritation of the left hemidiaphragm.
Acute onset of severe pain in the anterior part of the chest or neck or between the shoulders is the typical presenting symptom of acute aortic dissection, although it may occur with rupture or sudden expansion of a chronic dissecting or nondissecting aneurysm (see Chapter 25 ). Acute chest pain may also result from a nondissecting intramural hematoma of the aorta or erosion of a penetrating arteriosclerotic ulcer into the surrounding tissues. Stroke or evidence of ischemia of the kidneys, abdominal viscera, and lower extremities may result from embolization of atheroma or thrombus from a severely arteriosclerotic aorta.
Signs
Direct physical signs of the presence of a thoracic aortic aneurysm are uncommon. In earlier times, a pulsating mass of the anterior chest was the first evidence of a syphilitic aneurysm of the ascending aorta; rarely, such an aneurysm eroded the sternum and ruptured, resulting in fatal hemorrhage. Signs of aortic regurgitation (bounding peripheral pulses, an aortic diastolic murmur) may be present in patients with large ascending aortic aneurysms that involve the aortic sinuses. A pulsatile mass in the upper abdomen may be present in patients with thoracoabdominal aneurysms. Evidence for embolization of atheroma or thrombus from an aneurysm or from a severely arteriosclerotic aorta to the lower extremities (blue toe syndrome) may occasionally be the first indication of severe aortic disease.
Diagnostic Techniques
Chest Radiography
Findings on the chest radiograph may be diagnostic of a thoracic aortic aneurysm. Ascending aortic aneurysms produce a convex shadow to the right of the cardiac silhouette ( Fig. 26-5 ), those of the arch an anterior and left-sided shadow ( Fig. 26-6 ), and those of the descending aorta a shadow to the left and posteriorly ( Fig. 26-7 ). However, approximately 17% of patients with documented aneurysms or dissections have no abnormalities on chest radiography. Pooled data place the sensitivity of detecting a widened mediastinum or abnormal aortic contour in patients with aortic dissection at 64% and 71%, respectively. Substantial enlargement of the ascending aorta may be confined to the retrosternal area, so that the aortic silhouette appears normal. Aneurysms that involve the ascending aorta and aortic arch cannot always be differentiated from tumors or other masses.
Computed Tomography
CT is the most widely used noninvasive technique for diagnosing thoracic aortic disease. It provides information about size, location, and extent of disease ( Fig. 26-8 ). It is of particular value in documenting the growth rate of aneurysms, determining timing of operative intervention in asymptomatic patients, and evaluating patients postoperatively. It is useful in identifying anatomic variants and branch vessel involvement, and provides three-dimensional (3D) data ( Fig. 26-9 ). Because approximately 25% of patients have aneurysms in more than one area of the aorta, both the thoracic and the abdominal aorta should be examined. CT is also useful for detecting intramural hematoma (see Fig. 26-2 ) and penetrating arteriosclerotic ulcers, and for determining severity and extent of thickening of the aortic wall in patients with severe aortic arteriosclerosis. It is of particular value in diagnosing thoracic aortic dissection. The principal disadvantage of CT is that it requires use of contrast medium for precise delineation of aortic disease, which may be contraindicated in patients with allergies to contrast agents or with renal insufficiency.
Radiation-induced malignancy in patients with thoracic aortic disease who require periodic CT imaging is a concern. Techniques to reduce radiation exposure (e.g., appropriate shielding, radiation dose reduction and management, algorithms to improve system efficiency) have been implemented to minimize this risk.
Magnetic Resonance Imaging
MRI is emerging as a premier imaging method for diagnosing diseases of the thoracic and thoracoabdominal aorta. Standard techniques do not require contrast agents ( Fig. 26-10, A ). In certain applications, a single study can provide information similar to that obtained from a combination of echocardiography, CT, and angiography. It provides excellent imaging of aortic dissections and can accurately identify thrombus formation and sites of entry. It can also differentiate periaortic hematoma from thrombosis of a false aneurysm. Breath-holding and 3D magnetic resonance angiography permit examination of the entire thoracic aorta, its major branches, the pericardium, the aortic valve, and the contractile pattern of the left ventricle. Contrast-enhanced, time-resolved, 3D magnetic resonance angiography using agents such as gadolinium provide excellent images of the aorta and its major branches, comparable with those obtained by conventional aortography ( Fig. 26-10, B ).
Compared with CT, current disadvantages of MRI include a longer time to complete the study, greater cost, inaccessibility to patients who are connected to ventilators and monitoring devices, contraindication in patients with metallic implants, pacemakers, and defibrillators, and limited availability. Use of MRI with a contrast agent (gadolinium compounds) is associated with a risk of nephrogenic systemic sclerosis.
Transesophageal Echocardiography
Transesophageal echocardiography (TEE) with Doppler color flow imaging is being used with increasing frequency for diagnosing thoracic aortic disease and caring for patients who undergo operations on the thoracic aorta. It is superior to transthoracic echocardiography for these purposes. It can be performed rapidly, with minimal morbidity, and has emerged as the most useful and accurate technique for diagnosing acute aortic dissection (see Chapter 25 ).
Before and during operations on the thoracic aorta, TEE is invaluable for assessing presence of arteriosclerosis, including mobile or pedunculated atheroma in the thoracic aorta, hemopericardium, malperfusion, competency of the aortic valve before CPB is established, and adequacy of reparative procedures on the valve. It also provides information about ventricular function and function of the mitral and tricuspid valves.
Disadvantages of TEE include lack of availability at small centers and during off hours, need for sedation, and occasionally endotracheal intubation.
Aortography
Aortography can be performed in patients who are to undergo elective operations on the thoracic aorta. It provides information about location of aneurysms, particularly in relation to major branches of the aorta in the chest and upper abdomen ( Fig. 26-11 ). It also defines areas of relatively normal aorta proximal and distal to aneurysms. It can detect presence of aortic regurgitation. Selective injections of the coronary, brachiocephalic, visceral, and renal arteries provide important information that permits more accurate assessment of operative risk and may demonstrate need for modifications in operative technique.
A disadvantage of aortography is that the size of large aneurysms may be underestimated because of the presence of thrombus. Other disadvantages include risk of allergic reactions after injection of contrast medium and risk of renal failure in patients with impaired renal function. Multidetector CT has largely replaced angiography for anatomic studies that are required for treating and monitoring aortic disease.
Epiaortic Ultrasonography
Intraoperative epiaortic ultrasound imaging of the ascending and descending thoracic aorta is useful for detecting arteriosclerosis. Presence of severe arteriosclerosis, including mobile or pedunculated atheroma, may necessitate alterations in surgical technique to avoid embolization of atheromatous debris to the brain and other organs during cardiac and thoracic aortic operations (see Fig. 26-4, A ). Epiaortic imaging is more accurate than palpation of the aorta and, in comparative studies, more accurate than TEE for detecting atheromatous disease in the ascending aorta.
Preoperative Evaluation
Because myocardial infarction, respiratory failure, renal failure, and stroke are the principal causes of mortality and morbidity after operations on the thoracic aorta, preoperative assessment of the function of these organ systems is essential.
Cardiac Function
Because of the high prevalence of ischemic heart disease in older individuals, particularly those with degenerative aneurysms, assessment of cardiac function is necessary when elective operation is contemplated, especially for those with a history of myocardial infarction or angina pectoris and those older than 50 years. Patients with symptoms or electrocardiographic (ECG) changes indicative of myocardial ischemia should undergo stress testing and coronary angiography when indicated. Patients with valvar heart disease are evaluated with echocardiography and cardiac catheterization. Clinically important coronary artery disease should be treated with percutaneous catheter interventional techniques or bypass grafting, and valvar heart disease by valve repair or replacement before or, in some cases, at the time of the procedure on the thoracic aorta.
Pulmonary Function
History of smoking and presence of chronic pulmonary disease are important predictors of respiratory failure, and they are frequently present in patients who require operations on the descending thoracic and thoracoabdominal aorta. Pulmonary function tests should be performed in patients with these risk factors. Spirometric tests and arterial blood gas analysis should be performed in patients with chronic pulmonary disease. If reversible restrictive disease or excessive sputum production is present, antibiotics and bronchodilators should be administered preoperatively. Cessation of smoking is advisable.
Renal Function
Preoperative renal dysfunction is the most important predictor of acute renal failure after operations on the thoracic aorta. Although creatinine and blood urea nitrogen are routinely measured preoperatively, their predictive value for postoperative renal failure is limited. Preoperative hydration and avoidance of intravenous contrast agents, hypotension, low cardiac output, and hypovolemia in the perioperative period are important mechanisms for reducing the prevalence of this complication.
Neurologic Function
To minimize risk of stroke or reversible ischemic neurologic deficits, duplex imaging of the carotid arteries and angiography of the brachiocephalic and intracranial arteries, when indicated, should be performed preoperatively in patients with a history of stroke, transient ischemic attack, or other risk factors for cerebrovascular disease. Patients with greater than 80% to 90% stenosis of one or both common or internal carotid arteries should be considered for carotid endarterectomy or stenting before elective operations on the thoracic aorta.
Natural History
Aneurysm
In contrast to the extensive data on the natural history of infrarenal abdominal aortic aneurysms that have not been surgically treated, substantially less information is available for thoracic aortic aneurysms. This is primarily due to the lack (until recent times) of a widely available noninvasive diagnostic test that can accurately measure the size of thoracic aneurysms.
In three of the largest studies of thoracic aortic aneurysms, which include 264 patients who had not undergone operative treatment at the time of diagnosis, rupture of the aneurysm was the most common cause of death, occurring in 42% to 70% of patients. In all three series, rupture of chronic dissecting aneurysms substantially exceeded that of nondissecting aneurysms. Five-year survival ranged from 13% to 39%. Survival for patients with thoracic, thoracoabdominal, and abdominal aneurysms in the study of Perko and colleagues is shown in Fig. 26-12 . In two studies of patients with thoracoabdominal aneurysms who did not undergo operative treatment, rupture of the aneurysm was also the most common cause of death.
Other studies have focused on rates of growth and influence of the size of thoracic aortic aneurysms on the probability of rupture. In an analysis of 171 patients with serial CT images of aortic aneurysms, Hirose and colleagues found that thoracic aneurysms enlarged more rapidly than abdominal aneurysms (0.42 vs. 0.28 cm · year −1 ). Aneurysms of the aortic arch enlarged at the fastest rate (0.56 cm · year −1 ). Similar findings were reported by Griepp and colleagues. Size of a thoracic aneurysm at initial evaluation appears to be the most important predictor of rupture. Aneurysms that are 5 to 6 cm in diameter have a faster rate of growth and a greater propensity for rupture than smaller ones. In the study by Perko and colleagues, the cumulative 5-year hazard for rupture increased fivefold for thoracic aneurysms that were 6 cm or greater in diameter. Rupture is often preceded by symptoms. Bickerstaff and colleagues reported that once symptoms developed, the mean time to rupture was 2 years.
Medical treatment is of limited value in managing thoracic aneurysms. Control of systemic hypertension, when present, is important to reduce wall stress even though no clear correlation between expansion rate of thoracic aneurysms and presence of hypertension has been demonstrated. Hypertension is a risk factor for aortic enlargement and need for reoperation after repair of type A aortic dissection, however. Administration of β-adrenergic blocking agents decreases progression of aortic dilatation in Marfan syndrome patients and may slow the rate of aortic dilatation in those with chronic aortic dissection in the absence of this syndrome. Angiotensin receptor blockers and angiotensin-converting enzyme inhibitors may slow the growth rate of aneurysms in patients with Marfan syndrome. Whether these agents can similarly affect other diseases of the aorta is unknown. Although statin therapy has been associated with decreased long-term mortality in patients with abdominal aortic aneurysms, no similar effect has been observed in patients with thoracic aneurysms. No prospective trials have demonstrated a beneficial effect of cessation of smoking on rates of progression of thoracic aortic disease.
Other Conditions
The natural history of penetrating arteriosclerotic ulcers is variable. In the largest reported series, the majority of ulcers detected by CT imaging were not associated with symptoms and remained stable or regressed. A small percentage progressively enlarged, with formation of saccular aneurysms. Intramural hematoma, dissection, embolization, and rupture can also occur.
Intramural hematoma is a dynamic entity that may regress, expand, or progress to aortic dissection. Its natural history varies according to location of the hematoma in the thoracic aorta and geographic location. A higher prevalence of dissection and death has been observed among patients with hematomas in the ascending aorta and arch than in those with hematomas in the descending aorta. The experience from Asia suggests more frequent resolution of the hematomas with conservative management than that reported from Western countries.
Patients with severe arteriosclerotic plaques (>4 mm in thickness) involving the ascending aorta and aortic arch have a high prevalence of atheromatous emboli in the cerebral circulation. These emboli are probably a major cause of cerebral infarction. Patients with severe ascending aortic arteriosclerosis are at risk for embolization and stroke after manipulation of the ascending aorta during coronary artery bypass grafting and other cardiac surgical procedures. When severe atheromatous disease is present in the distal aortic arch and descending thoracic aorta, embolization to the visceral, renal, and peripheral arteries can occur.
Among patients with the conditions just described, death due to coexisting cardiovascular disease is common.
Technique of Operation
Preparations for Thoracic and Thoracoabdominal Aortic Surgery
After anesthesia induction, venous access is obtained with a large-bore central catheter and several large peripheral catheters. A radial arterial catheter is inserted for monitoring blood pressure and withdrawing blood samples. This is placed in the left radial artery in patients with ascending aortic and proximal arch disease, and in the right radial artery in patients with descending thoracic or thoracoabdominal aortic disease. If chronic aortic dissection is present and the potential for malperfusion exists (see “Malperfusion Syndromes” under Special Situations and Controversies in Chapter 25 ), a second arterial catheter is placed in a femoral artery or the opposite radial artery. If entrance into the left chest after a median sternotomy is anticipated, or if a lateral thoracotomy or thoracoabdominal incision is used, a double lumen endotracheal tube is inserted. Alternatively, an occlusive balloon can be placed through a single-lumen endotracheal tube. Leads II and V 5 of the ECG are continuously monitored. A pulmonary artery catheter is placed to measure pulmonary artery pressure, oxygen saturation, and cardiac output. Thermistor probes are placed for measuring nasopharyngeal and bladder temperature. If an interval of hypothermic circulatory arrest is planned, electroencephalographic monitoring is also necessary, and monitoring of cerebral oxygen saturation is advisable. Cerebrospinal fluid drainage is performed in patients with extensive descending thoracic aortic disease and thoracoabdominal aneurysms. TEE is performed intraoperatively to assess function of the cardiac valves, size of the aorta, and type and extent of aortic disease, and to monitor myocardial function.
Ascending Aorta Replacement
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