Updated: Nov 17, 2009
Aneurysmal degeneration can occur anywhere in the human aorta. By definition, an aneurysm is a localized or diffuse dilation of an artery with a diameter at least 50% greater than the normal size of the artery.
A blood vessel has 3 layers: the intima (inner layer made of endothelial cells), media (contains muscular elastic fibers), and adventitia (outer connective tissue). Aneurysms are either true or false. The wall of a true aneurysm involves all 3 layers, and the aneurysm is contained inside the endothelium. The wall of a false or pseudoaneurysm only involves the outer layer and is contained by the adventitia. An aortic dissection is formed by an intimal tear and is contained by the media; hence, it has a true lumen and a false lumen.
Most aortic aneurysms (AA) occur in the abdominal aorta; these are termed abdominal aortic aneurysms (AAA). Although most abdominal aortic aneurysms are asymptomatic at the time of diagnosis, the most common complication remains life-threatening rupture with hemorrhage.
Aneurysmal degeneration that occurs in the thoracic aorta is termed a thoracic aneurysm (TA). Aneurysms that coexist in both segments of the aorta (thoracic and abdominal) are termed thoracoabdominal aneurysms (TAA). Thoracic aneurysms and thoracoabdominal aneurysms are also at risk for rupture. A recent population-based study suggests an increasing prevalence of thoracic aortic aneurysms. Thoracic aortic aneurysms are subdivided into 3 groups depending on location: ascending aortic, aortic arch, and descending thoracic aneurysms or thoracoabdominal aneurysms. Aneurysms that involve the ascending aorta may extend as proximally as the aortic annulus and as distally as the innominate artery, whereas descending thoracic aneurysms begin beyond the left subclavian artery. Arch aneurysms are as the name implies.
Dissection is another condition that may affect the thoracic aorta. An intimal tear causes separation of the walls of the aorta. A false passage for blood develops between the layers of the aorta. This false lumen may extend into branches of the aorta in the chest or abdomen, causing malperfusion, ischemia, or occlusion with resultant complications. The dissection can also progress proximally, to involve the aortic sinus, aortic valve, and coronary arteries. Dissection can lead to aneurysmal change and early or late rupture. A chronic dissection is one that is diagnosed more than 2 weeks after the onset of symptoms. Dissection should not be termed dissecting aneurysm because it can occur with or without aneurysmal enlargement of the aorta.
The shape of an aortic aneurysm is either saccular or fusiform. A fusiform (or true) aneurysm has a uniform shape with a symmetrical dilatation that involves the entire circumference of the aortic wall. A saccular aneurysm is a localized outpouching of the aortic wall, and it is the shape of a pseudoaneurysm.
Treatment of abdominal aortic aneurysms, thoracoabdominal aneurysms, and thoracic aneurysms involves surgical repair in good-risk patients with aneurysms that have reached a size sufficient to warrant repair. Surgical repair may involve endovascular stent grafting (in suitable candidates) or traditional open surgical repair.
The development of treatment modalities for thoracic aneurysms followed successful treatment of abdominal aortic aneurysms. Estes' 1950 report revealed that the 3-y survival rate for patients with untreated abdominal aortic aneurysms was only 50%, with two thirds of deaths resulting from aneurysmal rupture.1 Since then, increased attempts were made to devise methods of durable repair.
Most of these initial successful repairs involved the use of preserved aortic allografts, thus triggering the establishment of numerous aortic allograft banks. Simultaneously, Gross and colleagues successfully used allografts to treat complex thoracic aortic coarctations, including those with aneurysmal involvement.2
In 1951, Lam and Aram reported the resection of a descending thoracic aneurysm with allograft replacement.3 Ascending aortic replacement required the development of cardiopulmonary bypass and was first performed in 1956 by Cooley and DeBakey.4 They successfully replaced the ascending aorta with an aortic allograft. Successful replacement of the aortic arch, with its inherent risk of cerebral ischemia, was understandably more challenging and was not reported until 1957 by DeBakey et al.5
Although the use of aortic allografts as aortic replacement was widely accepted in the early 1950s, the search for synthetic substitutes was well underway. Dacron was introduced by DeBakey. By 1955, Deterling and Bhonslay believed that Dacron was the best material for aortic substitution.6 Numerous types of intricately woven hemostatic grafts have since been developed and are now used much more extensively than their allograft counterparts. Such Dacron grafts are used to replace ascending, arch, thoracic, and thoracoabdominal aortic segments.
However, some patients required replacement of the aortic root, as well. Subsequently, combined operations that replaced the ascending aneurysm in conjunction with replacement of the aortic valve and reimplantation of the coronary arteries were performed by Bentall and De Bono in 1968, using a mechanical valve with a Dacron conduit.7 Ross, in 1962, and Barratt-Boyes, in 1964, successfully implanted the aortic homograft in the orthotopic position.8,9 In 1985, Sievers reported the use of stentless porcine aortic roots.10
More recently, less invasive therapy for descending thoracic aortic aneurysm have been developed. Dake et al reported the first endovascular thoracic aortic repair in 1994.11 In March 2005, the US Food and Drug Administration (FDA) approved the first thoracic aortic stent graft, the GORE TAG graft (W.L. Gore and Associates; Newark, Del).12
Aneurysms are usually defined as a localized dilation of an arterial segment greater that 50% its normal diameter. Most aortic aneurysms occur in the infrarenal segment (95%). The average size for an infrarenal aorta is 2 cm; therefore, abdominal aortic aneurysms are usually defined by diameters greater than 3 cm.
The normal size for the thoracic and thoracoabdominal aorta is larger than that of the infrarenal aorta, and aneurysmal degeneration in these areas is defined accordingly. The average diameter of the mid-descending thoracic aorta is 26-28 mm, compared with 20-23 mm at the level of the celiac axis.
Although findings from autopsy series vary widely, the prevalence of aortic aneurysms probably exceeds 3-4% in individuals older than 65 years.
Death from aneurysmal rupture is one of the 15 leading causes of death in most series. The estimated incidence of thoracic aortic aneurysms is 6 cases per 100,000 person-years. In addition, the overall prevalence of aortic aneurysms has increased significantly in the last 30 years. This is partly due to an increase in diagnosis based on the widespread use of imaging techniques. However, the prevalence of fatal and nonfatal rupture has also increased, suggesting a true increase in prevalence. Population-based studies suggest an incidence of acute aortic dissection of 3.5 per 100,000 persons; an incidence of thoracic aortic rupture of 3.5 per 100,000 persons; and an incidence of abdominal aortic rupture of 9 per 100,000 persons. An aging population probably plays a significant role.
Aneurysmal degeneration occurs more commonly in the aging population. Aging results in changes in collagen and elastin, which lead to weakening of the aortic wall and aneurysmal dilation. According to the Laplace law, luminal dilation results in increased wall tension and the vicious cycle of progressive dilation and greater wall stress. Pathologic sequelae of the aging aorta include elastic fiber fragmentation and cystic medial necrosis. Arteriosclerotic (degenerative) disease is the most common cause of thoracic aneurysms.
A previous aortic dissection with a persistent false channel may produce aneurysmal dilation; such aneurysms are the second most common type. False aneurysms are more common in the descending aorta and arise from the extravasation of blood into a tenuous pocket contained by the aortic adventitia. Because of increasing wall stress, false aneurysms tend to enlarge over time.
Aneurysmal degeneration occurs more commonly in the aging population. Aging results in changes in collagen and elastin, which lead to weakening of the aortic wall and aneurysmal dilation. According to the law of Laplace, luminal dilation results in increased wall tension and the vicious cycle of progressive dilation and greater wall stress. Pathologic sequelae of the aging aorta include elastic fiber fragmentation and cystic medial necrosis. Arteriosclerotic (degenerative) disease is the most common cause of thoracic aneurysms.The occurrence and expansion of an aneurysm in a given segment of the arterial tree probably involves local hemodynamic factors and factors intrinsic to the arterial segment itself.
The medial layer of the aorta is responsible for much of its tensile strength and elasticity. Multiple structural proteins comprise the normal medial layer of the human aorta. Of these, collagen and elastin are probably the most important. The elastin content of the ascending aorta is high and diminishes progressively in the descending thoracic and abdominal aorta. The infrarenal aorta has a relative paucity of elastin fibers in relation to collagen and compared with the thoracic aorta, possibly accounting for the increased frequency of aneurysms in this area. In addition, the activity and amount of specific enzymes is increased, which leads to the degradation of these structural proteins. Elastic fiber fragmentation and loss with degeneration of the media result in weakening of the aortic wall, loss of elasticity, and consequent dilation.
Hemodynamic factors probably play a role in the formation of aortic aneurysms. The human aorta is a relatively low-resistance circuit for circulating blood. The lower extremities have higher arterial resistance, and the repeated trauma of a reflected arterial wave on the distal aorta may injure a weakened aortic wall and contribute to aneurysmal degeneration. Systemic hypertension compounds the injury, accelerates the expansion of known aneurysms, and may contribute to their formation.
Hemodynamically, the coupling of aneurysmal dilation and increased wall stress is defined by the law of Laplace. Specifically, the law of Laplace states that the (arterial) wall tension is proportional to the pressure times the radius of the arterial conduit (T = P x R). As diameter increases, wall tension increases, which contributes to increasing diameter. As tension increases, risk of rupture increases. Increased pressure (systemic hypertension) and increased aneurysm size aggravate wall tension and therefore increase the risk of rupture.
Aneurysm formation is probably the result of multiple factors affecting that arterial segment and its local environment.
Most patients with aortic aneurysms are asymptomatic at the time of discovery. Thoracic aneurysms are usually found incidentally after chest radiographs or other imaging studies. Abdominal aortic aneurysms may be discovered incidentally during imaging studies or a routine physical examination as a pulsatile abdominal mass.
The most common complication of abdominal aortic aneurysms is rupture with life-threatening hemorrhage manifesting as pain and hypotension. The triad of abdominal pain, hypotension, and a pulsatile abdominal mass is diagnostic of a ruptured abdominal aortic aneurysm, and emergent operation is warranted without delay for imaging studies.
Patients with a variant of abdominal aortic aneurysm may present with fever and a painful aneurysm with or without an obstructive uropathy. These patients may have an inflammatory aneurysm that can be treated with surgical repair.
Other presentations of abdominal aortic aneurysm include lower extremity ischemia, duodenal obstruction, ureteral obstruction, erosion into adjacent vertebral bodies, aortoenteric fistula (ie, GI bleed), or aortocaval fistula (caused by spontaneous rupture of aneurysm into the adjacent inferior vena cava [IVC]). Patients with aortocaval fistula present with abdominal pain, venous hypertension (ie, leg edema), hematuria, and high output cardiac failure.
Patients with thoracic aneurysms are often asymptomatic. Most patients are hypertensive but remain relatively asymptomatic until the aneurysm expands. Their most common presenting symptom is pain. Pain may be acute, implying impending rupture or dissection, or chronic, from compression or distension. The location of pain may indicate the area of aortic involvement, but this is not always the case. Ascending aortic aneurysms tend to cause anterior chest pain, while arch aneurysms more likely cause pain radiating to the neck. Descending thoracic aneurysms more likely cause back pain localized between the scapulae. When located at the level of the diaphragmatic hiatus, the pain occurs in the mid back and epigastric region.
Large ascending aortic aneurysms may cause superior vena cava obstruction manifesting as distended neck veins. Ascending aortic aneurysms also may develop aortic insufficiency, with widened pulse pressure or a diastolic murmur, and heart failure. Arch aneurysms may cause hoarseness, which results from stretching of the recurrent laryngeal nerves. Descending thoracic aneurysms and thoracoabdominal aneurysms may compress the trachea or bronchus and cause dyspnea, stridor, wheezing, or cough. Compression of the esophagus results in dysphagia. Erosion into surrounding structures may result in hemoptysis, hematemesis, or gastrointestinal bleeding. Erosion into the spine may cause back pain or instability. Spinal cord compression or thrombosis of spinal arteries may result in neurologic symptoms of paraparesis or paraplegia. Descending thoracic aneurysms may thrombose or embolize clot and atheromatous debris distally to visceral, renal, or lower extremities.
Patients who present with ecchymoses and petechiae may be particularly challenging because these signs probably indicate disseminated intravascular coagulation (DIC). The risk of significant perioperative bleeding is extremely high, and large amounts of blood and blood products must be available for resuscitative transfusion.
The most common complications of thoracic aortic aneurysms are acute rupture or dissection. Some patients present with tender or painful nonruptured aneurysms. Although debate continues, these patients are thought to be at increased risk for rupture and should undergo surgical repair on an emergent basis.
Indications for surgery of thoracic aortic aneurysms are based on size or growth rate and symptoms. Because the risk of rupture is proportional to the diameter of the aneurysm, aneurysmal size is the criterion for elective surgical repair. Elefteriades published the natural history of thoracic aortic aneurysms and recommends elective repair of ascending aneurysms at 5.5 cm and descending aneurysms at 6.5 cm for patients without any familial disorders such as Marfan syndrome.13,14 These recommendations are based on the finding that the incidence of complications (rupture and dissection) exponentially increased when the size of the ascending aorta reached 6.0 cm (31% risk of complications) or when the size of the descending aorta reached 7.0 cm (43% risk).15,14 Patients with Marfan syndrome or familial aneurysms should undergo earlier repair, when the ascending aorta grows to 5.0 cm or the descending aorta grows to 6.0 cm.
In addition, relative aortic aneurysm size in relation to body surface area may be more important than absolute aortic size in predicting complications.16 Using the aortic size index (ASI) of aortic diameter (in cm) divided by body surface area (m2), patients are stratified into 3 groups: ASI <2.75 cm/m2 are at low risk for rupture (4%/y), ASI 2.75-4.25 cm/m2 are at moderate risk (8%/y), and ASI >4.25cm/m2 are at high risk (20-25%/y).16,17
Rapid expansion is also a surgical indication. Growth rates average 0.07 cm/y in the ascending aorta and 0.19 cm/y in the descending aorta.14 A growth rate of 1 cm/y or faster is an indication for elective surgical repair.
Symptomatic patients should undergo aneurysm resection regardless of size. Acutely symptomatic patients require emergent operation. Emergent operation is indicated in the setting of acute rupture. Rupture of the ascending aorta may occur into the pericardium, resulting in acute tamponade. Rupture of the descending thoracic aorta may cause a left hemothorax.
Patients with acute aortic dissection of the ascending aorta require emergent operation. They may present with rupture, tamponade, acute aortic insufficiency, myocardial infarction, or end-organ ischemia. Acute dissection of the descending aorta does not require surgical intervention, unless complicated by rupture, malperfusion (eg, visceral, renal, neurologic, leg ischemia), progressive dissection, persistent recurrent pain, or failure of medical management.
Patients who undergo surgery for symptomatic aortic insufficiency or stenosis with an associated enlarged aneurysmal aorta should have concomitant aortic replacement if the aorta reaches 5 cm in diameter. Concomitant aortic replacement should be consider for patients with bicuspid aortic valves with an aorta >4.5 cm in diameter.
Summary of indications
Ascending aortic aneurysms occur as proximally as the aortic annulus and as distally as the innominate artery. They may compress or erode into the sternum and ribs, causing pain or fistula. They also may compress the superior vena cava or airway. When symptomatic by rupture or dissection, they may involve the pericardium, aortic valve, or coronary arteries. They may rupture into the pericardium, causing tamponade. They may dissect into the aortic valve, causing aortic insufficiency, or into the coronary arteries, causing myocardial infarction.
Aortic arch aneurysms involve the aorta where the innominate artery, left carotid, and left subclavian originate. They may compress the innominate vein or airway. They may stretch the left recurrent laryngeal nerve, causing hoarseness.
Descending thoracic aneurysms originate beyond the left subclavian artery and may extend into the abdomen. Thoracoabdominal aneurysms are stratified based on the Crawford classification. Type I involves the descending thoracic aorta from the left subclavian artery down to the abdominal aorta above the renal arteries. Type II extends from the left subclavian artery to the renal arteries and may continue distally to the aortic bifurcation. Type III begins at the mid-to-distal descending thoracic aorta and involves most of the abdominal aorta as far distal as the aortic bifurcation. Type IV extends from the upper abdominal aorta and all or none of the infrarenal aorta. Descending thoracic aneurysms and thoracoabdominal aneurysms may compress or erode into surrounding structures, including the trachea, bronchus, esophagus, vertebral body, and spinal column.
Aneurysm surgery has no strict contraindications. The relative contraindications are individualized, based on the patient's ability to undergo extensive surgery (ie, the risk-to-benefit ratio). Patients at higher risk for morbidity and mortality include elderly persons and individuals with end-stage renal disease, respiratory insufficiency, cirrhosis, or other comorbid conditions. For descending thoracic aneurysms, endovascular stent grafting is less invasive and is an ideal alternative (with appropriate anatomic considerations) to open repair for patients at high risk for complications of open repair. Stent grafts are also a reasonable alternative (with the appropriate anatomy) to open repair in patients who are not at high risk for complications. Patients must understand that life-long follow-up is required and that long-term durability is unknown.
Histologic findings may include elastic fiber fragmentation, loss of elastic fibers, loss of smooth muscle cells, cystic medial necrosis, intraluminal thrombus, and atherosclerotic plaque and ulceration.
All aneurysms must be treated with risk-factor reduction. Systemic hypertension probably contributes to the formation of aneurysms and certainly contributes to expansion and rupture. This is especially true of thoracic aneurysms. Strict control of hypertension is implemented in all patients, regardless of aortic aneurysm size.
Tobacco use contributes to aneurysm formation, although the exact pathophysiology is not well understood. Cessation of smoking is recommended. Control of other risk factors for peripheral arterial obstructive disease may be beneficial.
For acute aortic dissections, the first-line treatment of hypertension is with a short-acting beta-blocker (eg, esmolol). Beta blockade decreases the force of contraction, thus decreasing the dP/dt and shear force exerted on the dissection by minimizing the rate of rise of the aortic pressure. It also decreases the heart rate and the inotropic state of the myocardium, and reduces the likelihood of propagation of the dissection. A second-agent added is a vasodilator (eg, nitroprusside), which reduces the systolic blood pressure to, in turn, decrease the aortic wall stress and the possibility of rupture.
Most aneurysm repairs involve aortic replacement with a Dacron tube graft. Dacron grafts allow ingrowth in the interstices to form a pseudoendothelial layer to minimize the risk of embolization. They may be knitted or woven. Knitted grafts are more porous and incorporate tissue well; however, they are prone to more bleeding. Woven grafts are more impervious and therefore are the most commonly used for aortic replacement. Grafts are typically impregnated with collagen to avoid preclotting the graft and to promote optimal healing.
Ascending aortic aneurysms
Surgical treatment of ascending aortic aneurysms depends on the extent of the aneurysm both proximally (eg, involvement of the aortic valve, annulus, sinuses of Valsalva, sinotubular junction, coronary orifices) and distally (eg, involvement to the level of the innominate artery). The choice of operation also depends on the underlying pathology of the disease, the patient's life expectancy, the desired anticoagulation status, and the surgeon's experience and preference.18
Ascending aortic aneurysms with normal aortic valve leaflets, annulus, and sinuses of Valsalva are typically replaced with a simple supracoronary Dacron tube graft from the sinotubular junction to the origin of the innominate artery, with the patient under cardiopulmonary bypass.
If the aortic valve is diseased but the aortic sinuses and annulus are normal, the aortic valve is replaced separately and the ascending aortic aneurysm is replaced with a supracoronary synthetic graft, leaving the coronary arteries intact (ie, Wheat procedure).
Sinus of Valsalva aneurysms with normal aortic valve leaflets and aortic insufficiency due to dilated sinuses may be repaired with a valve-sparing aortic root replacement. Two valve-sparing procedures have been developed: the remodeling method and the reimplantation method. The remodeling method involves resecting the aneurysmal sinus tissue while maintaining the tissue along the valve leaflets and scalloping the Dacron graft to form new sinuses to remodel the root. The reimplantation method involves reimplanting the scalloped native valve into the Dacron graft. Both require reimplantation of the coronary ostia into the Dacron graft.19
Patients with an abnormal aortic valve and aortic root require aortic root replacement (ARR). In nonelderly patients who can undergo anticoagulation with reasonable safety, the aortic root may be replaced with a composite valve-graft consisting of a mechanical valve inserted into a Dacron graft coronary artery reimplantation (eg, classic or modified Bentall procedure, Cabrol procedure).20,21
For elderly patients, young active patients who do not desire anticoagulation, women of childbearing age, and patients with contraindications to warfarin, the options include stentless porcine roots,22 aortic homografts, and pulmonary autografts (ie, Ross procedure).23 For elderly patients who cannot undergo a complex operation, another option is reduction aortoplasty (ie, wrapping of the ascending aorta with a prosthetic graft).
Patients with Marfan syndrome have abnormal aortas and cannot undergo tube graft replacement alone. They must have either a valve-sparing aortic root replacement or a complete aortic root replacement.
Aortic root replacement with a homograft is ideal in the setting of aortic root abscess from endocarditis.
Aortic arch aneurysms
Arch aneurysms pose a formidable technical challenge. Deep hypothermic circulatory arrest (DHCA) with or without antegrade or retrograde cerebral perfusion is usually used to facilitate reanastomosis of the arch vessels. Aortic arch reconstruction techniques vary depending on the arch pathology.
In patients with proximal arch involvement extending from the ascending aorta, a hemiarch replacement may be performed. The ascending aorta is replaced with a Dacron graft beveled as a tongue along the undersurface of the arch. In patients whose conditions mandate replacement of the entire arch, the distal anastomosis is the Dacron graft to the descending thoracic aorta. The head vessels are reimplanted individually or as an island. Grafts have been developed with a trifurcated head-vessel attachment and with a fourth attachment for the cannula. In this case, the head vessels are attached individually to the trifurcated branches.
For patients in whom the arch replacement is part of a staged procedure, preceding the delayed repair of a concomitant descending thoracic aneurysm, an "elephant trunk" is used. That is, the Dacron graft used to reconstruct the transverse arch ends distally in an extended sleeve that is telescoped into the descending thoracic aorta, facilitating later replacement of the descending thoracic/abdominal aneurysm (2-stage procedure).
Descending thoracic aortic aneurysms and thoracoabdominal aneurysms
Descending thoracic aneurysms may be repaired with open surgery or, if appropriate, with endovascular stent grafting techniques.24,25,26,27,17,28 Stent graft repair of descending thoracic aortic aneurysms should be performed if the predicted operative risk is lower than that of an open repair. Patient age, comorbidities, symptoms, life expectancy, aortic diameter, characteristics and extent of the aneurysm, and landing zones, should also be taken into consideration.
Surgically, descending thoracic aneurysms may be repaired with or without the use of a bypass circuit from the left atrium to the femoral artery or femoral vein–femoral artery cardiopulmonary bypass, depending on the length of the anticipated ischemic cross-clamping and the experience of the surgeon. Discrete aneurysms with an anticipated clamp time of less than 30 minutes may be repaired without left heart or cardiopulmonary bypass (ie, "clamp and go" technique). More complex or larger aneurysms are probably safer to repair with the aid of either left heart, partial, or full cardiopulmonary bypass with hypothermic circulatory arrest. The use of left heart or cardiopulmonary bypass is favored to reduce hemodynamic instability and the risk of spinal cord paraplegia.
Descending thoracic aneurysms with the appropriate anatomy may now be repaired by endovascular stent grafts. The GORE TAG is an FDA-approved nitinol-based stent graft designed for descending thoracic aneurysm repair. An appropriate proximal neck of 2 cm prior to the aneurysm is required. Ideally, the proximal landing zone is beyond the left subclavian artery, though, in some circumstances, the stent may be placed proximal to the left subclavian artery. Distally, a sufficient landing zone of 2 cm prior to the celiac artery is required. The aortic inner neck diameters in the proximal and distal landing zones must fall within 23-37 mm. In addition, appropriately sized femoral and iliac arteries (typically >8 mm in diameter) that lack tortuosity and calcium are required for implantation.
The GORE TAG graft has been FDA-approved since March 2005.12 More recently, the Zenith TX2 endovascular graft (Cook Medical Inc.; Bloomington, Ind) was approved in March 2008, followed by the Talent Thoracic Stent Graft (Medtronic Inc.; Minneapolis, Minn) in June 2008.29,30 The Valiant Thoracic Stent Graft (Medtronic Inc.; Minneapolis, Minn) is approved for use outside the United States.
Thoracoabdominal aneurysms, comprising approximately 10% of thoracic aneurysms, may be repaired with the use of a partial bypass of the left atrium to the femoral artery. Crawford type I thoracoabdominal aneurysms involve Dacron graft replacement of the aorta from the left subclavian artery to the visceral and renal arteries as a beveled distal anastomosis, using sequential cross-clamping of the aorta. Crawford type II thoracoabdominal aneurysm repair requires a Dacron graft from the left subclavian to the aortic bifurcation with reattachment of the intercostal arteries, visceral arteries, and renal arteries. Crawford type III or IV thoracoabdominal aneurysm repairs, which begin lower along the thoracic aorta or upper abdominal aorta, may use either the partial bypass of the left atrial artery to the femoral artery or a modified atrio-visceral and/or renal bypass. Prevention of paraplegia is one of the principal concerns in the repair of descending and thoracoabdominal aneurysms.
Under investigational trials, Dr. Timothy Chuter at the University of California at San Francisco Medical Center and Dr. Roy Greenberg at the Cleveland Clinic have treated thoracoabdominal aneurysms using custom-built fenestrated and branched stent grafts. Such devices require precise anatomic tailoring of the grafts to the specific patient's anatomy for placement of the scallops (for visceral flow) or branches (for direct stenting into the visceral vessels).
Ascending aortic aneurysm
Preoperative assessment of coronary artery disease is essential to determine the need for concomitant coronary artery bypass grafting. Transesophageal echocardiography is crucial preoperatively to examine the need for aortic valve replacement. Patients with aortic stenosis or aortic insufficiency in whom the valve leaflets are anatomically abnormal require replacement, whereas patients with aortic insufficiency and normal aortic valve leaflets may be candidates for valve-sparing procedures. Transesophageal echocardiography is valuable for accurate delineation of the aortic root at the sinuses of Valsalva and sinotubular junction.
Aortic arch aneurysm
The major morbidities from aortic arch aneurysm repair are neurologic, cardiac, and pulmonary in nature. All patients require preoperative assessment of cardiac function and evaluation for coronary artery disease. In the operating room, transesophageal echocardiography is used to monitor ventricular function and to assess for atherosclerosis of the aorta.
A major concern in arch surgery is neurologic injury, both transient neurologic dysfunction and permanent neurologic injury. Patients with a higher risk of stroke undergo preoperative noninvasive carotid ultrasound, and those with a history of stroke undergo a brain CT scan. In the operating room, steroids are often given at the onset of the procedure if hypothermic circulatory arrest is anticipated. Evidence suggests that steroids given preoperatively several hours before the operation may have benefit. Some institutions monitor electroencephalogram silence to assess for adequate duration and temperature of cerebral cooling for hypothermic circulatory arrest.
Descending thoracic aneurysms and thoracoabdominal aneurysms
A devastating complication of descending thoracic aneurysm and thoracoabdominal aneurysm repair is spinal cord injury with paraparesis or paraplegia. Preoperatively, some groups perform spinal arteriograms to attempt to localize the artery of Adamkiewicz for reimplantation during surgery. Neurologic monitoring with somatosensory evoked potentials or motor evoked potentials is used by some to assess spinal cord ischemia and identify critical segmental arteries for spinal cord perfusion. Lastly, preoperative placement of catheters for cerebrospinal fluid drainage is performed to increase spinal cord perfusion pressure during aortic cross-clamping.
Spinal cord injury is less prevalent with endovascular stent grafting than with open repair but exists with both types of surgical treatment.24,25,27,28 For endovascular stent grafting, cerebrospinal fluid (CSF) drainage and avoidance of hypotension are the primary mechanisms used to prevent paraplegia. The use of CSF drainage is selective among most centers. For some discrete aneurysms, stent graft coverage may allow for preservation of spinal arteries. Others require coverage of the entire descending thoracic aorta. Indications for use of CSF drains include anticipated endograft coverage of T9-T12, coverage of the long segment of the thoracic aorta, compromised collateral pathways from prior infrarenal AAA repair, and symptomatic spinal ischemia.
Brain protection
Methods used for brain protection during deep hypothermic circulatory arrest (DHCA) include intraoperative EEG monitoring, evoked somatosensory potential monitoring, hypothermia (to temperatures <20o C), packing the patient's head in ice, Trendelenburg positioning (ie, head down), mannitol, CO2 flooding, thiopental, steroids, and antegrade and retrograde cerebral perfusion.
General monitoring and anesthesia
Venous access is obtained with 2 large-bore peripheral IVs and a central line. Filling pressures and cardiac output monitoring are performed with a pulmonary artery catheter. Continuous blood pressure monitoring is performed with a radial arterial line. Nasopharyngeal and bladder probes monitor systemic temperature. Intraoperative transesophageal echocardiography is used to assess myocardial and valvular function.
Ascending aortic replacement
Cardiopulmonary bypass is established and the aorta is cross-clamped just below the innominate artery. The heart is arrested with cardioplegia. The aorta is transected at the sinotubular junction and sized for the appropriate Dacron tube graft. The tube graft is sutured to the proximal aorta with running 4-0 Prolene with a strip of felt. The tube graft is measured to length distally and sutured to the distal aorta using running 4-0 Prolene with a strip of felt.
Valve-sparing aortic root replacement
Once the aorta is transected at the sinotubular junction, the valve is inspected for normal anatomy. If sparing is feasible, the appropriate size tube graft is chosen to allow coaptation of the aortic valve leaflets without aortic insufficiency. In the remodeling technique, the tube graft is tailored to form aortic sinuses. The sinuses of Valsalva of the native aorta are removed, and the coronary ostia are mobilized. The neosinuses of the tube graft are sutured to the scalloped aortic valve with running 4-0 Prolene and a strip of felt.
In the reimplantation technique, Tycron sutures are placed along the subannular horizontal plane and passed through the tube graft. The scalloped aortic valve is placed within the tube graft, and the proximal suture line is secured. The scalloped aortic valve is positioned in the graft to achieve valve competence, and the subcoronary suture line along the scalloped valve is performed with running 4-0 Prolene. The valve is examined for competence within the graft. The coronary ostia are reimplanted in the graft. The graft is measured to length distally and sutured to the distal aorta.
In the reimplantation technique, Tycron sutures are placed along the subannular horizontal plane and passed through the tube graft. The scalloped aortic valve is placed within the tube graft, and the proximal suture line is secured. The scalloped aortic valve is positioned in the graft to achieve valve competence, and the subcoronary suture line along the scalloped valve is performed with running 4-0 Prolene. The valve is examined for competence within the graft. The coronary ostia are reimplanted in the graft. The graft is measured to length distally and sutured to the distal aorta.
Aortic root replacement
The aorta is transected, and the aortic valve is removed. The annulus is sized, and the appropriate valved conduit, stentless root, mechanical composite, or homograft is brought to the field. The coronary ostia are mobilized. Annular sutures are placed and are passed through the valve conduit. The proximal suture is thus secured. The coronary ostia are reimplanted. The distal suture line is performed for the mechanical valve composite, but an additional Dacron graft extension may be required for the stentless roots or homografts, depending on their length.
Patients who have undergone ascending aneurysm repairs are observed for signs of coronary ischemia, particularly if the coronary ostia were reimplanted, and for signs of aortic insufficiency when the aortic valve is repaired. Following the repair of arch aneurysms, particular attention must be given to neurological status, and patients who have had the elephant trunk repair must be observed for signs of paraplegia because the telescoped sleeve in the descending aorta may obstruct critical spinal vessels.
Paraplegia is the main concern in patients who have had repair of the descending and thoracoabdominal aorta. Cerebrospinal fluid drainage may be continued for up to 72 hours postoperatively if necessary, along with motor evoked potential monitoring. Paraplegia and paraparesis may be acute or delayed postoperatively. If paraparesis or paraplegia is delayed, increased mean arterial pressure with pressors and reinstitution of cerebrospinal fluid drainage may augment spinal cord perfusion to reverse this complication. Paraplegia due to occlusion of critical spinal arteries that were not reimplanted cannot be reversed by these maneuvers. Acute postoperative renal dysfunction may be due to extended periods of ischemic cross-clamping or to hypothermic circulatory arrest.
Patients undergoing endovascular stenting are often extubated early postoperatively with a decreased ICU length of stay.
Development of another aneurysm postoperatively is not uncommon in these patients. For this reason, serial evaluations (ie, CT scans or MRI for ascending, arch, or descending aneurysms; echocardiography for ascending aneurysms) may be performed every 3-6 months during the first postoperative year and every 6 months thereafter.
For excellent patient education resources, see eMedicine's patient education article Aortic Aneurysm.
Early morbidity and mortality are related to bleeding, neurologic injury (eg, stroke), cardiac failure, and pulmonary failure (eg, acute respiratory distress syndrome [ARDS]). Risk factors include emergent operation, older age, dissection, congestive heart failure (CHF), prolonged cardiopulmonary bypass time, arch replacement, previous cardiac surgery, need for concomitant coronary revascularization, and reoperation for bleeding. Late mortality is usually related to cardiac disease or distal aortic disease.
Bleeding is a potential complication for all aneurysm repairs. It is minimized by the use of antifibrinolytics, felt strips, and factors, including fresh frozen plasma and platelets. For patients who undergo hypothermic circulatory arrest, the use of aprotinin is controversial, but most groups routinely use aminocaproic acid (Amicar). Coagulopathy and bleeding in severe cases may warrant the use of recombinant factor VII.
Aprotinin (Trasylol), an antifibrinolytic agent used to reduce operative blood loss in patients undergoing open heart surgery, is now only available via a limited-access protocol. Fergusson et al reported an increased risk for death compared with tranexamic acid or aminocaproic acid in high-risk cardiac surgery.31
Stroke is a major cause of morbidity and mortality and typically results from embolization of atherosclerotic debris or clot. Transesophageal echocardiography and epiaortic ultrasound may be beneficial in localizing appropriate areas to clamp. Patients undergoing arch repairs are at the highest risk of permanent and transient neurologic injury. Retrograde cerebral perfusion is beneficial for flushing out embolic debris, but it may be detrimental, with increased intracranial pressure and cerebral edema. Antegrade cerebral perfusion is beneficial for reducing neurologic injury during hypothermic circulatory arrest. Stroke incidence for open surgical repair versus endovascular repair of descending thoracic aneurysms is equivalent.
Myocardial infarction may occur with technical problems with coronary ostia implantation during root replacement for ascending aortic aneurysms and may require reoperation. Pulmonary dysfunction and renal dysfunction are other potentially morbid complications.
Paraparesis and paraplegia, either acute or delayed, are the most devastating complications of descending thoracic aneurysm and thoracoabdominal aneurysm repairs. Despite cerebrospinal drainage, reimplantation of intercostal arteries, evoked potential monitoring, mild hypothermia, and atrial femoral bypass, spinal cord injury still occurs. Endovascular stent grafting has not eliminated spinal cord paraplegia; the incidence varies widely, with an overall incidence of 2.7%.24,25,27,28
Complications specific to endovascular stenting include endoleaks, stent fractures, stent graft migration or thrombosis, iliac artery rupture, retrograde dissection, microembolization, aortoesophageal fistula, and complications at the site of delivery (eg, groin infection, lymphocele, seroma).
According to Culliford et al from 1982,32 Cabrol et al from 1988,33 and Donaldson and Ross from 1982,34 the early hospital mortality rate following repair of ascending aneurysms is 4-10%. Contemporary surgical series demonstrated a continued wide range in operative mortality (2-17%). Stroke occurs in 2-5% of patients.
As would be expected, the early mortality rate after repair of arch aneurysms is considerably higher, approaching 25% in series by Crawford and Saleh from 1981,35 by Crawford et al from 1979,36 by Columbi et al from 1983,37 by Ergin et al from 1982,38 and by Galloway et al from 1989.39 More contemporary results from Coselli and Ueda demonstrate operative mortality of 6-12%. Stroke rate varied from 3-22%. Renal failure that required dialysis occurred in 7% of patients.
The mortality rate after repair of descending thoracic aneurysms is lower, approximately 5-15% according to Crawford et al from 1981,35 to Donahoo et al from 1977,40 to Livesay et al from 1985,41 and to Pressler and McNamara from 1985.2 Contemporary results are unchanged, with 12-15% mortality.
As a group, including all repairs, according to Crawford et al from 1978,42 Crawford et al from 1981,35 and Kitamura et al from 1983,43 survival rates after surgery for chronic aortic aneurysms are approximately 60% at 5 years and 30-40% at 10 years.
The results of a phase II multicenter trial for the GORE-TAG thoracic endovascular stent demonstrated 1.5% 30-day mortality. Temporary or permanent spinal cord paraplegia occurred in 3% of patients and stroke in 4% of patients.44 At 2 years, aneurysm survival was 97% and overall survival 75%.44 For the Medtronic Talent device, the incidence of paraplegia in the stent group was 0-9%, stroke 3.7-8.1%, 30-day mortality 2.9-9.7%, and procedural success >95%.26
When endovascular stent grafting was compared to open surgery for the GORE-TAG device, the rate of paraplegia was 3% in the stent group vs 14% in the open group;24 operative mortality was 1% vs 6%, and early death was 2% vs 10%.45 The patients in the stent group had a shorter ICU and hospital stay, a quicker recovery time, and a lower incidence of major adverse events (except for vascular complications). Complications at 2 years included 4% proximal stent migration, 6% migration of the graft components, and 15% of patients had an endoleak. Survival rates were the same (80% in both the open and stent groups).
Midterm results comparing open descending thoracic aneurysm repair with endovascular stent grafting demonstrate less early operative mortality with endovascular repair (10% for stent grafting vs 15% for open repair) but similar late survival (actuarial survival rate at 48 months of 54% for stent grafting vs 64% for open repair).
Ascending aortic aneurysm repair has been well established and is performed safely with low morbidity and mortality. The controversies lie in the use of valve-sparing root replacements in patients with Marfan syndrome with regard to the durability of the repair. However, because most patients with Marfan syndrome undergo the operation while they are young, they likely require reoperation eventually and the additional years of sparing their native aortic valve and living without anticoagulation are valuable.
Arch aneurysms still carry the most morbidity and mortality because neurologic injury is a great risk. Most controversies involve the methods of cerebral protection. More and more evidence suggests that antegrade cerebral perfusion is an optimal choice to reduce both temporary and permanent neurologic injury.
Recent advances in the treatment of descending thoracic aneurysms and thoracoabdominal aneurysms have used endovascular stent grafting, which offers a less invasive alternative to open surgical repair. The first FDA-approved device for descending thoracic aneurysm repair was approved in March 2005. The nonrandomized prospective comparison of open surgical versus endovascular stenting demonstrated a reduced incidence of operative mortality and reductions in paraplegia, blood loss, operative time, and length of ICU stay. The incidence of stroke between the two groups was similar.
Midterm results suggest that, although early operative mortality rates are lower with endovascular repair than with open surgical repair, late survival rates are equivalent. Paraplegia rates in the real world (as opposed to in carefully selected patient populations of clinical trials) suggest an increased incidence of paraplegia with endovascular stent grafting but range from 0-12% (average 2.7%).
Future studies will examine comparisons of open versus endovascular repair of thoracoabdominal aneurysms and aortic arch aneurysms.
Aneurysms are the most commonly diagnosed conditions of the thoracic aorta that require surgery. Recently, many advances in aortic substitutes, cerebral protection, and perioperative care have led to improved survival rates and outcomes.
Estes JE Jr. Abdominal aortic aneurysm: A study of 102 cases. Circulation. 1950;2:258.
Gross RE, Hurwitt ES, Bill AH Jr. Preliminary observations on the use of human arterial grafts in the treatment of certain cardiovascular defects. N Engl J Med. 1948;239:578.
Lam CR, Aram HH. Resection of the descending thoracic aorta for aneurysm; a report of the use of a homograft in a case and an experimental study. Ann Surg. Oct 1951;134(4):743-52. [Medline].
Cooley DA, De Bakey ME. Resection of entire ascending aorta in fusiform aneurysm using cardiac bypass. J Am Med Assoc. Nov 17 1956;162(12):1158-9. [Medline].
De Bakey ME, Crawford ES, Cooley DA, Morris GC Jr. Successful resection of fusiform aneurysm of aortic arch with replacement by homograft. Surg Gynecol Obstet. Dec 1957;105(6):657-64. [Medline].
Deterling RA, Bhonslay SB. An evaluation of synthetic materials and fabrics suitable for blood vessel replacement. Surgery. Jul 1955;38(1):71-91. [Medline].
Bentall H, De Bono A. A technique for complete replacement of the ascending aorta. Thorax. Jul 1968;23(4):338-9. [Medline].
Ross DN. Homograft replacement of the aortic valve. Lancet. Sep 8 1962;2:487.
Barratt-Boyes BG. Homograft aortic valve replacement in aortic incompetence and stenosis. Thorax. Mar 1964;19:131-50. [Medline].
Sievers HH, Podszus G, Lange PE, Bürsch JH, Bernhard A. Replacement of the aortic root by free implantation of a stentless aortic porcine bioprosthesis in a patient with aneurysm of the sinuses of Valsalva. Thorac Cardiovasc Surg. Dec 1985;33(6):360-1. [Medline].
Dake MD, Miller DC, Semba CP, Mitchell RS, Walker PJ, Liddell RP. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med. Dec 29 1994;331(26):1729-34. [Medline].
US Food and Drug Administration (FDA). FDA Approves First-of-Kind Device to Treat Descending Thoracic Aneurysms. FDA Web site. Available at http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2005/ucm108424.htm. Accessed October 5, 2009.
Davies RR, Gallo A, Coady MA, Tellides G, Botta DM, Burke B. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg. Jan 2006;81(1):169-77. [Medline].
Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg. Nov 2002;74(5):S1877-80; discussion S1892-8. [Medline].
Coady MA, Rizzo JA, Hammond GL, Mandapati D, Darr U, Kopf GS, et al. What is the appropriate size criterion for resection of thoracic aortic aneurysms?. J Thorac Cardiovasc Surg. Mar 1997;113(3):476-91; discussion 489-91. [Medline].
Davies RR, Gallo A, Coady MA, et al. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg. Jan 2006;81:169-77. [Medline].
Svensson LG, Kouchoukos NT, Miller DC, Bavaria JE, Coselli JS, Curi MA. Expert consensus document on the treatment of descending thoracic aortic disease using endovascular stent-grafts. Ann Thorac Surg. Jan 2008;85(1 Suppl):S1-41. [Medline].
Ergin MA, Spielvogel D, Apaydin A, Lansman SL, McCullough JN, Galla JD, et al. Surgical treatment of the dilated ascending aorta: when and how?. Ann Thorac Surg. Jun 1999;67(6):1834-9; discussion 1853-6. [Medline].
Patel ND, Williams JA, Barreiro CJ, Bethea BT, Fitton TP, Dietz HC. Valve-sparing aortic root replacement: early experience with the De Paulis Valsalva graft in 51 patients. Ann Thorac Surg. Aug 2006;82(2):548-53. [Medline].
Cabrol C, Pavie A, Mesnildrey P, Gandjbakhch I, Laughlin L, Bors V, et al. Long-term results with total replacement of the ascending aorta and reimplantation of the coronary arteries. J Thorac Cardiovasc Surg. Jan 1986;91(1):17-25. [Medline].
Kouchoukos NT, Marshall WG Jr, Wedige-Stecher TA. Eleven-year experience with composite graft replacement of the ascending aorta and aortic valve. J Thorac Cardiovasc Surg. Oct 1986;92(4):691-705. [Medline].
LeMaire SA, Green SY, Sharma K, Cheung CK, Sameri A, Tsai PI, et al. Aortic root replacement with stentless porcine xenografts: early and late outcomes in 132 patients. Ann Thorac Surg. Feb 2009;87(2):503-12; discussion 512-3. [Medline].
Ross D. Replacement of the aortic valve with a pulmonary autograft: the "switch" operation. Ann Thorac Surg. Dec 1991;52(6):1346-50. [Medline].
Bavaria JE, Appoo JJ, Makaroun MS, Verter J, Yu ZF, Mitchell RS. Endovascular stent grafting versus open surgical repair of descending thoracic aortic aneurysms in low-risk patients: a multicenter comparative trial. J Thorac Cardiovasc Surg. Feb 2007;133(2):369-77. [Medline].
Criado FJ, Abul-Khoudoud OR, Domer GS, McKendrick C, Zuzga M, Clark NS. Endovascular repair of the thoracic aorta: lessons learned. Ann Thorac Surg. Sep 2005;80(3):857-63; discussion 863. [Medline].
Fattori R, Nienaber CA, Rousseau H, Beregi JP, Heijmen R, Grabenwoger M, et al. Results of endovascular repair of the thoracic aorta with the Talent Thoracic stent graft: the Talent Thoracic Retrospective Registry. J Thorac Cardiovasc Surg. Aug 2006;132(2):332-9. [Medline].
Zipfel B, Hammerschmidt R, Krabatsch T, Buz S, Weng Y, Hetzer R. Stent-grafting of the thoracic aorta by the cardiothoracic surgeon. Ann Thorac Surg. Feb 2007;83(2):441-8; discussion 448-9. [Medline].
Leurs LJ, Bell R, Degrieck Y, Thomas S, Hobo R, Lundbom J. Endovascular treatment of thoracic aortic diseases: combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg. Oct 2004;40(4):670-9; discussion 679-80. [Medline].
US Food and Drug Administration (FDA). Zenith® TX2® Thoracic TAA Endovascular Graft with the H&LB One-Shot Introduction System - P070016. FDA Web site. Available at http://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/DeviceApprovalsandClearances/Recently-ApprovedDevices/ucm074075.htm. Accessed October 5, 2009.
US Food and Drug Administration (FDA). Talent Thoracic Stent Graft System - P070007. FDA Web site. Available at http://www.fda.gov/MedicalDevices/ProductsandMedicalProcedures/DeviceApprovalsandClearances/Recently-ApprovedDevices/ucm074063.htm. Accessed October 5, 2009.
[Best Evidence] Fergusson DA, Hebert PC, Mazer CD, Fremes S, MacAdams C, Murkin JM, et al. A comparison of aprotinin and lysine analogues in high-risk cardiac surgery. N Engl J Med. May 29 2008;358(22):2319-31. [Medline].
Culliford AT, Ayvaliotis B, Shemin R, et al. Aneurysms of the ascending aorta and transverse arch: surgical experience in 80 patients. J Thorac Cardiovasc Surg. May 1982;83(5):701-10. [Medline].
Cabrol C, Gandjbakhc I, Pavie A. Surgical treatment of ascending aortic pathology. J Card Surg. Sep 1988;3(3):167-80. [Medline].
Donaldson RM, Ross DN. Composite graft replacement for the treatment of aneurysms of the ascending aorta associated with aortic valvular disease. Circulation. Aug 1982;66(2 Pt 2):I116-21. [Medline].
Crawford ES, Saleh SA. Transverse aortic arch aneurysm: improved results of treatment employing new modifications of aortic reconstruction and hypothermic cerebral circulatory arrest. Ann Surg. Aug 1981;194(2):180-8. [Medline].
Crawford ES, Saleh SA, Schuessler JS. Treatment of aneurysm of transverse aortic arch. J Thorac Cardiovasc Surg. Sep 1979;78(3):383-93. [Medline].
Colombi P, Rossi C, Porrini AM, Pellegrini A. Aneurysms involving the aortic arch. Report on thirteen surgically treated patients. Thorac Cardiovasc Surg. Aug 1983;31(4):234-8. [Medline].
Ergin MA, Spielvogel D, Apaydin A, et al. Surgical treatment of the dilated ascending aorta: when and how?. Ann Thorac Surg. Jun 1999;67(6):1834-9; discussion 1853-6. [Medline].
Galloway AC, Colvin SB, LaMendola CL, et al. Ten-year operative experience with 165 aneurysms of the ascending aorta and aortic arch. Circulation. Sep 1989;80(3 Pt 1):I249-56. [Medline].
Donahoo JS, Brawley RK, Gott VL. The heparin-coated vascular shunt for thoracic aortic and great vessel procedures: a ten-year experience. Ann Thorac Surg. Jun 1977;23(6):507-13. [Medline].
Livesay JJ, Cooley DA, Ventemiglia RA, et al. Surgical experience in descending thoracic aneurysmectomy with and without adjuncts to avoid ischemia. Ann Thorac Surg. Jan 1985;39(1):37-46. [Medline].
Crawford ES, Snyder DM, Cho GC, Roehm JO Jr. Progress in treatment of thoracoabdominal and abdominal aortic aneurysms involving celiac, superior mesenteric, and renal arteries. Ann Surg. Sep 1978;188(3):404-22. [Medline].
Kitamura S, Onishi K, Nakano S, et al. Early and late results of the Bentall operation for annulo-aortic ectasia. J Cardiovasc Surg (Torino). Jan-Feb 1983;24(1):5-12. [Medline].
Makaroun MS, Dillavou ED, Kee ST. Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg. Jan;41(1):1-9 2005;41(1):1-9. [Medline]. [Full Text].
R. Scott Mitchell, Michel S. Makaroun, Gregario Sicard. A comparative trial of open versus stent graft repair of descending thoracic aneurysms. AATS 2005 Meeting Abstract. 2005.
Anderson CA, Rizzo RJ, Cohn LH. Ascending aortic aneurysms. In: Edmunds LH, Cohn LH, eds. Cardiac Surgery in the Adult. 2nd ed. New York, NY: McGraw-Hill; 2003:1123-48.
Bickerstaff LK, Pairolero PC, Hollier LH, et al. Thoracic aortic aneurysms: a population-based study. Surgery. Dec 1982;92(6):1103-8. [Medline].
Clouse WD, Hallett JW Jr, Schaff HV, et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc. Feb 2004;79(2):176-80. [Medline].
Coselli JS, Conklin LD, LeMaire SA. Thoracoabdominal aortic aneurysm repair: review and update of current strategies. Ann Thorac Surg. Nov 2002;74(5):S1881-4; discussion S1892-8. [Medline].
Coselli JS, Moreno PL. Descending and thoracoabdominal aneurysm. In: Edmunds LH, Cohn LH, eds. Cardiac Surgery in the Adult. 2nd ed. New York, NY: McGraw-Hill; 2003:1169-89.
Crawford ES, Crawford JL. Diseases of the Aorta: Including an Atlas of Angiographic Pathology and Surgical Technique. Baltimore, Md: Lippincott Williams & Wilkins; 1984.
Crawford ES, Walker HS 3rd, Saleh SA, Normann NA. Graft replacement of aneurysm in descending thoracic aorta: results without bypass or shunting. Surgery. Jan 1981;89(1):73-85. [Medline].
David TE, Ivanov J, Armstrong S, et al. Aortic valve-sparing operations in patients with aneurysms of the aortic root or ascending aorta. Ann Thorac Surg. Nov 2002;74(5):S1758-61; discussion S1792-9. [Medline].
Ergin MA, O'Connor J, Guinto R, Griepp RB. Experience with profound hypothermia and circulatory arrest in the treatment of aneurysms of the aortic arch. Aortic arch replacement for acute arch dissections. J Thorac Cardiovasc Surg. 84(5):649-55. [Medline].
Gowda RM, Misra D, Tranbaugh RF. Endovascular stent grafting of descending thoracic aortic aneurysms. Chest. Aug 2003;124(2):714-9. [Medline].
Griepp RB, Ergin MA, Galla JD, et al. Natural history of descending thoracic and thoracoabdominal aneurysms. Ann Thorac Surg. Jun 1999;67(6):1927-30; discussion 1953-8. [Medline].
Guerit JM, Dion RA. State-of-the-art of neuromonitoring for prevention of immediate and delayed paraplegia in thoracic and thoracoabdominal aorta surgery. Ann Thorac Surg. Nov 2002;74(5):S1867-9; discussion S1892-8. [Medline].
Hagl C, Ergin MA, Galla JD, et al. Neurologic outcome after ascending aorta-aortic arch operations: effect of brain protection technique in high-risk patients. J Thorac Cardiovasc Surg. Jun 2001;121(6):1107-21. [Medline].
Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl J Med. Jun 26 1997;336(26):1876-88. [Medline].
LeMaire SA, Miller CC, Conklin LD, et al. Estimating group mortality and paraplegia rates after thoracoabdominal aortic aneurysm repair. Ann Thorac Surg. Feb 2003;75(2):508-13. [Medline].
Ling E, Arellano R. Systematic overview of the evidence supporting the use of cerebrospinal fluid drainage in thoracoabdominal aneurysm surgery for prevention of paraplegia. Anesthesiology. Oct 2000;93(4):1115-22. [Medline].
Minatoya K, Karck M, Hagl C, et al. The impact of spinal angiography on the neurological outcome after surgery on the descending thoracic and thoracoabdominal aorta. Ann Thorac Surg. Nov 2002;74(5):S1870-2; discussion S1892-8. [Medline].
Moffatt SD, Mitchell RS. Endovascular stent management of thoracic aneurysms and dissections. Cardiac Surgery in the Adult. 2003;1191-204.
Morasch MD. Percutaneous techniques for aneurysm repair. J Vasc Surg. Feb 2006;43 Suppl A:69A-72A. [Medline].
Olsson C, Thelin S, Stahle E, Ekborn A, Granath F. Thoracic aortic aneurysm and dissection: Increasing prevalence and improved outcomes reported in a nationwide population-based study of more than 14,000 cases from 1987 to 2002. Circulation. 2006;114:2611-8.
Pressler V, McNamara JJ. Aneurysm of the thoracic aorta. Review of 260 cases. J Thorac Cardiovasc Surg. Jan 1985;89(1):50-4. [Medline].
Reich DL, Uysal S, Ergin MA, Griepp RB. Retrograde cerebral perfusion as a method of neuroprotection during thoracic aortic surgery. Ann Thorac Surg. Nov 2001;72(5):1774-82. [Medline].
Roe BB. Air embolism prevention. Ann Thorac Surg. Aug 1987;44(2):212-3. [Medline].
Roe BB. Prevention of air embolism with intravascular carbon dioxide washout. J Thorac Cardiovasc Surg. Apr 1976;71(4):628-30. [Medline].
Shum-Tim D, Tchervenkov CI, Laliberte E, et al. Timing of steroid treatment is important for cerebral protection during cardiopulmonary bypass and circulatory arrest: minimal protection of pump prime methylprednisolone. Eur J Cardiothorac Surg. Jul 2003;24(1):125-32. [Medline].
Spielvogel D, Mathur MN, Griepp RB. Aneurysms of the aortic arch. In: Edmunds LH, Cohn LH, eds. Cardiac Surgery in the Adult. 2nd ed. New York, NY: McGraw-Hill; 2003:1149-68.
Stone DH, Brewster DC, Kwolek CJ, et al. Stent-graft versus open-surgical repair of the thoracic aorta: mid-term results. J Vasc Surg. Dec 2006;44(6):1188-97. [Medline].
Sullivan TM, Sundt TM 3rd. Complications of thoracic aortic endografts: spinal cord ischemia and stroke. J Vasc Surg. Feb 2006;43 Suppl A:85A-88A. [Medline].
Wheat MW Jr, Boruchow IB, Ramsey HW. Surgical treatment of aneurysms of the aortic root. Ann Thorac Surg. Dec 1971;12(6):593-607. [Medline].
Wheat MW, Wilson JR, Bartley TD. Successful replacement of the entire ascending aorta and aortic valve. JAMA. May 25 1964;188:717-9. [Medline].
thoracic aortic aneurysm, aortic aneurysm, ascending thoracic aortic aneurysm, thoracic aortic aneurysm repair, aneurysm repair, descending thoracic aortic aneurysm, abdominal aortic aneurysm, thoracic aneurysm, thoracoabdominal aneurysm, aneurysm rupture
Elaine Tseng, MD, Assistant Professor of Surgery, Division of Cardiothoracic Surgery, University of California at San Francisco
Elaine Tseng, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Surgeons, American Medical Association, and Massachusetts Medical Society
Disclosure: Nothing to disclose.
Mabelle H Cohen, MD, Fellow, Department of Cardiothoracic Surgery, University of California, San Francisco
Mabelle H Cohen, MD is a member of the following medical societies: American College of Surgeons and American Medical Association
Disclosure: Nothing to disclose.
Benson B Roe, MD, Emeritus Chief, Division of Cardiothoracic Surgery, Emeritus Professor, Department of Surgery, University of California at San Francisco Medical Center
Benson B Roe, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Cardiology, American College of Surgeons, American Heart Association, American Medical Association, American Society for Artificial Internal Organs, American Surgical Association, California Medical Association, Society for Vascular Surgery, Society of Thoracic Surgeons, and Society of University Surgeons
Disclosure: Nothing to disclose.
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment
Shreekanth V Karwande, MBBS, Chair, Professor, Department of Surgery, Division of Cardiothoracic Surgery, University of Utah School of Medicine and Medical Center
Shreekanth V Karwande, MBBS is a member of the following medical societies: American Association for Thoracic Surgery, American College of Chest Physicians, American College of Surgeons, American Heart Association, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association
Disclosure: Nothing to disclose.
Paolo Zamboni, MD, Professor of Surgery, Chief of Day Surgery Unit, Chair of Vascular Diseases Center, University of Ferrara, Italy
Paolo Zamboni, MD is a member of the following medical societies: American Venous Forum and New York Academy of Sciences
Disclosure: Nothing to disclose.
Mary C Mancini, MD, PhD, Professor and Chief, Cardiothoracic Surgery, Department of Surgery, Louisiana State University Health Sciences Center-Shreveport
Mary C Mancini, MD, PhD is a member of the following medical societies: American Association for Thoracic Surgery, American College of Surgeons, American Surgical Association, Phi Beta Kappa, Society of Thoracic Surgeons, and Southern Surgical Association
Disclosure: Nothing to disclose.
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