segments of the aorta are evaluated and replaced if abnormal, including the aortic valve, sinuses of

Valsalva, the tubular portion of the ascending aorta, and the aortic arch. Cardiopulmonary bypass is

established through right atrial (venous) cannulation and either aortic, femoral, or axillary arterial

cannulation. The left ventricle is vented via the right superior pulmonary vein. The use of the axillary

artery for cannulation allows for selective antegrade cerebral perfusion if circulatory arrest is needed

during the replacement of the aorta (Fig. 85-4).33,34 The axillary artery is exposed via a 4-cm transverse

incision 2 cm below and parallel to the clavicle. Once through the pectoral muscles, the axillary vein is

isolated and retracted, exposing the axillary artery. After systemic heparinization, an 8- or 10-mm

Dacron graft is anastomosed in an end-to-side fashion onto the artery. The arterial cannula is then

secured to the Dacron graft. Myocardial protection is achieved by infusion of antegrade blood

cardioplegia into the coronary ostia and retrograde cardioplegia into the coronary sinus accompanied by

a topical hypothermia.

If the aneurysm is contained to the root or ascending aorta and does not involve the aortic arch or

head vessels, the heart can be arrested with the cross-clamp proximal to the innominate artery, and mild

hypothermia can be used for systemic protection while the patient is maintained on cardiopulmonary

bypass. A tube graft is then anastomosed distally and proximally using running monofilament suture.

The aortic valve is also assessed with the aorta open and the valve repaired or replaced as necessary

(Fig. 85-5). If the dilation of the aorta extends into the arch, deep HCA allows for complete resection

and reconstruction of the diseased aorta and an open distal anastomosis in a bloodless field. Cerebral

protection can be augmented by maintaining antegrade cerebral perfusion via the right axillary cannula

and clamping the proximal innominate artery. The distal anastomosis is then performed in a timely

manner. The cross-clamp is then reapplied to the graft, and full cardiopulmonary bypass can then

resume. The proximal anastomosis is then completed encompassing all diseased portions of the

ascending aorta and the aortic root.

Figure 85-4. Cannulation of the right axillary artery with the use of a side graft. Once established, axillary artery cannulation can

allow for antegrade cerebral perfusion throughout the aortic replacement procedure.

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Figure 85-5. Common repair options include: (A) graft replacement of the ascending aorta from the sinutubular junction to the

aortic arch, (B) graft replacement with concomitant aortic valve replacement, (C) total aortic root replacement and ascending

aortic replacement with a valve conduit and coronary reimplantation (Bentall procedure), and (D) Valve-sparing aortic root

reimplantation where the native aortic valve is left in-situ (David procedure).

Aneurysms involving the aortic root require isolation of the right and left coronary ostia and

reimplantation into the Dacron tube graft. Care must be taken to ensure the coronary arteries are not

kinked. In this setting the native aortic valve can be spared (valve-sparing root replacement) if the

leaflets are normal or can be replaced with a valved conduit (Bentall procedure).

Aortic Arch Aneurysms

Operations involving replacement of the thoracic aortic arch are approached from a median sternotomy

and use HCA. In this setting, the patient is cooled to 16°C to 24°C and the cardiopulmonary bypass

circuit is turned off for up to 45 to 60 minutes. The use of selective antegrade cerebral perfusion

(cannulation and perfusion of the right axillary artery with a clamp on the proximal innominate artery)

allows perfusion of the right carotid and vertebral arteries during operations of the aortic arch, and

reduces the risk of embolism and associated morbidity by maintaining some perfusion to the brain.35

With selective antegrade cerebral perfusion, the patient may require less systemic hypothermia allowing

for reduced bypass times. Replacement of the arch is often best performed with the use of a

multibranched aortic graft to allow individual anastomoses to each of the three great vessels (Fig. 85-

6).35,36 This approach, rather than reimplanting an island of aortic tissue with all the great vessels, has

been suggested to reduce the risk of embolization but, more importantly, minimizes the risk of late

aneurysmal degeneration of the aortic patch.36

Descending Thoracic Aortic Aneurysms

Open surgical repair of the descending thoracic aorta is performed through a left posterolateral

thoracotomy. The exact interspace depends on the proximal and distal extent of the disease. Prior to

positioning, a double-lumen endotracheal tube is placed for single-lung ventilation. A variety of adjuncts

have been devised to ameliorate the most common complications of stroke, paralysis, and visceral organ

malperfusion during descending thoracic aneurysm repair.36 Cerebrospinal fluid (CSF) drainage with a

lumbar drain allows intra- and postoperative monitoring of CSF pressure and drainage and has been

shown to reduce the incidence of paraparesis and paraplegia caused by spinal cord ischemia.37 Other

modalities used to mitigate risk of spinal cord injury include monitoring of sensory evoked potentials

and motor evoked potentials.38,39 Pharmacologic agents, including barbiturates, naloxone, and steroids,

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may also help reduce neurologic injury when administered during the procedure. In addition, epidural

catheters are extremely beneficial for pain control and can improve early mobilization and pulmonary

function.

Figure 85-6. Traditional total arch repairs. A: Island approach. B: Branched graft approach. C:. Traditional elephant trunk (shown

with concomitant island approach).

Figure 85-7. Schematic of left heart bypass whereby partial bypass is used to maintain perfusion to the viscera and lower

extremities. The inflow to the Bio-Medicus pump is the left inferior pulmonary vein, and the outflow is the left femoral artery.

This technique avoids the need for an oxygenator.

There are two options to perform this procedure: sequential clamping versus HCA. The use of left

heart or partial cardiopulmonary bypass has been shown to decrease the risk of visceral and spinal cord

ischemia. If the arch is relatively spared and enough normal aorta can be identified distal to the left

common carotid artery, a proximal clamp can be placed, which allows for left heart bypass. In using left

heart bypass, the left atrium via the left inferior pulmonary vein and the femoral artery are cannulated.

A centrifugal pump, heparin-bonded tubing, and minimal heparinization can be used, which can result in

less bleeding than in traditional cardiopulmonary bypass. With this technique, mild hypothermia is used

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with sequential aortic clamping, reimplantation of critical intercostal arteries, and the distal anastomosis

constructed with peripheral and visceral perfusion via the femoral artery (Fig. 85-7).40 Conversely, for

patients in whom the transverse arch cannot be safely clamped, profound HCA is used for both cardiac

protection and central and peripheral nervous system protection. With this technique, full

cardiopulmonary bypass with cannulation of the femoral artery and femoral vein allows for cooling of

the patient and deep HCA and the proximal anastomoses can be performed in a bloodless field. 41

After clamping the aorta (or initiating HCA), the aneurysm is opened and the proximal cuff is

fashioned. An interposition graft is sutured to the proximal aorta in an end-to-end fashion. Once

completed, cardiopulmonary bypass can be reinstituted and the graft clamped to perform the distal

anastomoses when using HCA. The distal aorta and graft are then fashioned and an anastomosis created.

Significant lumbar artery identified via preoperative computed tomographic aortography or

intraoperative assessment can be reimplanted into the interposition graft. There is continued

controversy regarding the necessity to perform this as this process can often take more than 30 minutes

during which the aorta may be clamped. Once the affected portion of aorta has been successfully

replaced, the patient can be appropriately warmed and hemostasis ensured. The patient is removed from

cardiac support and thoracotomy closed in the usual manner. If the diaphragm was taken down, it

should be reapproximated with interrupted nonabsorbable suture.

Endovascular Therapy

4 Thoracic endovascular aneurysm repair (TEVAR) for the descending thoracic aorta has become the

preferred treatment approach not only for aneurysms but also for dissections and traumatic aortic

injuries as they often can be performed with less morbidity than that associated with open surgical

treatment. Endovascular stent grafts are available in a wide range of sizes and are made of

polytetrafluoroethylene (PTFE) or woven polyester with steel or nitinol stents to maintain their shape.

Absolute contraindications for TEVAR include insufficient proximal and distal landing zones, or

excessive aortic tortuosity. Relative and debated contraindications include connective tissue disease

(such as Marfan’s), young age, or patients unlikely to follow-up. Patients who are not candidates for

endovascular repair require open repair.

Planning for TEVAR requires careful review of all imaging. Proximal and distal landing zones with a

minimum of 2-cm “normal” aorta are preferred. To prevent endoleaks, stent grafts are oversized by

approximately 10% to 15% from the CT cross-sectional diameter. The size of the femoral and iliac

arteries must be large enough to allow safe passage of the delivery sheaths. In general, vessels should

be 7 to 8 mm depending on the size of the chosen stent graft. In some cases, an adequate proximal

landing zone can only be accomplished by coverage of the left subclavian artery. If the left subclavian is

covered, a carotid to subclavian bypass can be considered to prevent spinal cord ischemia, subclavian

steal, and limb ischemia. In cases where the patient has a patent left internal mammary bypass graft or

an incomplete circle of Willis with a left vertebral artery that terminates in a posterior inferior

cerebellar artery, a carotid subclavian bypass should be performed prior to TEVAR.

TEVAR is performed by first obtaining femoral or iliac access. For smaller grafts this can be done with

all percutaneous access and use of closure devices. In other cases, a femoral or iliac cutdown is

performed. A stiff wire is advanced into the aortic root under fluoroscopic guidance. A separate pigtail

catheter is advanced over a wire into the aortic root for aortography. The stent graft is then advanced

into the appropriate position over the stiff wire. Once in place, an aortogram is performed to ensure

proper positioning. A completion angiogram is performed to ensure no positioning, presence of kinks or

endoleaks, or continued filling of the aneurysm sac. A type 1A (proximal) or type 1B (distal) endoleak

typically requires placement of an additional stent graft (Fig. 85-8).

Hybrid Procedures

As endovascular approaches have evolved, so too have the options for hybrid procedures combining

open and endovascular surgery. Patients with combined arch and descending thoracic aneurysms are

often ideal candidates for hybrid procedures. The traditional approach has been a two-stage open

procedure (elephant trunk). In the first operation, the arch aneurysm is repaired under HCA via a

median sternotomy. The distal end of the Dacron graft replacing the arch is sewn to the proximal

descending aorta with a long cuff to allow for future repair of the descending aortic aneurysm in the

second stage. In the second stage, the traditional procedure has been an open descending aneurysm

repair using the long cuff left at the initial operation as the proximal new aorta. Stent graft therapy has

allowed for the second stage to be performed less invasively with an endovascular approach. An

alternative approach to these patients is debranching of the arch vessels via sternotomy using a

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trifurcated graft off the ascending aorta to the great vessels. This can be performed without the use of

cardiopulmonary bypass using a side-biting clamp on the ascending aorta. This is followed by

endovascular repair of the arch and descending aorta covering the native take off of the great vessels.

Other patients who benefit from hybrid procedures include those with thoracoabdominal aneurysms

who require debranching of visceral vessels prior to stent graft repair. The inflow for these debranching

bypasses is traditionally from the iliac vessels but can include the proximal abdominal or descending

thoracic aorta.

Figure 85-8. Reconstruction of a CT scan in a patient with a descending thoracic aneurysm (A) prior to repair, and (B) after

endovascular stent graft repair showing successful exclusion of the aneurysm sac.

Outcomes and Complications

With advances in surgical techniques significant improvements in morbidity and mortality with aortic

aneurysm surgery have been made. Important outcomes following aortic surgery include mortality,

stroke, paralysis, renal failure, and freedom from reoperation. Operative mortality for elective

ascending aortic aneurysm repair is low, ranging from 1.2% to 3.7% in contemporary series.42–45 Risk

factors for mortality include advanced age, coronary artery disease, heart failure, reoperative

sternotomy, and need for HCA. Interestingly, patients with connective tissue disorders, such as Marfan

syndrome, have a low operative mortality of 1.5%, partially due to their young age at time of

presentation.46 The primary morbidity following ascending aortic surgery is bleeding and stroke.

Reexploration for bleeding occurs in 5.6% to 9.9% of patients.45 Precise suturing with even tension and

minimal aortic tissue trauma is essential to minimize bleeding risks. Use of Teflon felt material and

hemostatic agents may further reduce bleeding. Neurologic injury following surgery occurs in 3.2% to

9.8% of patients.45 Stroke is usually due to embolization of debris or thrombus from the aorta resulting

in focal deficits. Diffuse injury is attributed to microemboli, insufficient cooling, and prolonged

circulatory arrest. The use of cerebral perfusion appears to improve these outcomes.47 The need for late

reoperation occurs because of pseudoaneurysm formation, graft infection, or progressive aortic

enlargement. Reoperation carries significantly greater operative mortality ranging from 4% to 22%.48

Up to 60% of reoperations occur because of inadequate repair during the primary operation and can be

avoided if all aneurysmal tissue is resected.49 Some patients, particularly those with connective tissue

disorders, have progressive aortic pathology and are prone to reoperation. Pseudoaneurysm formation

may be the result of a technical error, infection, or inadequate resection of diseased segments. Graft

infections are reported in 1.0% to 6.0% of patients, are associated with very high operative mortality

and often require a homograft for repair.50

More extensive aortic operations involving the aortic arch are associated with greater risks of

mortality and morbidity. Operative mortality has ranged from 5% to 8% in contemporary series with

stroke risks of 5% to 12%.51,52 As arch surgery requires longer circulatory arrest times, increased

incidences of renal failure of 3% to 7% are noted.

Similar to ascending aneurysm surgery, mortality with open repair of descending thoracic aneurysms

has significantly improved. Contemporary open elective repair is associated with an operative mortality

of 5%.53 The major complications include stroke (2% to 10%), paralysis (5% to 10%), renal failure

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(13%), and recurrent laryngeal nerve injury (40%). Increased extent of aortic replacement correlates

with risks of paralysis. The use of adjuncts such as CSF drainage, intercostal artery reimplantation, and

distal aorta perfusion with cardiopulmonary bypass or left heart bypass has significantly reduced

incidence of paraplegia and renal failure.54,55

Endovascular therapy has emerged as the first-line therapy for descending TAAs. In most series,

perioperative mortality ranges from 1.9% to 3.1% for elective TEVAR.56 Complications include stroke

(4% to 8%), paralysis (3% to 11%), and access site complications. The risk of stroke with TEVAR

increases with more proximal deployment in the arch, the presence of mobile atheroma in the arch, and

history of cerebrovascular disease. Longer segment aortic coverage increases risk of paralysis. Use of

adjuvants such as CSF drainage or carotid-subclavian bypass when the left subclavian is covered reduces

incidence of paraplegia. Multiple studies have supported these findings reporting lower mortality,

paraplegia, and renal failure following endovascular therapy versus open surgery for the descending

thoracic aorta.24,57

Long-term data on TEVAR are limited due to its recent and evolving development. In a 5-year followup of the Gore TAG Food and Drug Administration trial, aneurysm-related mortality was 2.8%

compared to 11.7% for nonrandomized open surgical controls.57 The rate of endoleak was 4.3%, which

in other studies, ranged from 4% to 8%. The most common endoleak is a type 1A (proximal). Graft

migration can occur in 1% to 2% of patients. The rate of reintervention is estimated to be 10.8% at a

median 5.6 months, primarily for type 1 and type 3 endoleaks.

THORACIC AORTIC DISSECTION

History

In 1760, King George II of England died at Kensington palace while “straining on the toilet.” His

personal physician, Dr. Frank Nicholls performed an autopsy and provided the first description of a

thoracic aortic dissection. He stated “in the trunk of the aorta we found a transverse fissure on its inner

side, about an inch and half long, through which some blood had recently passed under its external coat

and formed an elevated ecchymosis.”58 King George died from acute aortic dissection with rupture and

cardiac tamponade. The first successful surgical approaches to acute aortic dissection were described by

DeBakey and associates in 1954.59

Prevalence and Classification

Acute aortic dissection is the most frequent lethal condition of the aorta. Aortic dissections are classified

based on anatomic involvement and extent. Two classification systems are widely utilized: the Debakey

and the Stanford systems. In the Debakey system, a type 1 dissection extends from the ascending aorta

into the descending thoracic aorta, possibly to the aortic bifurcation (Fig. 85-9). Type 2 dissection

involves the ascending aorta and terminates proximal to the left subclavian artery. Type 3 dissection

starts distal to the left subclavian artery and involves the descending or abdominal aorta. The Stanford

classification has become more commonly used as it readily translates to clinical decision making.60 A

Stanford type A dissection involves the ascending aorta and includes Debakey type 1 and type 2. A

Stanford type B dissection involves the descending aorta only, similar to Debakey type 3. Type B

dissections are now further subclassified as complicated versus uncomplicated. Complicated type B

dissections are defined by uncontrolled pain, impending rupture, or visceral organ malperfusion. Acute

aortic dissection is three times more frequent than thoracic or abdominal aortic rupture.15 The estimated

worldwide prevalence is 2.95 per 100,000 per year, with an estimated 2,000 new cases in the United

States each year.61 Stanford type A dissection constitutes 75% of acute aortic dissections.

Etiology and Risk Factors

Aortic dissection is initiated when a weakened aortic wall is exposed to a high impulse force. The most

common primary tear occurs in the right anterior aspect of the ascending aorta, likely due to the

impulse force of blood ejected from the left ventricle. Once this entry tear occurs, blood enters the

aortic media and propagates, creating a false channel of flow. The false channel may propagate

antegrade, retrograde, or both. When the false channel encounters a branch vessel, the origin of the

branch vessel may tear off, leading to a fenestration with communication between the true and false

lumens. The branch vessel will then derive some or all of its blood flow from the false lumen. The

patency and origin of branch vessel perfusion is critical in determining treatment plans for patients with

2461

acute aortic dissection. Although the false lumen may end blindly 4% to 12% of patients leading to

false-lumen thrombosis, the vast majority of patients have multiple fenestrations leading to false-lumen

patency. In chronic dissection, the false-lumen remodels over time, leading to further aneurysm

formation and possibly rupture.

Figure 85-9. Debakey classification system for aortic dissection. Stanford type A = Debakey type 1 or type 2. Stanford type B =

Debakey type 3A or 3B.

Diagnosis

Acute aortic dissection has been described as the “great imitator,” as symptoms are often ascribed to

other pathologies, such as myocardial infarction, peptic ulcer disease, or musculoskeletal back pain. For

this reason, diagnosis of aortic dissection can be delayed. Dissections usually present with pain

involving the chest, back, or abdomen. The location of maximum pain tends to change as the dissection

progresses. Involvement of branch vessels may lead to syncope, stroke, paralysis, myocardial ischemia,

mesenteric ischemia, or limb ischemia. Aortic root involvement may lead to acute aortic insufficiency

and symptoms of acute heart failure. Pericardial effusions can present with cardiac tamponade

symptoms.

Management and Natural History

5 Once aortic dissection occurs, mortality and morbidity are high. Fifty percent of patients with acute

Stanford type A dissection die within 48 hours if untreated. Data suggest a 1% per hour rate of

mortality from the onset of symptoms. The most frequent causes of death are aortic rupture,

tamponade, heart failure, and cerebral or visceral organ malperfusion. In contrast, acute mortality of

type B aortic dissection is lower with 90% in-hospital survival.62 Survivors of aortic dissection then

develop a chronic aortic dissection characterized by aortic remodeling and progressive aneurysm

enlargement. The annual growth rates for patients suffering from chronic dissections are significantly

higher than nondissected aneurysms, ranging from 0.24 to 0.48 cm/yr.

Acute Stanford type A aortic dissections mandate emergent surgery. Complicated type B aortic

dissections, characterized by uncontrolled pain, impending rupture, or visceral organ malperfusion, also

require intervention with open or endovascular techniques. Intervention for chronic dissection is

2462

indicated for aneurysm enlargement with size criteria similar to nondissected aneurysmal disease.

Surgery for Type A Aortic Dissections

Operative intervention for acute type A aortic dissection is focused on the aortic root, ascending aorta,

and aortic arch to eliminate the common causes of death of aortic rupture, cardiac tamponade,

myocardial ischemia, stroke, and heart failure. A successful operation for type A dissections reconstructs

the root with a well-functioning valve, replaces the ascending aorta and the proximal arch maintaining

true-lumen patency of the arch vessels. Depending on the extent of the dissection, arterial cannulation

can be challenging. The most common sites of cannulation include the right axillary and femoral

arteries, however, alternative strategies such as cannulating the true lumen of the dissected ascending

aorta using an ultrasound guided Seldinger technique may also be performed.63 Once the patient is

cooled on cardiopulmonary bypass to an adequate temperature for HCA, the ascending aorta is resected.

Often this performed with selective antegrade cerebral perfusion via the right axillary artery or with

retrograde cerebral perfusion by a separate cannula placed in the superior vena cava. The ascending

aorta is then replaced with an interposition graft from the sinotubular junction to the aortic arch. In rare

situations, the aortic arch is so disrupted, a total arch reconstruction is performed. If the aortic root is

dissected, the root is reconstructed and the aortic valve resuspended (Fig. 85-10). If there is significant

pre-existing aortic root disease a root replacement or valve-sparing root procedure may be performed.

Figure 85-10. Dissected aortic root. The right and left coronary arteries (A) are rarely avulsed but if so require bypass. The aortic

valve is resuspended using pledgeted mattress sutures (B) at the aortic valve commissures to allow valve coaptation. Felt and/or

bioglue (C) is utilized to fill the dissected space as “neo media.”

Endovascular Therapy

Endovascular therapy has a growing and vital role in the acute and chronic management of type A and

type B aortic dissections. For acute type A aortic dissections, endovascular therapy may be urgently

performed to alleviate abdominal malperfusion. In patients who present with mesenteric ischemia,

endovascular fenestration, celiac or superior mesenteric artery stenting may be utilized to improve

visceral perfusion prior to proximal aortic surgery.

TEVAR has an increasing and evolving role in patients with acute and chronic type B aortic dissections

and residual dissections following type A dissection repair. Preoperative CT angiography must be

carefully reviewed to understand the anatomy and extent of the proximal fenestrations, the true and

false lumen, as well as proximal and distal landing zones (Fig. 85-11). True-lumen arterial access may

be gained percutaneously or with a femoral cutdown. Intravascular ultrasound (IVUS) is typically

utilized to confirm true-lumen position. For dissections, grafts are not oversized to minimize the chance

of rupture or retrograde dissection. The extent of coverage depends on the pathology being treated, but

typically involves coverage of the entire descending thoracic aorta. Completion aortography is essential

to identify any endoleaks and ascertain visceral perfusion following device deployment.

Outcomes and Complications

Outcomes following surgery for type A aortic dissection have improved, however significant morbidity

and mortality remain. The International Registry of Acute Aortic Dissections (IRAD) reported the

outcomes of 526 patients at 18 centers.64 Overall hospital mortality was 25%. The most common causes

of death included aortic rupture (33%), stroke (14%), abdominal malperfusion (12%). Risk factors for

2463

increased mortality included age, extent of dissection, hemodynamic instability, and time since onset of

symptoms. Long-term survival for patients who survive was 96% at 1 year and 91% at 3 years.

Figure 85-11. TEVAR for acute type B dissection.

Similar improvements have been made with open surgery for complicated type B dissections. In the

most recent IRAD series, operative mortality was 29%, with a stroke rate of 9%, paraplegia rate of 5%,

and renal failure rate of 8%.62 Results have improved with TEVAR. In a recent meta-analysis of 609

patients with type B aortic dissection, perioperative mortality was 5% with a 3% rate of stroke and 2%

rate of retrograde aortic dissection.65 In the IRAD data, TEVAR was associated with a lower mortality

(11% vs. 34%) and complication rate (21% vs. 40%) compared to open surgery. Interestingly, mortality

following TEVAR was similar to those patients managed medically who presumably had uncomplicated

dissections. Importantly, the IRAD data were nonrandomized and subject to treatment bias which should

limit overarching conclusions. Nevertheless, the data suggest that TEVAR is associated with significantly

less morbidity and mortality than open surgical repair.

Based on this favorable data with complicated type B dissections, TEVAR is now being evaluated for

uncomplicated type B dissections. Uncomplicated acute type B aortic dissections have a favorable in

hospital survival of 89% to 93% with medical therapy alone.66 The long-term outcomes however are not

favorable with only 78% surviving at 3 years.67 Two European randomized trials have been conducted

to evaluate the outcomes of TEVAR for uncomplicated type B dissection. The INvestigation of STEnt

grafts in Aortic Dissection (INSTEAD) trial has been recently published.68 At 2 years, TEVAR failed to

improve 2-year survival in comparison to medical therapy alone. Favorable aortic remodeling, such as

true-lumen size and false-lumen thrombosis; however, occurred in 91% of TEVAR patients compared to

19% of medical only patients. The ADSORB (Acute Uncomplicated Aortic Dissection type B) trial also

demonstrated favorable aortic remodeling after TEVAR.69 In 61 randomized patients, TEVAR increased

true-lumen size, decreased false-lumen size, and reduced overall aortic diameter. In longer-term data,

this favorable aortic remodeling appeared to have led to improved survival. At 5 years, the INSTEAD

trial data demonstrated improved aorta-specific mortality with TEVAR (6.9% vs. 19.3%) compared to

medical therapy alone.70 More long-term data are required to determine the utility of TEVAR for

uncomplicated type B dissection.

CONCLUSIONS

Aneurysm disease of the thoracic aorta has a high morbidity and mortality, especially after the

development of an aortic dissection. Treatment of these patients requires careful preoperative planning,

meticulous protection of the viscera and spinal cord, and rigorous follow-up. Endovascular therapy has

become the preferred technique for descending thoracic aortic disease and offers patients less morbidity

than that associated with open surgical treatment. The best outcomes for all patients who suffer from

aneurysm disease of the thoracic aorta are provided by a multidisciplinary approach with a firm

understanding of the pathogenesis and natural history of the disease.

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