AUTHOR AND EDITOR INFORMATION

Section 1 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

INTRODUCTION

Section 2 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Background

Thoracic aortic aneurysm represents aneurysmal dilatation of ascending, arch, or descending thoracic aorta. Aneurysm is defined as a localized or diffuse dilatation of more than 50% normal diameter of the aorta. It occurs with the highest frequency of all of the diseases of the thoracic aorta that require surgical treatment. Atherosclerosis or connective tissue disorders may be contributing underlying disorders that facilitate aortic dilatation. Frequently associated factors include advanced age, hypertension, smoking, atherosclerosis, and aortic dissection.

Thoracic aneurysms are classified by the portion of aorta involved: the ascending thoracic aorta, the arch, or the descending thoracic aorta. This anatomic distinction is important because the etiology, natural history, and treatment of thoracic aneurysms vary for each of these segments.

Aneurysms of the descending aorta are most common, followed by aneurysms of the ascending aorta, whereas arch aneurysms occur less often. In addition, descending aortic thoracic aneurysms may extend distally to involve the abdominal aorta and create a thoracoabdominal aortic aneurysm.

Sometimes, the entire aorta may be ectatic, with localized aneurysms seen at sites in both the thoracic and abdominal aorta. Interestingly, thoracic aortic aneurysms are less common than aneurysms of the abdominal aorta.

Pathophysiology

Cystic medial necrosis

Aneurysms of the ascending thoracic aorta most often result from the process of cystic medial degeneration (or cystic medial necrosis).

Histologically, cystic medial degeneration has the appearance of smooth muscle cell necrosis and elastic fiber degeneration, with the presence in the media of cystic spaces filled with mucoid material. Although these changes occur most frequently in the ascending aorta, in some cases the entire aorta may be similarly affected.

The histologic changes lead to weakening of the aortic wall, which in turn results in the formation of a fusiform aneurysm. Such aneurysms often involve the aortic root and may consequently result in aortic regurgitation. The term annuloaortic ectasia is often used to describe this condition.

Cystic medial degeneration is found in virtually all cases of Marfan syndrome and may be associated with other connective tissue disorders as well, such as Ehlers-Danlos syndrome. Marfan syndrome is an autosomal dominant heritable disorder of connective tissue that has been discovered to be due to mutations in one of the genes for fibrillin, a structural protein that helps direct and orient elastin in the developing aorta.

These mutations result in a decrease in the amount of elastin in the aortic wall, together with a loss of the normally highly organized structure of elastin. As a consequence, a marfanoid aorta exhibits markedly abnormal elastic properties and increased systemic pulse wave velocities from an early age, and over time, the aorta exhibits progressively increasing degrees of stiffness and dilatation.

In patients without Marfan syndrome, however, it is not possible to recognize the histologic diagnosis of cystic medial degeneration prospectively (eg, without surgery or necropsy). This fact has significantly limited our understanding of medial degeneration and its natural history, and it remains unclear to what extent this syndrome may represent an independent disease process versus a manifestation of another disease state.

It has long been suspected that some patients who have annuloaortic ectasia and proven cystic medial degeneration without the classic phenotypic manifestations of Marfan syndrome may, in fact, have a variation, or forme fruste, of Marfan syndrome, although this theory remains unproved. On the contrary, many patients with ascending thoracic aortic aneurysms appear to have nothing more than idiopathic cystic medial degeneration.

Atherosclerosis

Atherosclerotic aneurysms infrequently occur in the ascending aorta and, when they do, tend to be associated with diffuse aortic atherosclerosis. Aneurysms in the aortic arch are often contiguous with aneurysms of the ascending or descending aorta. They may be due to atherosclerotic disease, cystic medial degeneration, syphilis, or other infections.

The predominant etiology of aneurysms of the descending thoracic aorta is atherosclerosis. These aneurysms tend to originate just distal to the origin of the left subclavian artery and may be either fusiform or saccular. The pathogenesis of such atherosclerotic aneurysms in the thoracic aorta may be similar to that of abdominal aneurysms but has not been extensively examined.

Syphilis

Syphilis was once a common cause of ascending thoracic aortic aneurysm, but today it has become a rarity in most major medical centers as a result of aggressive antibiotic treatment of the disease in its early stages.

The latent period from initial spirochetal infection to aortic complications is in the range of 5-40 years, but it is most commonly 10-25 years. During the secondary phase of the disease, spirochetes directly infect the aortic media, most commonly involving the ascending aorta. The muscular and elastic medial elements are destroyed by the infection and inflammatory response and are replaced by fibrous tissue that frequently calcifies.

Weakening of the aortic wall from medial destruction results in progressive aneurysmal dilatation. In addition, the infection may spread into the aortic root, and the subsequent root dilatation may result in aortic regurgitation.

Infectious aortitis

This rare cause of aortic aneurysm may result from a primary infection of the aortic wall causing aortic dilatation with the formation of fusiform or saccular aneurysms.

More commonly, infected or mycotic aneurysms may arise secondarily from an infection occurring in a preexisting aneurysm of another etiology. When an infected aneurysm involves the ascending aorta, it is often the consequence of direct spread from aortic valve bacterial endocarditis.

Miscellaneous

Other causes of thoracic aortic aneurysms include giant cell arteritis, aortic trauma, and aortic dissection.

Frequency

United States

The population incidence of detected thoracic aortic aneurysms is estimated to be 5.9 new aneurysms per 100,000 person-years. The lifetime probability of rupture in thoracic and thoracoabdominal aneurysms is 75 to 80%, with 5-year untreated survival rates or 10-20%. In nondissecting aneurysms, the median time to rupture has been reported to be 2-3 years.

International

The data are the same as for the United States.

Mortality/Morbidity

• In the largest modern series, survival rates for patients with thoracic aortic aneurysms not undergoing surgical repair were as follows: 65% survival at 1 year, 36% survival at 3 years, and 20% survival at 5 years. Aneurysm rupture occurs in 32-68% of patients not treated surgically, with rupture accounting for 32-47% of all deaths. Less than one half of patients with rupture may arrive at the hospital alive. The mortality rates for aneurysmal rupture are 54% at 6 hours and 76% at 24 hours.
• Hospital mortality rates for primary medical treatment remain relatively high, and a substantial percentage of patients require surgery during initial hospitalization. The main causes of death in both medical and surgical groups are rupture. Improvements in supportive medical care have increased patient survival.
• In the patients with aortic aneurysm, aortic dissection is the catastrophic event most feared. Rupture of a thoracic aortic aneurysm is more frequent than abdominal aortic rupture. The presence or absence of symptoms is another important predictor. Symptomatic patients have a poorer prognosis than those without symptoms. Onset of new symptoms is frequently a harbinger of rupture or death. Moreover, the high prevalence of additional cardiovascular disease in these patients may have a great impact on mortality. In fact, next to aneurysm rupture, the most common causes of death in persons with aortic aneurysm are other cardiovascular diseases.

Age

The incidence or thoracic aortic aneurysm is more common with increasing age.

Anatomy

Classification

The DeBakey and Stanford classifications are the 2 most widely used methods to describe the type of aortic dissection.

In the DeBakey classification, types I, II, and III are based on the origin and extent of the dissecting process.

In the Stanford system, type A signifies involvement of the ascending aorta, with or without involvement of the arch or the descending aorta (regardless of the site of the primary intimal tear). Type B represents all others, or dissections that do not involve the ascending aorta.

Dissection and rupture

The aortic layers, beginning at the innermost wall, are the intima, the media, and the adventitia.

In aortic dissection, a tear in the intima allows blood to escape from the true lumen of the aorta, rapidly dissecting the inner from the outer layer of the media and expanding the aorta to above normal size. A false channel forms in the outer half of the aortic media, whose walls are exceedingly thin and highly susceptible to rupture.

Size is an important predictor of the risk of aneurysm rupture.

Acute versus chronic dissections

Dissections or rupture detected within 14 days of the onset of pain or other initial clinical symptom related to the dissection are classified as acute, and death may occur suddenly or within the first hours or days after onset.

Chronic dissection, which is diagnosed 2 weeks after the initial tear, may expand in the weakened aortic wall to develop an aneurysm. As in aortic aneurysm, causative factors are difficult to establish. The risk of rupture within 1 year for aneurysms with diameters of 6 cm is 43%. The risk with diameters of 8 cm and greater is 80%, and the risk for those with diameters smaller than 5 cm is 4%.

Expansion

Dapunt and colleagues monitored 67 patients with thoracic aortic aneurysms by means of serial CT and found a mean rate of expansion of 0.43 cm/y. The only independent predictor of rapid expansion (>0.5 cm/y) was an initial aortic diameter larger than 5 cm.

Growth rates were as follows: for aneurysms 5 cm or smaller, 0.17 cm/y, and for aneurysms larger than 5 cm, 0.79 cm/y. Only 1 of 25 aneurysms 4 cm or smaller at baseline showed rapid growth. No aneurysm smaller than 5 cm ruptured during the follow-up period. The only predictor of survival was initial aneurysm size.

For dissecting aneurysms, the median time to rupture is approximately 3 days in patients with acute dissection. Patients with aneurysms 5 cm or larger, those with documented aneurysm enlargement, or those with chest or back pain indicating expansion are considered candidates for elective surgery.

Clinical Details

Signs and symptoms associated with aortic dissection are variable and depend on the extent of aortic and branch vessel involvement. Patients with the ultimate diagnosis of aortic dissection are often initially thought to have other conditions such as myocardial ischemia, congestive heart failure, or pulmonary embolus. Several clinical syndromes are particularly suggestive of aortic dissection: pain that progresses over hours or days from chest to neck to arms to abdomen, chest pain with concomitant neurologic deficits, and chest pain with pulse deficits.

Approximately 40% of patients with thoracic aortic aneurysms are asymptomatic at the time of diagnosis. Aneurysms are typically discovered as incidental findings on a routine physical examination or chest radiography. When patients experience symptoms, the symptoms tend to reflect either a vascular consequence of the aneurysm or a local mass effect.

Vascular consequences include (1) aortic regurgitation from dilatation of the aortic root, which is often associated with secondary congestive heart failure; (2) sinus of Valsalva aneurysms that may rupture into the right side of the heart and cause a continuous murmur and congestive heart failure; and (3) thromboembolism causing stroke, lower extremity ischemia, renal infarction, or mesenteric ischemia.

A local mass effect from an ascending or arch aneurysm may cause superior vena cava syndrome as a result of obstruction of venous return via compression of the superior vena cava or innominate veins.

Aneurysms of the arch or descending aorta may compress the trachea or main stem bronchus and produce tracheal deviation, wheezing, cough, dyspnea (with symptoms that may be positional), hemoptysis, or recurrent pneumonitis. Compression of the esophagus may produce dysphagia, and compression of the recurrent laryngeal nerve may cause hoarseness.

Chest pain occurs in 37% of nondissecting aneurysms and back pain, in 21%. These result from direct compression of other intrathoracic structures or the chest wall or from erosion into adjacent bone. Typically, the pain is steady, deep, boring, and sometimes severe.

As with abdominal aortic aneurysms, the most worrisome consequence of thoracic aneurysms is leakage or rupture. Rupture is accompanied by the dramatic onset of excruciating pain, usually in the region where less severe pain had previously existed. Rupture occurs most commonly into the left intrapleural space or the intrapericardial space and is manifested as hypotension. The third most common site of rupture is from the descending thoracic aorta into the adjacent esophagus (an aortoesophageal fistula), which causes life-threatening hematemesis.

Acute aneurysm expansion, which may herald rupture, can cause similar chest or back pain.

Thoracic aneurysms may also be accompanied by aortic dissection.

Preferred Examination

Although aortic dissection might be suspected on the basis of history and physical findings, diagnostic imaging is necessary to establish the diagnosis. A clear and efficient imaging strategy is required. The clinical team involved in the diagnosis and treatment of patients with aortic dissection should prospectively agree on a strategy. Their approach should consider the technology available at the institution and the ease of performing each test, especially after hours.

The preferred examinations for diagnosis are aortic angiography, MRI, magnetic resonance angiography (MRA), and echocardiography.

Aortography has been the criterion standard against which other modalities were measured, but it is rarely used with the advent of transesophageal echocardiography (TEE) and CT, though aortography is still the preferred modality for the preoperative evaluation of thoracic aortic aneurysms and for precise definition of the anatomy of the aneurysm and great vessels.

CT is a reliable test for diagnosing aortic dissection, and it is the primary diagnostic test of choice in most institutions. CT scans usually show dilation of the aorta, an intimal flap, and both the false and true lumina. Rapid scanning after an intravenous bolus injection of contrast material allows the detection of differential filling rates in the true and false lumina.

TEE is helpful due to the proximity of the esophagus to the aorta and the ability to use higher transducer frequencies help to better delineate the aorta. It is highly sensitive but less specific. TEE, however, is excellent at detecting pericardial effusion and aortic regurgitation, and can be quickly performed at the patient's bedside under sedation without radiation or the injection of contrast material. Evaluating the ascending aorta and proximal arch may be difficult.

MRI is useful in defining thoracic aortic anatomy and detecting aneurysms and is of particular utility in patients with preexisting aortic disease. MRI is an appealing option in the detection of aortic dissection. Sensitivity and specificity are excellent, but it is time consuming and cumbersome to perform.

MRA may prove especially useful in defining the anatomy of aortic branch vessels.

Regarding echocardiography, TTE is not accurate for diagnosing thoracic aneurysms, and it is particularly limited in its ability to examine the descending thoracic aorta. TEE is a far more accurate method for assessing the thoracic aorta and has become widely used for detection of aortic dissection. There has been less experience with TEE, however, in the evaluation of nondissecting thoracic aneurysms.

Reports have shown high sensitivity for TEE, CT, and MRI for the diagnosis of aortic dissection. However, the specificity of CT and MRI was significantly better than that of TEE.

Limitations of Techniques

Limitations are few.

DIFFERENTIALS

Section 3 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Other Problems to Be Considered

Acute coronary syndrome
Pulmonary embolism
Acute pericarditis
Pericardial effusion or tamponade
New aortic regurgitation
Penetrating aortic ulcer
Aortic intramural hemorrhage
Esophageal rupture
Musculoskeletal and/or spinal conditions

RADIOGRAPH

Section 4 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Findings

Many thoracic aneurysms are readily visible on chest radiographs and are characterized by (1) widening of the mediastinal silhouette, (2) enlargement of the aortic knob, or (3) displacement of the trachea from the midline.

Chest radiographs are usually abnormal in 80-90% of patients, but the abnormalities are nonspecific. For example, mediastinal widening occurs in more than 75% of cases and may occur in the ascending aorta, the aortic arch, or the descending portion of the thoracic aorta. This finding may be difficult to differentiate from the aortic tortuosity that is associated with long-standing hypertension. Up to 12% of patients with aortic dissection have a normal chest image.

The calcium sign is a rare radiographic finding in aortic dissection. Generally, intimal calcification is seen along the outer border of the aorta. With dissection of the aortic media, the calcium deposit becomes separated from the outermost portion of the aorta by more than 0.5 cm.

Other radiographic signs include a double-opacity appearance of the aorta suggesting true and false channels, a localized bulge along a normally smooth aortic contour, a disparity in the caliber between the descending and ascending aorta, obliteration of the aortic knob, and displacement of the trachea to the right by the dissection.

Degree of Confidence

The degree of confidence is moderate.

False Positives/Negatives

Unfortunately, smaller aneurysms, especially saccular ones, may not be evident on the chest radiograph. Therefore, this technique cannot exclude the diagnosis of aortic aneurysm.

CT SCAN

Section 5 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Findings

Thoracic aortic aneurysm is characterized by an increase in aortic diameter and outward displacement of calcium of the aortic wall.

CT is an effective method for defining the maximum diameter of the aneurysm and monitoring the diameter over time. A diameter exceeding 4 cm is considered aneurysmal. A diameter exceeding 6 cm, on the contrary, is usually an indication for surgery of thoracic aortic aneurysm.

Degree of Confidence

The degree of confidence is high.

False Positives/Negatives

The rate of false-positive and false-negative findings is low.

MRI

Section 6 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Findings

MRI and CT are now the procedures most frequently used for diagnosing and monitoring thoracic aortic diseases.

A number of reports attest to the effectiveness of MRI for the evaluation of aortic aneurysms, both true and false. Velocity-encoded cine MRI provides a measurement of the differential flow velocity in the true and false channels. By using multiple images per cardiac cycle, a velocity-time curve can be generated to display the disparate flow pattern in the 2 channels.

MRI and MRA are also used to monitor the maximum diameter and extent of the thoracic aortic aneurysms. A maximum diameter exceeding 6 cm indicates the need for surgical repair. Regular monitoring is also important in patients with Marfan syndrome and other conditions associated with progressive aortic dilatation.

Velocity-encoded cine MRI can be used in thoracic aortic disease to quantify the volume of concomitant aortic regurgitation in patients with aortoannular abnormalities.

Gadolinium-based contrast agents (gadopentetate dimeglumine [Magnevist], gadobenate dimeglumine [MultiHance], gadodiamide [Omniscan], gadoversetamide [OptiMARK], gadoteridol [ProHance]) have recently been linked to the development of nephrogenic systemic fibrosis (NSF) or nephrogenic fibrosing dermopathy (NFD). For more information, see the eMedicine topic Nephrogenic Fibrosing Dermopathy. The disease has occurred in patients with moderate to end-stage renal disease after being given a gadolinium-based contrast agent to enhance MRI or MRA scans. As of late December 2006, the FDA had received reports of 90 such cases. Worldwide, over 200 cases have been reported, according to the FDA. NSF/NFD is a debilitating and sometimes fatal disease. Characteristics include red or dark patches on the skin; burning, itching, swelling, hardening, and tightening of the skin; yellow spots on the whites of the eyes; joint stiffness with trouble movingor straightening the arms, hands, legs, or feet; pain deep in the hip bones or ribs; and muscle weakness. For more information, see the FDA Public Health Advisory or Medscape.

Degree of Confidence

The degree of confidence is high. Because MRI and MRA are noninvasive and provide images along both the short and long axis of the thoracic aorta, they are now the preferred method for the follow-up of patients with thoracic aortic diseases. MRA in the sagittal plane is effective for depicting the origins of the arch branches and visceral arteries of the abdominal aorta and their relationship to the aneurysm.

False Positives/Negatives

The rate of false-positive and false-negative findings is low.

ULTRASOUND

Section 7 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Findings

TEE is reliable for surveys of the following:

• Aortic valve disease

• Aortic dilatation

• Ascending aortic aneurysm

• Aortic dissection

• Thrombi

• Atherosclerotic disease

• Mitral valve disease

TEE provides an assessment of cardiac structure and function and is highly sensitive in aortic pathology diagnosis.

Intraoperatively, TEE can be used to monitor cardiac function; detect atherosclerosis in the thoracic aorta; establish the competency of the aortic valve before surgery; and lower the incidence of stroke, by enabling surgeons to better navigate the placement of clamps and to avoid loosening any atherosclerotic plaques, which could otherwise embolize to the brain.

Degree of Confidence

The degree of confidence is high. The accuracy of TEE in imaging intimal membranes for signs of aortic dissection has been reported to be 90%.

False Positives/Negatives

TEE poorly depicts aneurysms below the diaphragm and in the transverse aortic arch. TEE requires a skilled cardiologist to interpret the study data because a high rate of false-positive results has been observed with those who are unfamiliar with the diagnostic limitations.

ANGIOGRAPHY

Section 8 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Findings

Angiography

The findings of aortic dissection seen at angiography include the following: (1) filling of a false channel with or without an intervening intimal flap, (2) distortion of the true lumen by either a patent or a thrombosed false lumen, (3) thickening of the aortic wall by more than 0.5 cm from a thrombosed false lumen, and (4) displaced intimal calcification. Aortography is accurate for determining the site of the intimal tear and the extent of the dissection.

Aortic regurgitation is easily demonstrated with aortography and demonstrates the extent and location of dissection into aortic side branches.

Aortography

Generally, all patients electively undergo aortography to assess the operative risks and make possible modifications in operative technique.

The aortogram depicts aortic root dilatation and clearly defines the geography of the aorta and the condition of the smaller vessels.

Absolute indications for aortography include renovascular hypertension, intermittent claudication, atherosclerotic occlusive abdominal aorta, and symptoms of carotid stenosis.

Cardiac catheterization and coronary angiography

Cardiac catheterization may be required to evaluate any concomitant atherosclerotic occlusive disease of the coronary arteries, which can be corrected before or at the same time as the aortic aneurysm.

Degree of Confidence

Aortography is highly specific. However, it is an invasive procedure, and it increases the risk of renal failure owing to the use of radiopaque dyes.

False Positives/Negatives

False-positive and false-negative findings are rare.

INTERVENTION

Section 9 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

The treatment of thoracic aortic aneurysm is mainly surgical. Better imaging technology has led to the earlier recognition of acute aortic dissection, permitting the identification of more patients with complex conditions who are candidates for surgery.

Aortic root

For the aortic root, the approach is through a median sternotomy; the patient is placed on cardiopulmonary bypass. Profound hypothermia with circulatory arrest is required in cases of acute aortic dissection or aneurysms extending into the aortic arch.

Aortic valve or graft replacement, or both, depends on the patient's presentation.

Allograft replacement may be suitable for physically active patients or patients with endocarditis. Separate valve or graft replacement may be applicable for older patients with minor to moderate sinus dilatation. Patients with Marfan syndrome or aortic root dilatation most often require composite valve graft. The coronary arteries are reattached to the graft.

Repair of the diseased aortic root can be accomplished safely, depending on risk factors, with an overall short-term mortality rate of 2-15%.

Major short-term complications include thromboembolism and bleeding at the anastomotic site requiring repeat operation. Long-term complications include endocarditis, thromboembolic events, and pseudoaneurysm.

Ascending aorta and arch

If aneurysmal disease is limited to the tubular portion of the ascending aorta, it is possible to use the closed technique. The aorta can be clamped, resected, and replaced with a graft, without the need for profound hypothermia. The short-term mortality rate is around 5%.

Acute type A versus type B dissection

Treatment of type A proximal dissection is surgical. Treatment of uncomplicated type B distal dissection is usually medical, with a beta-blocker and nitroprusside to control blood pressure and dP/dt shearing forces.

Acute type A aortic dissection of the proximal aorta is treated as a surgical emergency to avoid rupture into the pericardium and subsequent cardiac tamponade because acute type A dissections may rupture in a matter of hours.

Acute type B dissection can be treated medically before being treated surgically, with the objective to correct hypertension and stabilize the patient. These dissections essentially follow the pattern of nondissecting aneurysms, with a median rupture time of 1-3 years.

Endovascular stent grafting

Exclusion of large thoracic aneurysms from the circulation by means of stent grafting is a fast growing procedure. Among the best candidates for stent grafts is their potential for patients who would otherwise be poor surgical candidates. The early mortality rate for thoracic endovascular stent grafts was reported to be 9%. Major complications included stroke in 7% and paraplegia in 3% of the patients. Twenty-four percent of the grafts demonstrated early endoleak, of which 18% required additional intervention. Roughly 5% of the grafts had to be removed or otherwise excluded.

The approach is reasonably successful and may be appropriate for patients who would not otherwise be surgical candidates. Lack of long-term data, however, should preclude the use of such grafts in younger patients or in those with an expected survival time of longer than 5 years. If patients are too ill to be treated by open technique, the value of providing any treatment to a patient with a short life expectancy must be considered when contemplating use of an endovascular technique.

The treatment of descending thoracic aortic aneurysms using endovascular stents is a less invasive alternative to open surgical repair. Although the technology is still in its infancy, significant improvements have lately been made in the design and deployment of the endovascular stent-grafts. The placement of endoluminal stent-grafts to exclude the dissected or ruptured site of thoracic aortic aneurysms is a technically feasible and relatively safe procedure.

The basic components of each device include a delivery system, mobile and fixed components of the prosthetic graft, and anchoring or fixation devices. Some of the commercially available systems include the following:

• AnueRx (AnueRx; Santa Rosa, Calif)



• EVT/Ancure (Guidant, Indianapolis, Ind)



• Excluder (Gore Medical Associates; Sunnyvale, Calif)



• Stentor (Mintec; Bahamas)



• Talent (Norid Medical Manufacturing Corporation; Fort Lauderdale, Fla)



• Vanguard (Boston Scientific/Meditech; Wayne, NJ)



• Zenith (Zenith; Bloomington, Ind)

Commercial graft systems are used more frequently in countries other than the United States. In the United States, the Food and Drug Administration (FDA) initially set strict inclusion and exclusion criteria for the systems used in the first clinical trials. The FDA first approved two devices for commercial use, the Ancure tube (Guidant Endovascular Technologies; Indianapolis, Ind) and the AneuRx bifurcated stent graft system (Medtronic; Minneapolis, Minn). It is important to have an understanding of the devices and the steps of this technically demanding procedure.

Medical/Legal Pitfalls

• High clinical suspicion is required.
• Imaging techniques, including MRI, TEE or CT, should be quickly utilized.
• Time is of the essence.
• Surgical complications, including stroke and spinal cord malfunction, can have serious medicolegal ramifications.
• Antihypertensive treatment does not eliminate the need to closely monitor patients with thoracic aortic aneurysm.

MULTIMEDIA

Section 10 of 11  

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

Media file 1:  Chest radiograph showing widening of the superior mediastinum.
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Media file 2:  Descending thoracic aortic aneurysm with mural thrombus at the level of the left atrium.
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Media type:  Image

Media file 3:  Ascending aortogram showing ascending aortic aneurysm.
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Media type:  X-RAY

Media file 4:  CT scan from same patient as in Image 3.
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Media type:  CT

Media file 5:  Chest radiograph following aneurysm surgery.
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Media type:  X-RAY

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Differentials
• Radiograph
• CT SCAN
• MRI
• Ultrasound
• Angiography
• Intervention
• Multimedia
• References

• Chryssidis S, Davies RP, Tie ML. Gadolinium-enhanced computed tomographic aortography. Australas Radiol. Mar 2002;46(1):97-100. [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].
• Davies RR, Goldstein LJ, Coady MA, et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg. Jan 2002;73(1):17-27; discussion 27-8. [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].
• Gonzalez-Fajardo JA, Gutierrez V, San Roman JA, et al. Utility of intraoperative transesophageal echocardiography during endovascular stent-graft repair of acute thoracic aortic dissection. Ann Vasc Surg. May 2002;16(3):297-303. [Medline].
• Gott VL, Cameron DE, Alejo DE, et al. Aortic root replacement in 271 Marfan patients: a 24-year experience. Ann Thorac Surg. Feb 2002;73(2):438-43. [Medline].
• Lankipalli RS, Pellecchia M, Burke JF. Magnetic resonance angiography in the evaluation of aortic pseudoaneurysm. Heart. Feb 2002;87(2):157. [Medline].
• Miller WT. Thoracic aortic aneurysms: plain film findings. Semin Roentgenol. Oct 2001;36(4):288-94.
• Mitchell RS. Stent grafts for the thoracic aorta: a new paradigm?. Ann Thorac Surg. Nov 2002;74(5):S1818-20; discussion S1825-32. [Medline].
• Nguyen BT. Computed tomography diagnosis of thoracic aortic aneurysms. Semin Roentgenol. Oct 2001;36(4):309-24. [Medline].
• Pereles FS, McCarthy RM, Baskaran V, et al. Thoracic aortic dissection and aneurysm: evaluation with nonenhanced trueFISP MR angiography in less than 4 minutes. Radiology. Apr 2002;223(1):270-4. [Medline].
• Rachel ES, Bergamini TM, Kinney EV, et al. Endovascular repair of thoracic aortic aneurysms: a paradigm shift in standard of care. Vasc Endovascular Surg. Mar-Apr 2002;36(2):105-13. [Medline].
• Roberts DA. Magnetic resonance imaging of thoracic aortic aneurysm and dissection. Semin Roentgenol. Oct 2001;36(4):295-308. [Medline].
• Saccani S, Nicolini F, Beghi C, et al. Thoracic aortic stents: a combined solution for complex cases. Eur J Vasc Endovasc Surg. Nov 2002;24(5):423-7. [Medline].
• Scott CH, Keane MG, Ferrari VA. Echocardiographic evaluation of the thoracic aorta. Semin Roentgenol. Oct 2001;36(4):325-33. [Medline].
• Soulen MC. Catheter angiography of thoracic aortic aneurysms. Semin Roentgenol. Oct 2001;36(4):334-9. [Medline].
• Von Segesser LK, Marty B, Ruchat P, et al. Routine use of intravascular ultrasound for endovascular aneurysm repair: angiography is not necessary. Eur J Vasc Endovasc Surg. 23(6):537-42. [Medline].

Article Last Updated: Apr 24, 2007