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[] Read [CK] TAA vs AAA

SUMMARY AND RECOMMENDATIONS
Patients diagnosed with thoracic aortic aneurysm (TAA) should be evaluated for possible underlying genetic syndromes known to be related to thoracic aortic aneurysm and dissection (TAAD). The patient should also be evaluated for other associated aneurysms (eg, brain, abdominal aorta, mesenteric, iliac, femoral, or popliteal arteries) using computed tomographic (CT) angiography or ultrasound. Among symptomatic patients, this evaluation is obtained postoperatively. (See 'Management of asymptomatic TAA' above and 'Identifying associated genetic conditions' above and 'Identifying associated aneurysm' above.)
The natural history of TAA is one of progressive expansion. The rate of expansion depends upon the location and diameter of the aneurysm and its underlying etiology. Most TAAs produce no symptoms. Patients with asymptomatic TAA should be followed for the development of signs and symptoms that may be associated with the TAA. The surveillance schedule is based upon the etiology, site, and diameter of the aneurysm at presentation, and expansion rates identified at follow-up. Ideally, serial CT or magnetic resonance (MR) angiography studies should be performed using the same imaging technique at the same center. (See 'Aneurysm surveillance' above.)
Following the initial study that identified TAA, we suggest imaging six months after the initial study to ensure the stability of the aneurysm diameter and extent.
If the TAA does not demonstrate expansion after six months, we suggest annual imaging.
If the TAA demonstrates expansion or is approaching the diameter threshold for repair, we suggest imaging every three to six months.
For patients with asymptomatic TAA who are being conservatively managed, control of hypertension is recommended to limit further aortic expansion. We suggest beta blocker therapy rather than other agents (Grade 2C). The goal systolic pressure is 105 to 120 mmHg. An angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) for blood pressure control is an acceptable alternative for those who do not tolerate beta blocker therapy. The majority of patients have concomitant cardiovascular disease; thus, managing cardiovascular risk factors (eg, smoking cessation, antiplatelet therapy, statin therapy) is also important. Statin therapy may also reduce aortic expansion, but this is unproven for TAA. (See 'Antihypertensive therapies' above and 'Management of asymptomatic TAA' above.)
Symptoms such as chest pain in a patient with TAA (known or unknown) can represent rapid aneurysm expansion or be due to a variety of life-threatening complications, including aortic dissection, acute aortic regurgitation, aortic leakage, or overt aortic rupture. Patients who develop symptoms attributable to TAA should undergo urgent repair (open surgical, endovascular), provided the risk for repair is not prohibitive. (See 'Symptomatic (nonruptured) and ruptured TAA' above and "Clinical manifestations and diagnosis of thoracic aortic aneurysm", section on 'Symptomatic TAA'.)
Elective repair of asymptomatic TAA is not undertaken until the risk of rupture or other complications exceeds the risks associated with repair. Candidates for repair are selected depending upon diameter, location, expansion rate, and patient comorbidities, taking into account the presence of underlying contributing etiologies. The most important factor determining the risk for TAA complications is the diameter of the aneurysm. Among patients with genetically mediated TAA, aortic diameter thresholds are lower, and a decision for repair also needs to consider the diameter of the aortic root and functional status of the aortic valve.
For most patients with asymptomatic TAA, we use the following thresholds as criteria for elective repair. (See 'Summary of indications' above.)
Ascending TAA:
-End-diastolic aortic diameter >5.5 cm or aortic size index (aortic diameter [cm] divided by body surface area [m2]) ≥2.75 cm/m2 [8]. A body surface area calculator can be found in the link (calculator 1).
-For patients with genetically mediated TAAD, including syndromic conditions such as Marfan, Loeys-Dietz, vascular Ehlers-Danlos, and Turner syndromes, and nonsyndromic conditions like familial TAAD or bicuspid aortic valve, a lower diameter or aortic size index is suggested as an indicator for repair.
-Non-Turner's patients undergoing aortic valve surgery: End-diastolic aortic diameter >4.5 cm in diameter at the time of aortic valve surgery.
Descending TAA:
-For most average-sized adults: Diameter >5.5 cm.
-Patient with high surgical risk: Diameter ≥7 cm.
-For patients with genetically mediated conditions (syndromic or nonsyndromic), a lower diameter (eg, 4.0 to 6.0 cm depending on the condition) or aortic size index is suggested as an indicator for repair. (See 'Genetically mediated thoracic aortic aneurysm and dissection' above.)
-For smaller patients, including many women, a diameter greater than twice the diameter of the nonaneurysmal aorta (normal segment) or aortic size index can be used. (See 'Accounting for body size' above.)
Rapid expansion ≥10 mm per year for aneurysms <5.0 cm in diameter. For patients with associated genetically mediated conditions, a lower expansion rate (eg, >5 mm/year) is suggested as an indicator for repair.
For patients who do not meet the above criteria, we suggest not performing elective repair (Grade 2C). These patients are followed conservatively and are considered for repair if symptoms develop. (See 'Indications for repair' above and 'Summary of indications' above and 'Counseling the high-risk patient' above.)
The approach to TAA repair (open, endovascular) takes into account the location and anatomic extent of the aneurysm, etiology, and the patient's expected survival (short-term and long-term), which depends upon the patient's age and medical comorbidities. Ascending TAA is managed with an open surgical approach using cardiopulmonary bypass and often requires aortic root replacement or coronary artery reimplantation. Descending TAA can be repaired with an open or endovascular approach, the choice of which depends upon whether the etiology is sporadic or genetically mediated. For patients with sporadic (degenerative) descending TAA, we suggest an endovascular approach for initial repair rather than an open approach, provided the thoracic aortic anatomy is suitable for endografting (Grade 2C). Endovascular repair is associated with reduced perioperative morbidity and mortality; however, the long-term durability of endovascular TAA repair compared with open surgical repair remains uncertain. An open approach should be used for those with syndromic TAAD. The approach for those with nonsyndromic TAAD is less well defined. (See 'Thoracic aneurysm repair' above and "Endovascular repair of the thoracic aorta" and "Overview of open surgical repair of the thoracic aorta".)
Patients with TAA with indications for repair should receive treatment at a facility where expertise in the management of thoracic aortic disease and the perioperative resources necessary for major aortic surgery are available (eg, operating room personnel, an appropriately trained surgeon, perioperative intensive care). For patients who present to a facility where these are not available, referral (or transfer) to a high-volume cardiovascular center is appropriate. (See 'Thoracic aneurysm repair' above.)

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