A plain chest x-ray is inadequately sensitive or specific enough to either diagnose or exclude aortic dissection. However, it may provide signs that further diagnostic testing is warranted. Mediastinal widening or absence of the normal aortic knob may indicate aortic aneurysm or abnormal mediastinal contents. A “calcium sign” indicates separation of the intimal calcium from the adventitial aortic wall. Double density within the aorta is a sign of hematoma or hemorrhage in a secondary or false lumen. Deviation of the trachea or a nasogastric tube within the esophagus toward the right may be a sign of a large aneurysm or dissection. Cardiomegaly may be a sign of pericardial effusion, and left pleural effusion may be due to hemothorax or a sympathetic effusion.

Transthoracic echocardiography (TTE) is a noninvasive imaging technique that can be performed at the bedside and may be useful in critically ill patients to establish a diagnosis rapidly. It is useful for rapid evaluation of cardiac function, pericardial effusion, cardiac tamponade, and aortic insufficiency. However, the sensitivity of TTE for identifying aortic dissection is limited by low resolution and variable chest wall anatomy, and absence of positive findings does not preclude the presence of an acute dissection.

Transesophageal echocardiography (TEE) is preferable to TTE due to its superior anatomic resolution and higher sensitivity ( Fig. 22.7 ). TEE provides a sensitivity and specificity for diagnosis of aortic dissection comparable to that of magnetic resonance imaging (MRI) and computed tomography (CT). Although it is an invasive procedure, it can be performed fairly rapidly at the bedside and may be ideal for unstable patients who cannot travel to a cross-sectional scanner. One downside of TEE is the presence of a blind spot at the distal ascending aorta to proximal aortic arch, but overall, the sensitivity and specificity for dissection are reported to be as high as 100% and 98%, respectively. In addition to identifying the dissection flap, TEE can identify pericardial fluid, evidence for pericardial tamponade, aortic regurgitation, involvement of proximal coronary arteries in the dissection process, and wall motion abnormalities of right and left ventricles. Use of TEE as the initial diagnostic study has waned over time as other imaging modalities improved.

Transesophageal echocardiogram of acute aortic dissection in the longitudinal plane of the ascending aorta showing a DeBakey type I (type A) dissection with intimal flap extending from the aortic root distally.

Computed tomographic angiography (CTA) is now the preferred imaging modality for patients suspected of having aortic dissection. It is widely available at all hours and provides rapid acquisition of high-resolution imaging. Modern aortic dissection CT protocols with electrocardiogram (ECG) gating minimize motion artifact and result in high-quality imaging that not only identifies the aortic dissection but demonstrates the entry tear, fenestrations, branch vessel involvement, radiologic signs of malperfusion, pericardial effusion, pleural effusion, mediastinal hemorrhage, and images the entire aorta ( Figs. 22.8 and 22.9 ). Sensitivity of CTA is 100% and specificity is 98% to 99%. ^{, ,}

Computed tomographic scan of a DeBakey type I (Stanford type A) aortic dissection. The primary tear is located in the ascending aorta and the dissection flap extends into the descending aorta.

Computed tomographic scan of a DeBakey type III (Stanford type B) aortic dissection. The dissection starts distal to the origin of the left subclavian artery and extends distally to the abdominal aorta.

MRI provides excellent imaging of the aorta without the need for contrast, although magnetic resonance angiography (MRA) using gadolinium contrast further enhances image quality. It provides detailed imaging of both ascending and descending thoracic aortic dissections and can accurately identify sites of entry and thrombus formation ( Fig. 22.10 ). ^, The sensitivity and specificity of MRA for diagnosing aortic dissection is near 100%. ^, However, its use for this purpose is limited by more restricted availability, longer acquisition times, greater cost, and the presence of a magnetic field, which may interfere with care of critically ill patients during the prolonged acquisition phase.

Sagittal spin-echo magnetic resonance image of DeBakey type III (Stanford type B) aortic dissection. Dissection begins at origin of left subclavian artery. Proximal entry is clearly defined 3 cm distal to this origin and appears as a disruption of dissecting membrane (arrow) . Distal part of false lumen appears partially thrombosed (arrowhead) .

(From Nienaber CA, von Kodolitsch Y, Brockhoff CJ, Koschyk DH, Spielmann RP. Comparison of conventional and transesophageal echocardiography with magnetic resonance imaging for anatomical mapping of thoracic aortic dissection. A dual noninvasive imaging study with anatomical and/or angiographic validation. Int J Card Imaging . 1994;10(1):1-14.)

Aortography is an accurate method for establishing the diagnosis of aortic dissection. The false lumen can be visualized, as can, at times, the intimal tear ( Fig. 22.11 ). It provides accurate information about branch artery involvement and presence of aortic valve regurgitation. However, it is an invasive procedure and is rarely used for this purpose in the modern era. Its main diagnostic utility is in cases of iatrogenic aortic dissection caused during cardiac catheterization procedures. Additionally, it is an essential component of interventional procedures to treat acute aortic dissection, such as fenestration and endovascular stent-grafting.

Aortography in acute aortic dissection. (A) Aortogram (lateral view) in DeBakey type I dissection. Intimal tear is evident in anterior aspect of ascending aorta. (B) Aortogram in DeBakey type II dissection. There is deformity of noncoronary aortic cusp, with regurgitation. True lumen of ascending aorta is compressed by large false lumen. (C) Aortogram (front view) in DeBakey type III dissection. True lumen is compressed by false lumen, which begins just beyond left subclavian artery and extends into abdominal aorta.

Selective coronary angiography to identify coronary artery involvement in acute ascending aortic dissection or to identify obstructive coronary artery disease (CAD) is not usually indicated due to the emergent nature of the disease process. The rare exception is in patients with known CAD who are hemodynamically stable and may have had previous coronary artery bypass grafting (CABG). Preoperative knowledge of native coronary artery and bypass graft anatomy is important in these cases.

A majority of aortic dissections have an identifiable intimal tear on imaging exams. With type A dissection, the location of the primary entry tear is most commonly located in the ascending aorta or aortic root in approximately 80% of patients. The primary tear originates in the aortic arch less frequently in 7% to 10% of patients. In a minority of patients, an intimal tear is not identified. In type B aortic dissections, the primary tear is located in the descending aorta in 82% of patients, with no apparent entry in 18%. The primary tear is most frequently seen just distal to the origin of the left subclavian artery. Aortic dissection with no identified entry tear may have a pathogenesis similar to intramural hematoma with rupture of aortic vasa vasorum as the inciting event leading to medial hemorrhage and subsequent dissection. ^, Dissection originating in the ascending aorta often propagates proximally and distally, whereas those originating in the descending aorta often propagate only distally as type B dissections. Rarely is the intimal tear low in the descending thoracic or abdominal aorta.

The dissection often propagates distally into the thoracoabdominal aorta in a spiraling pattern. The intima usually remains attached to the adventitia on one side, and circumferential dissection is rare. When medial dissection occurs, the walls of any of the branches of the aorta may be involved with the dissection, may be sheared off from the lumen and occluded by the dissecting media and intima, may stay in communication with the aorta but only by the false lumen, or may be uninvolved. Extension of dissection into the branch wall is more common in large arteries such as the brachiocephalic, carotid, subclavian, and renal than in smaller ones. Dissection more frequently involves the left rather than right iliac artery. Extent and nature of involvement of the branches, including coronary and iliac arteries, are important determinants of the clinical syndrome with which the patient presents.

The true lumen can be differentiated from the false lumen by its size and shape. The true lumen is often the smaller lumen and has an oval shape with circumferentially visible intima. Thus, the true lumen may be seen as thicker, containing all three aortic layers, whereas the false lumen is only thin media and adventitia. The false lumen develops in the outer segment of the aortic media; as a consequence, its external wall is thinner than the internal wall. The false lumen usually involves half to two-thirds of the circumference of the aorta and rarely the entire circumference. The false lumen may be contained by the thin outer layer of media and adventitia, which may rupture into the pericardium, the pleural space (usually the left), or, less commonly, the abdomen. Even when initial rupture does not occur, blood from the false lumen may extravasate through weak areas of media and adventitia to form a mediastinal or pericardial hematoma.

Usual preparations are made for operations in which CPB is used. Arterial pressures are monitored by right radial artery or other right upper extremity arterial access, which are informative of cerebral blood flow given the common origin of the right common carotid artery from the brachiocephalic artery. If malperfusion to the right upper extremity is suspected based on pulse exam or preoperative imaging, then an alternative site may be employed. Monitoring of cerebral oxygen saturation using near-infrared spectroscopy is a useful technique for detecting compromised blood flow to the carotid arteries during the operation.

A median sternotomy is the standard approach to repair, allowing for access to the entire ascending aorta and arch. After median sternotomy, the pericardium is incised, often starting with a pinpoint opening, to allow pericardial fluid and blood to drain slowly. Rapid release of intrapericardial pressure and cardiac tamponade may lead to a sudden increase in blood pressure and aortic rupture. The often-hemorrhagic ascending aorta is not disturbed at this point ( Fig. 22.13 ).

Intraoperative photo of an acute ascending aortic dissection. The ascending aorta is hemorrhagic with purple discoloration. The epicardial fat is inspissated with blood.

Arterial cannulation may be achieved via the femoral artery, axillary artery, brachiocephalic artery, or direct aortic cannulation. Blood flow to the brain and organs may be affected by the chosen cannulation strategy due to the dynamic nature of the dissection flap. The site of arterial cannulation must be planned based on the choice of cerebral perfusion strategy during aortic arch repair. For example, right axillary artery cannulation may be helpful if antegrade cerebral perfusion (ACP) is planned, as it is uniquely suited for providing flow to the right carotid artery by clamping the brachiocephalic artery.

Femoral artery cannulation is the classic method of arterial cannulation, and it remains relevant today. It allows for rapid arterial access and initiation of CPB, and it can be performed concomitantly as the sternum is opened. The right femoral artery is preferred to save the left groin for potential use during future downstream thoracoabdominal aortic operations. The common femoral artery is exposed through a small oblique incision in the inguinal fold. The dissection rarely extends to the level of the common femoral artery, but if dissection is present upon opening it, the true lumen should be cannulated. Femoral venous access is readily available via the inguinal incision if emergent CPB is necessary. Although there has been a recent shift away from femoral artery cannulation, numerous groups have reported excellent outcomes using this strategy with outcomes comparable to other cannulation strategies, and the incidence of malperfusion or other complications caused by retrograde arterial perfusion was rare (0-2%). Femoral cannulation provides retrograde blood flow, which is at risk for causing embolism of debris and thrombus from the distal aorta. Meta-analyses have suggested inferior outcomes with regard to mortality and stroke using femoral artery cannulation, but it must be noted that the femoral artery was often used as a bailout option in the sickest patients. Unfortunately, randomized comparisons of cannulation strategies do not exist.

Axillary artery cannulation, usually via the right axillary artery, emerged as an alternative cannulation technique, which provides unique advantages compared to femoral cannulation. Axillary artery cannulation provides antegrade true lumen blood flow, which minimizes the risk of causing malperfusion and, in fact, resolves many types of malperfusion by providing true lumen perfusion. This configuration also allows for ACP through the brachiocephalic and right carotid arteries during periods of circulatory arrest. The artery is accessed via an incision in the deltopectoral groove in the subclavicular region. The pectoralis muscles are divided, and the axillary vein is retracted inferiorly to expose the artery. The axillary artery may be cannulated directly with a flexible cannula. However, the axillary artery can be quite fragile or small in diameter, leading to complications with direct cannulation. Indirect cannulation of the axillary artery by placement of an 8- or 10-mm graft reduces the incidences of these complications and may be associated with improved outcomes ( Fig. 22.14 ). The disadvantage of axillary artery cannulation is the additional time necessary to access the vessel, which may make this approach disadvantageous in hemodynamically unstable patients. Due to its location in the same surgical field, it is difficult to perform concomitantly with the sternotomy.

Axillary artery cannulation in case of dissected innominate artery. CPB, cardiopulmonary bypass; LAX, left axillary; LCC, left common carotid; RAX, right axillary; RCC, right common carotid.

(From Rylski B, Czerny M, Beyersdorf F, et al. Is right axillary artery cannulation safe in type A aortic dissection with involvement of the innominate artery? J Thorac Cardiovasc Surg . 2016;152(3):801-807.e1.)

Brachiocephalic artery cannulation provides many of the advantages of right axillary artery cannulation, with an additional advantage in terms of speed. This technique has been used in aortic arch surgery and may be applied during repair of ascending aortic dissections that do not extend into the brachiocephalic artery. Outcomes with brachiocephalic artery cannulation for aortic dissection are comparable to other cannulation methods. It provides access to the right carotid circulation, similar to right axillary artery cannulation, which aids in antegrade cerebral protection strategies. However, it requires manipulation of the brachiocephalic artery near its origin in the arch, which may risk release of atherosclerotic debris.

Direct ascending aortic true lumen cannulation has emerged as a safe and expedient method of establishing CPB and true lumen blood flow. A modified Seldinger technique is utilized to access the true lumen of the aorta under epiaortic ultrasound and transesophageal echocardiographic guidance. ^, The ascending aorta is scanned with ultrasound to identify the optimal spot for cannulation, preferably where the intima and adventitia are not separated or have minimal separation. Concentric purse-string sutures are placed, and needle and wire access of the true lumen are obtained. The aortic puncture is serially dilated, and a cannula is advanced into the true lumen over the wire ( Fig. 22.15 A-B). This technique requires no extra incisions and offers speed similar to normal ascending aortic cannulation. Outcomes with this cannulation strategy are comparable to other techniques. An alternative method of direct cannulation, sometimes referred to as the “Samurai” cannulation, involves transection of the ascending aorta during a low-flow state and placement of a cannula under direct vision into the true lumen, which is then secured by several concentric tapes around the distal ascending aorta. ^,

(A) Epiaortic ultrasound guided direct aortic puncture into the true lumen of the ascending aortic dissection. (B) Aortic cannula is directly inserted into the true lumen over the guidewire.

A majority of ascending aortic dissections, aside from some DeBakey type II dissections, require replacement of a part or all of the aortic arch. Arch replacement requires preparation for circulatory arrest during the arch reconstruction portion of the case to protect the brain. Deep hypothermic circulatory arrest provides adequate brain protection for short periods of circulatory arrest, but adjunctive retrograde cerebral perfusion (RCP) or ACP are recommended to increase the safe time of circulatory arrest.

If dissection is confined to the ascending aorta (DeBakey type II) and hypothermic circulatory arrest is not needed, a single two-stage cannula for venous drainage can be inserted through a purse-string suture in the right atrial appendage. If RCP is planned, purse-string sutures are placed for cannulation of both superior and inferior venae cavae. If ACP is planned, preparation for perfusion to one or both carotid arteries is necessary and may require cannulation of the right axillary or brachiocephalic artery or insertion of catheters directly into the carotid arteries. CPB is established, and a venting catheter is inserted through the right superior pulmonary vein and advanced into the left ventricle. The vent prevents distension as the heart fibrillates due to hypothermia, especially in cases with aortic insufficiency. If only the ascending aorta requires repair and circulatory arrest is not required, perfusate temperature is taken to 32°C. If circulatory arrest is necessary, the patient’s systemic temperature is reduced to less than 18°C for deep hypothermia cases and 24°C to 28°C for moderate hypothermia with ACP.

Given the emergent nature of acute ascending aortic dissection, it is not often reasonable to perform coronary angiography preoperatively to assess for CAD. Nevertheless, modern high-resolution CT angiography may be somewhat revealing to the degree of coronary calcification, which may suggest the possibility of obstructive CAD or indicate whether existing bypass grafts are patent. In the rare case of a stable patient with a history of known history of CAD or history of prior coronary revascularization, the risk of proceeding with preoperative coronary angiography may be justified to define the degree of CAD and decrease the risk of postoperative coronary ischemia. In a majority of patients, the coronary arteries may be assessed by direct inspection after initiating CPB. The coronary arteries are palpated, and areas of disease are noted. Each coronary distribution is assessed for potential bypass targets in case ischemia is noted when attempting to separate from CPB. Concomitant CABG may be required to address coronary artery dissection or concomitant CAD. Regardless of the reason, the need for concomitant CABG is associated with a significant increase in operative mortality.

Limited dissection is carried out, carefully separating the ascending aorta from the pulmonary trunk proximal to the origin of the brachiocephalic artery, and the aorta is clamped using a soft padded clamp after transiently reducing CPB flow. Whenever possible, the clamp should be placed several centimeters proximal to the brachiocephalic artery to avoid further injury of the aorta at this site, where an anastomosis may be performed. The aorta is incised transversely, and this often enters into the false lumen ( Fig. 22.16 ). If clot is present in the false lumen, it is carefully removed to identify the intimal dissection flap, which is then incised as well ( Fig. 22.17 ). With the true aortic lumen exposed, cardioplegic solution is promptly infused directly into the coronary ostia using a soft-tipped catheter to prevent injury to the coronary ostia. Retrograde cardioplegia may be administered, as necessary, by placing a balloon catheter in the coronary sinus via the right atrium. A majority of primary entry tears are located in the ascending aorta and should be identified at this time. Resection of the primary entry tear is important for reducing the risk of late reinterventions. The ascending aorta is resected down to within 3 to 5 mm of the level of the sinutubular junction ( Fig. 22.18 ). Any false lumen thrombus in the root is carefully removed, and the intima is reapproximated to the adventitia. Root anatomy and aortic valve cusp quality are assessed, and the need for valve or root replacement is assessed.

Repair of acute DeBakey type I or II (type A) aortic dissection. After cardiopulmonary bypass is established, aorta is clamped proximal to origin of brachiocephalic artery. After incising outer layer of aorta, origin of intimal tear is often visualized just distal to aortic valve. Cardioplegic solution is infused directly into coronary arteries whenever possible for optimal myocardial management.

Thrombus is seen within the false lumen, between the intima and adventitia of the ascending aorta. This thrombus must be carefully extracted.

Aortic wall is transected circumferentially 4 to 5 mm above level of aortic commissures.

The sinuses of Valsalva are inspected and correlated to preoperative CT findings. An aortic root with diameter <4.5 cm on imaging and without significant dilation of the sinuses of Valsalva may be safely preserved. Root-sparing surgery is suitable for a majority of acute type a aortic dissection patients even when significant aortic valve regurgitation (AR) is present. Valvar dysfunction is primarily due to collapse of one or more aortic valve commissures rather than true native aortic valve pathology. Restoring root geometry by resuspension of the valve commissures and obliteration of the false lumen within the aortic root resolves aortic insufficiency in most cases. Aortic root replacement in the setting of acute dissection is a complex procedure requiring significantly longer bypass and cross-clamp times than root-sparing procedures. Coronary button reimplantation may be hazardous due to the fragile, dissected tissue. Postoperative hemorrhage and coronary ischemia can be potentially lethal. Given the substantial potential risks, root replacement should be conserved for those with significant root dilation. The need to optimize long-term benefits should be balanced with the primary goal of reducing operative risk and mortality. The durability of preserved aortic roots after type A dissection repair is excellent, with low incidence of proximal aortic events or reoperation.

A root-sparing, sinus-preserving repair strategy is the preferred approach for most patients. A nonectatic aortic root may be safely preserved by resuspending the aortic valve commissures and performing a supracoronary aortic replacement. The dissection flap often extends proximally to cause collapse of one or more of the aortic valve commissures. The false lumen often has thrombus, which should be carefully removed while avoiding injury to the fragile separated intimal layer. This allows for accurate reapproximation of the layers of the aortic wall. The prolapsing commissure is positioned at the appropriate height relative to the adventitial layer and the commissure is resuspended by placing a 4-0 pledgeted suture through and through the layers just above the commissure, taking care to avoid interference with the cusp tissue itself. Non-prolapsed commissures should be reinforced similarly ( Fig. 22.19 ).

Commissural resuspension. Pledgeted, double-armed, polypropylene sutures are placed above each commissure and through the adventitial layer of aorta. The sutures are tied over a second pledget.

The false lumen in the aortic root may be obliterated using a number of methods. Surgical adhesives, such as biological glue, have been used frequently to reapproximate and adhere the intimal and adventitial layers together, ^, but their use has waned due to reports of associated complications. Biological glues contain formaldehyde or glutaraldehyde, which can cause smooth muscle necrosis in aortic tissue. Such types of glue have led to tissue necrosis, anastomotic dehiscence, pseudoaneurysm formation, and embolization of glue particles, especially if used excessively. Surgical adhesives should be used sparingly, if at all, to prevent late complications.

The aortic root may also be remodeled and reinforced using a felt strip as a “neo-media.” Dissected aortic tissue is often thin and fragile, making it difficult to sew and prone to bleeding. Addition of felt neo-media purportedly strengthens the root tissue, and this type of remodeling has been used extensively worldwide with great success. ^, In this technique, a strip of felt is cut to fit around the part of the circumference of the root that is dissected. The felt is inserted between the intima and adventitia, incorporated into the anastomosis, and serves as a newly created media ( Fig. 22.20 A-B). However, the felt may prevent proper healing of the dissected layers of the aortic root, resulting in a persistent false lumen. Furthermore, reoperations may be complicated by the excess foreign material and persistent separation of layers. The need for a neo-media has been questioned, and some groups have found no benefit compared to reconstruction without a neo-media. ^{, ,}

(A) Disrupted layers of aorta are approximated between strips of polytetrafluoroethylene (PTFE) felt and secured with multiple polypropylene mattress sutures. (B) This cuff is sutured to a woven polyester graft using a continuous polypropylene suture.

In the author’s practice, neither surgical glues nor neo-media reconstruction are utilized. After resuspension of the aortic valve commissures, which itself lines up and reapproximates the dissected layers together, the proximal anastomosis is performed by direct suturing using fine 4-0 or 5-0 polypropylene suture. The suture line fixates the intima to the adventitia, and the fine filament suture reduces needle hole bleeding. The anastomosis is reinforced externally using overlapping horizontal-mattressed felt-pledgeted sutures laced circumferentially around the anastomosis, creating a continuous external ring of felt reinforcement. This technique allows full approximation of intimal and adventitial layers, and in the rare cases that required late reoperation, we noted complete fusion of the aortic layers with no residual false lumen.

Preservation of the aortic root is an effective and durable option, even in the presence of significant preoperative AR. Up to 69% of patients who underwent root-preserving repair have moderate or greater AR. Meticulous resuspension of the commissures with a particular focus on restoring the proper geometry of the sinutubular junction and valve commissures resolves AR in a majority of patients. Root-preserving type A dissection repair is not only safe but also very durable. Although some centers have noted an increased risk of reoperation or recurrent AR with root-sparing techniques compared to root replacement, ^, a majority have identified no difference. The long-term risk of reoperation is 3% to 8% at 10-year follow-up. ^,

In ascending aortic dissection, the most vulnerable segment of the aorta, which is at greater risk of rupture, is the tubular ascending aorta. The goal of surgery for ascending aortic dissection is to remove the entire tubular ascending aorta and thus minimize the risk of lethal aortic rupture. Although the distal aortic anastomosis may be performed with a “clamp-on” technique or an open distal anastomosis under circulatory arrest, debate has existed regarding the optimal approach. A clamp-on anastomosis is performed under normal CPB without the need for deep hypothermia or circulatory arrest, but it leaves a considerable portion of ascending aortic tissue at the distal ascending aorta. An open distal anastomosis allows for resection of all ascending aortic tissue but requires circulatory arrest. Many groups have identified no significant difference in operative outcomes or early outcomes between clamp-on and open distal anastomosis repairs. A multi-center study of the Nordic Consortium for Acute Type A Aortic Dissection showed worse operative mortality and survival with a clamp-on anastomosis despite its use in younger patients. Notably, the clamp-on technique was used in sicker patients with more preoperative organ dysfunction. An open distal anastomosis has the important benefit of improved long-term survival, potentially improved distal aortic remodeling, and decreased need for reintervention. ^{, ,}

DeBakey type II dissection is an exception in which the dissection is confined to the ascending aorta, and the distal anastomosis may be performed to undissected aortic tissue, often even with a clamp-on technique. If dissection involves only the proximal ascending aorta, the aortic clamp is placed just proximal to the origin of the brachiocephalic artery. The aorta is completely transected, and the aortic root is managed as previously described in this chapter. The distal anastomosis is performed in a standard fashion for ascending aortic repairs using continuous 3-0 or 4-0 polypropylene suture ( Fig. 22.21 A-B). Despite the possibility of a clamp-on anastomosis, an open distal anastomosis in patients with a dilated arch incurs the benefit of reducing late aortic reinterventions, and with DeBakey type II dissection, resection up to the arch can be a curative procedure if it eliminates all abnormal aorta.

(A) With DeBakey type II dissection, the intact ascending aorta beyond dissection is completely transected and sutured to the distal end of the aortic graft with a continuous polypropylene suture. (B) Completed procedure. A polypropylene suture is used to seal the site of insertion of a needle vent for aspiration of air.

Hemiarch replacement.

Hemiarch replacement is an effective technique for ascending aortic dissection repair, which offers an excellent balance between the immediate operative risk of the procedure and the late distal aortic outcomes. The incremental increase in difficulty compared to ascending aortic replacement is smaller than the jump to a total arch replacement, and as such, hemiarch replacement may be performed with reliable results by surgeons who may not have a specific subspecialization in aortic surgery.

When preoperative diagnostic studies or intraoperative TEE suggest a need for arch replacement, provisions are made for hypothermic circulatory arrest. An open distal aortic anastomosis technique provides the opportunity to inspect the aortic arch and proximal descending thoracic aorta directly to ensure resection of the primary entry tear whenever possible. The author routinely performs arch repairs using deep hypothermic circulatory arrest (DHCA) with RCP and target systemic temperature of 18°C. Selective ACP with moderate or deep hypothermia of 18°C to 28°C may be used alternatively, depending on institutional experience. The head is packed in ice during the cooling and circulatory arrest phases. While cooling, the ascending aorta is clamped with a soft padded clamp proximal to the brachiocephalic artery, and repair of the root and ascending aorta may commence.

Prior to initiation of circulatory arrest, 500 mg of methohexital is administered to reduce cerebral metabolism. When appropriate systemic temperatures, measured by nasopharyngeal, bladder, or rectal temperatures, are reached, the operating table is placed in steep Trendelenburg position. The caval tapes are secured, and the circulation is stopped. RCP is delivered through the superior vena cava cannula at 150 to 300 mL/min at 14°C, keeping central venous pressure at 25 to 30 mmHg. No clamps or tourniquets are placed on the brachiocephalic vessels. The aortic clamp is removed, blood aspirated, and interiors of the aortic arch and proximal descending thoracic aorta examined for presence of intimal tears and evidence of aneurysmal dilation or rupture. The aortic arch is resected out to the level of the left common carotid artery ( Fig. 22.22 A). The false lumen is inspected, and any thrombus near the level of the anastomosis is removed to prevent embolization. As with aortic root repair, the distal aorta may be prepared for anastomosis using felt neo-media or direct suture reapproximation ( Fig. 22.22 B).

Repair of acute DeBakey type I (type A) aortic dissection when aortic arch is included in repair. (A) Dashed line indicates the site of transection of the aorta, which includes resection of the lesser curvature of the aortic arch. (B) Disrupted layers of aorta are approximated with or without strips of polytetrafluoroethylene (PTFE) felt and secured with multiple polypropylene mattress sutures. A prepared polyester graft is cut obliquely. (C) The graft is sutured to the aorta so that it is aligned vertically with respect to the aortic arch. (D) After evacuating air from distal aorta and brachiocephalic arteries, the aortic graft is clamped, an arterial perfusion cannula is attached, and antegrade perfusion is reestablished. The graft is then anastomosed to proximal prepared aortic cuff with a continuous polypropylene suture.

Arch reconstruction is performed using a woven polyester graft with a prefabricated side branch. The graft is prepared with a slight bevel with the side branch positioned on the lesser curve toward the pulmonary artery side. The anastomosis is created using running 4-0 or 5-0 polypropylene suture, reapproximating the intimal and adventitial layers ( Fig. 22.22 C). The anastomosis is circumferentially externally reinforced with overlapping pledgeted 4-0 polypropylene mattress sutures. After completion of the anastomosis, the aortic cannula is secured to the side-branch of the graft, and CPB is resumed through the side-branch graft in the antegrade direction. Establishing antegrade flow in the aorta following repair reduces the possibility of malperfusion of brachiocephalic vessels and may reduce flow in the false lumen. The proximal end of the graft is elevated, and the operating table is shaken to loosen any entrapped air bubbles in the circulation. Retrograde cerebral perfusion is maintained until full flow is reestablished to flush out air or debris from the cerebral circulation. Suture lines are inspected to confirm they are hemostatic. The table is taken out of Trendelenburg position, and systemic warming is initiated, keeping a gradient of 10°C between the blood and core temperatures. A cross-clamp is applied just proximal to the side branch, and the remaining ascending aortic and root work is completed ( Fig. 22.22 D). CPB is discontinued in standard fashion at a core temperature of 35°C to 36°C.

Hemiarch replacement is a safe and durable technique with an operative risk that is similar to limited ascending aortic replacement. ^, It remains the most common technique for replacing the arch in ascending aortic dissections. ^, The cumulative risk of reintervention at 10 years after hemiarch replacement is as low as 5% to 15% in appropriately selected patients. ^{, ,}

Extended or total aortic arch replacement.

Total arch replacement may be considered in the setting of ascending aortic dissection, but proper patient selection is important, as immediate or late benefits must justify the additional risk incurred by a total arch procedure. An extended arch replacement may be reasonable if the primary entry tear extends to or originates in the arch and cannot be resected with a hemiarch procedure, if the arch is aneurysmal, or if the arch is ruptured and cannot be secured by hemiarch repair.

If inspection of the arch demonstrates a need for extended arch replacement, then resection of the arch ensues, beginning with a hemiarch resection out to the left common carotid artery. The arch is inspected to decide on the extent of arch replacement out to zone 1, zone 2, or zone 3 of the aorta. The periaortic tissues, vagus nerve, and recurrent laryngeal nerves are dissected free from the anterior surface of the arch. The aorta is transected at the appropriate level of the arch, distal to the origin of the left subclavian artery, if total arch replacement is necessary. If the ostia of the arch vessels are grouped together, then they may be reimplanted as an island patch, but if they are splayed apart, separate bypasses to each arch vessel using a prefabricated branched graft may be necessary. The distal aorta is prepared for anastomosis, similar to hemiarch replacement, with or without felt neo-media. The distal anastomosis is created to the polyester graft using 4-0 polypropylene suture and reinforced externally with circumferential overlapping mattressed 4-0 polypropylene sutures, ensuring proper orientation for the arch vessel reimplantation ( Fig. 22.23 A).

Repair of acute DeBakey type I (type A) aortic dissection when total arch replacement is necessary. (A) Aorta is completely transected distal to origin of left subclavian artery. Disrupted layers of aorta are approximated with or without strips of polytetrafluoroethylene (PTFE) felt. A full-thickness elliptical patch is created with the origins of the arch vessels. A polyester graft is sutured to the distal aortic cuff with a continuous polypropylene suture. (B) An opening is made into aortic graft corresponding to size of the patch including the arch vessel origins. The graft is sutured to aortic cuff with a continuous polypropylene suture. (C) Reperfusion is established through the ascending aortic graft prior to completing the proximal aortic anastomosis.

For island reimplantation, an elliptical opening is made in the aortic graft opposite the arch vessel island, and the island is sutured to the graft with a continuous 4-0 polypropylene suture, which is again reinforced with mattressed pledgeted sutures ( Fig. 22.23 B-C). With separate arch vessel bypasses, the ostium of each arch vessel, which may often contain atherosclerotic changes, is resected, and a prefabricated branch of the graft is anastomosed to each healthy arch vessel using running 5-0 polypropylene suture ( Fig. 22.24 ). The remainder of the procedure is completed as described earlier.

Repair of acute DeBakey type I (type A) aortic dissection with total arch replacement. When the aortic arch is aneurysmal and the arch vessel origins are widely separated, each individual arch vessel is bypassed with 8- or 10-mm prefabricated branches.

Some experienced aortic centers have reported that total arch replacement at the time of aortic dissection does not significantly increase mortality of the operation compared to less extensive arch strategies. ^{, ,} Understandably, these represent the results of highly experienced centers that carefully select patients who are most appropriate for an extensive arch reconstruction, and the outcomes should not be generalized to all patients. Indeed, large database studies and single-center reports have found both increased mortality and permanent neurologic injury ^, when extensive arch repair is performed. Total arch replacement has been proposed as a mechanism to promote thrombosis of the distal false lumen and reduce the frequency of late reoperation. Long-term follow-up, however, has not demonstrated that this procedure improves survival or reduces frequency of reoperation. ^{, , , , ,} Recently, a meta-analysis with a landmark analysis indicated that early risk of reoperation is no different, but beyond 7 years of follow-up, an aggressive surgical approach was associated with lower risk of reoperation. Longer follow-up will be necessary to determine if a true benefit exists.

Elephant trunk technique.

Addition of an elephant trunk to ascending aorta and total arch replacement has been proposed as a method to ensure a more secure distal aortic anastomosis and to promote thrombosis of the false lumen in the descending thoracic aorta. This can be accomplished with a polyester graft, and the operative risk of an unstented elephant trunk is not significantly different from a total arch replacement procedure. ^, Alternatively, an elephant trunk can be created with an endovascular stent graft inserted through the open aortic arch or a prefabricated FET device with a proximal surgical graft and distal stent-graft segment. The advantages of an elephant trunk include promoting thrombosis of the false lumen, reducing the frequency of subsequent operations for aneurysm formation of the residual dissected aorta, and simplifying any subsequent operative procedure on the distal aorta.

Efforts to induce downstream aortic remodeling without requiring total arch replacement led to the use of hemiarch replacement with antegrade stent-graft placement. In these procedures, the stent graft is deployed through the open aortic arch under circulatory arrest, which does not add significant time or complexity to the operation ( Fig. 22.25 ). However, care must be taken to ensure the graft is in the true lumen of the descending aorta. Compared to less extensive arch procedures, there is no significant difference in operative mortality or neurologic injury. Aortic remodeling and false lumen thrombosis are significantly improved with antegrade stent graft, but this was less apparent in the aorta distal to the stent. ^, However, there is no difference in the rate of open distal aortic reintervention. Interestingly, endovascular late reintervention is actually significantly higher in some series. While the appearance of aortic remodeling may be satisfying, lack of evidence showing decreased reintervention rates is sobering.

Repair of acute DeBakey type I (type A) aortic dissection with hemiarch replacement and antegrade stent-graft. The stent-graft is incorporated into the distal suture line along the lesser curvature of the arch.

(From Preventza O, Olive JK, Liao JL, et al. Acute type I aortic dissection with or without antegrade stent delivery: mid-term outcomes. J Thorac Cardiovasc Surg . 2019;158(5):1273-1281.)

Total arch replacement with FET is another arch repair strategy that has been gaining support worldwide. The FET procedure is most commonly performed using a hybrid device, which includes a proximal surgical polyester graft attached to a distal stent graft. Variations include prefabricated arch branches and a sewing skirt between the stented and non-stented segments to aid in performing the anastomosis. Use of a FET device is a complex procedure that increases operative and circulatory arrest times, potentially leading to more adverse events. With the prefabricated hybrid devices, the stented portion is placed into the true lumen of the descending thoracic aorta over a guidewire after resecting the aortic arch. The stent-graft portion is deployed, fixing the graft to the descending thoracic aorta. The distal aorta is anastomosed to the sewing skirt of the graft with running polypropylene suture and reinforced in routine fashion ( Fig. 22.26 ). The operation is then completed as described for total arch replacement.

Repair of acute DeBakey type I (type A) aortic dissection with total arch replacement and frozen elephant trunk. Deployed graft, containing 3 side branches for supra-aortic vessels, 1 sidearm for cardiopulmonary bypass, a sewing collar, and a self-expanding stented portion with nitinol ring stents.

(From Shrestha M, Kaufeld T, Beckmann E, et al. Total aortic arch replacement with a novel 4-branched frozen elephant trunk prosthesis: single-center results of the first 100 patients. J Thorac Cardiovasc Surg . 2016;152(1):148-159.e1.)

Centers experienced in the use of FET devices have employed them during repair of aortic dissections with success. Proper patient selection allowed for operative mortality after FET repair of ascending aortic dissection of 1% to 12%, which was similar to that of repair using hemiarch or total arch replacement without FET in comparative studies. ^, However, neurologic complications remain a concern in these complex cases requiring prolonged circulatory arrest. The incidence of stroke ranges from 1% to 18%, ^, and spinal cord injury (SCI) is seen in up to 8.1% of patients receiving FET. ^{, , , ,} SCI is a particularly devastating complication, which is associated with poor survival. In a large meta-analysis of FET during ascending aortic dissection repair, the pooled rate of SCI was 4.7% but was significantly higher when stent length exceeded 15 cm or coverage of the aorta extended to T8 or lower. Some studies have refuted a difference in SCI using FET, but it is unclear why the SCI rates were high even in the unstented patients. Nevertheless, limiting the length of the FET to 10 cm is recommended to decrease the risk of SCI. ^{, ,}

As with other extensive arch procedures, FET provides significant advantages in terms of distal aortic remodeling, especially in the stented segment. False lumen obliteration is common in the stented segment, seen in 86% to 94% of patients, but the aorta distal to the stent often has persistent dissection. True lumen expansion and false lumen shrinkage are also common findings. ^{, , ,} However, despite improved remodeling, the need for reintervention after FET is comparable to other repairs ^{, ,} and is actually increased in some series. Few series demonstrated a reduction in late reintervention, and a survival advantage is not readily apparent. For the limited percentage of patients requiring late distal reintervention, it is debatable whether the routine use of FET should be recommended. However, it may be beneficial for a select group of patients who are expected to have an increased risk of needing distal reintervention.

Malperfusion is defined as ischemia of a vascular bed due to obstruction of blood flow by the dissection flap; this may lead to ischemia-induced end-organ dysfunction. Malperfusion is a lethal complication of acute aortic dissection, which accounts for a significant proportion of morbidity and mortality. Malperfusion may be identified in radiologic studies, but the diagnosis of true malperfusion syndromes requires clinical evidence of end-organ dysfunction such as stroke, coma, myocardial infarction, pulselessness of a limb, acute renal insufficiency or failure, or elevated liver enzymes. ^{, ,} Malperfusion is present in greater than 15% to 40% of patients presenting with acute ascending aortic dissection and is a significant predictor of mortality and adverse events. ^{, , , ,}

Central aortic repair is the classic approach to treating malperfusion, and it remains relevant in the modern era as the primary approach to most types of malperfusion. ^{, ,} Malperfusion is most often caused by obstruction of a branch vessel of the aorta by the intimal dissection flap. Since a majority of primary entry tears are located in the ascending aorta or arch, central aortic repair serves to reestablish and improve true lumen blood flow and reduce the hemodynamic forces within the false lumen. This allows the true lumen to re-open and provide blood flow to critical organs. Central aortic repair is often successful in restoring blood flow with dynamic obstruction caused by the dissection flap, but static obstruction caused by thrombus formation may not be relieved by this technique alone. ^{, ,}

The presentations of cerebral malperfusion range from asymptomatic to syncope, stroke, or coma. As with general care of stroke patients, early reperfusion is beneficial for reducing the risk of neurologic complications and permanent neurologic deficit. The most common approach to correcting cerebral malperfusion is central aortic repair. Intervention on the carotid artery, such as carotid stenting, may be required in a minority of patients with static malperfusion. Many of the presenting neurologic deficits are reversible after repair and reperfusion. ^, In the IRAD database, 17.5% of patients with preoperative cerebral malperfusion had evidence of cerebrovascular accident postoperatively.

Coronary malperfusion may present with signs and symptoms similar to acute coronary syndromes, including ST changes on electrocardiogram, elevated troponin level, and wall motion abnormalities on echocardiography. Malperfusion of the coronary arteries leads to myocardial ischemia and dysfunction, which must be addressed rapidly due to their significant associated risk of mortality. Malperfusion is usually due to involvement of the coronary arteries with dissection by three potential mechanisms: type A lesions involve obstruction of the coronary ostium by the dissection flap; type B lesions have extension of the dissection flap into the coronary artery itself obstructing by the false lumen; and type C lesions are defined by complete avulsion of the intima of the coronary ostium ( Fig. 22.27 ). ^, Proximal aortic replacement and repair of the aortic root are adequate to treat type A and most type B lesions. Some type B and all type C lesions require CABG. Optionally, the coronary ostium may be reinforced with suture, pericardium, or felt. ^, If evidence of coronary ischemia persists despite successful aortic repair with direct coronary repair, additional CABG is necessary.

Three main types of coronary lesion due to proximal aortic dissection: type A, ostial dissection (A); type B, dissection with a coronary false channel (B); type C, circumferential detachment with an inner cylinder intussusception (C).

(From Neri E, Toscano T, Papalia U, et al. Proximal aortic dissection with coronary malperfusion: presentation, management, and outcome. J Thorac Cardiovasc Surg . 2001;121(3):552-560.)

Mesenteric malperfusion presents a particularly difficult challenge since it is difficult to diagnose, difficult to treat, and is associated with a high risk of poor outcomes and mortality. Signs and symptoms of mesenteric malperfusion are often not specific and overlap significantly with standard aortic dissection clinical presentation. Only 60% have abdominal pain, and laboratory evidence of visceral malperfusion, such as elevated liver function panel and lactate level, are late signs which may themselves be nonspecific. A delay in reestablishing perfusion leads to high mortality rates due to the risk of microvascular thrombosis and irreversible bowel ischemia or liver failure. The two debated approaches to mesenteric malperfusion are early central aortic repair versus treatment of the malperfusion syndrome with delayed central aortic repair. Central aortic repair improves true lumen flow and usually relieves the malperfusion, but an extensive aortic procedure requiring circulatory arrest is high-risk in patients who often have liver and bowel ischemia. Immediate central aortic repair is associated with a 30% to 70% operative mortality. ^, Alternatively, a period of medical management with or without endovascular techniques, such as fenestration or stenting, may relieve the malperfusion, restoring blood flow to the affected vascular bed. Surgery may be performed in a delayed fashion with significantly reduced risk, similar to patients without malperfusion at presentation, but up to 13% to 33% of patients are at risk of dying in the interim from malperfusion or aortic rupture. ^, The optimal strategy remains debated, but the best outcomes are likely to be achieved with a balanced strategy of delayed central aortic repair for patients in extremis with severe organ dysfunction and immediate central repair for those with earlier or less severe mesenteric malperfusion. In the IRAD database, the in-hospital mortality of patients with mesenteric malperfusion receiving medical therapy alone was 95.2%, endovascular revascularization was 72.7%, and hybrid therapy was 41.7%.

Lower extremity malperfusion presents with pain, pulselessness, paraplegia, or paraparesis and is most often caused by dynamic obstruction of the iliofemoral system by the dissection flap. Less commonly, a static obstruction is caused by thrombosis of the false lumen. Up to 65% to 85% of patients presenting with extremity malperfusion have resolution of the malperfusion with proximal aortic repair alone. ^{, ,} The remaining require additional vascular interventions to restore extremity blood flow, such as fenestration, stenting, patching, or extra-anatomic femoral bypass. Isolated lower limb ischemia is not associated with increased early mortality. ^, However, patients with lower limb ischemia are more likely to have mesenteric malperfusion, which portends a worse prognosis. ^, Revascularization of the extremities first with delayed aortic repair may be a reasonable approach in some patients, but up to 24% die before their aortic repair. After surgical repair, close monitoring for limb ischemia, reperfusion injury, and compartment syndrome is imperative. Prophylactic 4-compartment fasciotomy should be considered in the initial operation in cases of prolonged preoperative limb ischemia.

Renal and spinal malperfusion are less critical than the previously mentioned syndromes and are not associated with increased early mortality in large series. However, the diagnosis of true renal malperfusion is clouded by the inaccuracy associated with imaging-based diagnosis and the common occurrence of renal insufficiency even when malperfusion is not present. Renal malperfusion resolves radiographically in 80% of patients with proximal aortic repair, and whereas some have found no difference in the incidence of renal insufficiency or dialysis, others have noted a higher incidence of postoperative acute kidney injury and operative mortality in those with preoperative renal malperfusion. ^,

Acute ascending aortic dissection remains a highly lethal disease in the modern era despite significant improvements in operative outcomes throughout the world due to improved surgical technique, surgeon experience, and perioperative care. In the IRAD database, the in-hospital mortality of surgically managed type A dissections improved from 25% in the late 1990s to 18% in the 2010s (see Fig. 22.12 ). Similarly, the most recent reports from the Nordic Consortium for Acute Type A Aortic Dissection (NORCAAD) reported a 30-day mortality of 16%, the German Registry for Acute Aortic Dissection Type A (GERAADA) reported 17%, and the United Kingdom National Adult Cardiac Surgical Audit dataset reported an operative mortality of 18%, the STS database reported an operative mortality of 17%, and the US National Inpatient Sample demonstrated an overall mortality of 15%. Independent predictors of mortality include preoperative shock, cardiac tamponade, limb ischemia, and hypotension as a presenting symptom.

The median case volume of acute ascending aortic dissection repair is three per year, and only 10% of hospitals perform more than 10 cases per year. In high-volume aortic centers of excellence, the operative mortality for repair of acute ascending aortic dissection is approximately half that reported in the large national databases, with operative mortality as low as 5% to 11%. ^{, , , , , 270 ,} Focused surgical teams with greater aortic surgery experience are able to improve operative outcomes relative to general cardiac surgeons. A strong volume-outcome relationship exists for repair of acute ascending aortic dissection. Numerous studies have shown that high-volume hospitals have a lower risk of early mortality (11%-17%) compared to low-volume hospitals (21%-28%). ^, On an individual surgeon level, the volume-outcome relationship strongly persists ( Fig. 22.28 ). ^, Although the strong relationship clearly exists, the difficulty lies in defining the limits for what is considered high versus low volume, and significant variation exists in the literature. Nevertheless, development of a team focused on aortic surgery has merit for improved outcomes. ^,

Relationship between the ratio of observed to predicted mortality and annual case volume. (A) Annual type A dissection repair for individual surgeons. (B) Annual number of all cardiac surgery cases for individual surgeons.

(From Chikwe J, Cavallaro P, Itagaki S, Seigerman M, Diluozzo G, Adams DH. National outcomes in acute aortic dissection: influence of surgeon and institutional volume on operative mortality. Ann Thorac Surg . 2013;95(5):1563-1569.)

Acute ascending aortic dissection usually presents as an acute event in which patients present to their local emergency departments. Many patients present to hospitals without cardiac surgical services and require transfer to another hospital. Over 60% of surgically treated patients are actually transferred in from other hospitals. Nearly 25% of Medicare beneficiaries present to hospitals without cardiac surgery, and 50% present to low-volume hospitals. Given the significantly better outcomes achieved at high-volume hospitals, the concept of regionalization of care for aortic dissections has been debated. ^, Delaying surgery for transfer to another institution has not been associated with increased adverse events, and patients may benefit from treatment at experienced high-volume centers. ^, However, the desire to transfer to an experienced center must be weighed against the need for timely treatment.

Much of the risk associated with acute aortic dissection repair is related to the early operative risk associated with the initial presentation and the surgery itself. Mid- to long-term survival of those who survive the primary event is largely a function of age and comorbidities with some contribution from aortic events. The hazard risk for death rapidly declines in the early phase and is followed by a constant phase ( Fig. 22.29 ). Mid-term survival at 5 years is 68% to 82%. Long-term survival at 10 years is 51% to 74%. ^{, , , , ,} Predictors for long-term mortality include baseline maximum descending aortic diameter, primary entry tear size, and connective tissue disorder suggesting that these high-risk subgroups may benefit from earlier or more aggressive therapy.

Kaplan-Meier survival curve for type A dissection stratified by treatment type.

(From Booher AM, Isselbacher EM, Nienaber CA, et al. The IRAD classification system for characterizing survival after aortic dissection. Am J Med . 2013;126(8):730.e19-e24.)

The need for aortic reoperation is uncommon within the first 5 years, ^, but the risk of reinterventions, especially of the distal aorta, increases over time. The determinants for late reintervention are patient factors that are associated with aortic degeneration, such as connective tissue disorder and other aortopathies. ^{, , ,} The need for a more extensive primary operation is a marker of more aggressive disease that increases the risk of needing later reinterventions, and the cumulative risk of reintervention at 10 years in this higher risk subset exceeds 20%.

Proximal aortic reoperation is uncommon even with preservation of the native aortic root and resuspension of the native aortic valve. Freedom from reoperation on the aortic valve is 97%, 92%, and 84%, whereas freedom from moderate or severe aortic insufficiency is 92%, 84%, and 72% at 5, 10, and 15 years, respectively. Cumulative incidence of proximal aortic reoperation at 5 years is 1% to 2.5% ^, and at 10 years is approximately 8%. In a recent comparison of outcomes of root-sparing versus root replacement in ascending aortic dissections, the 15-year cumulative incidence of reoperation was 11% and 7% in the root-sparing and root replacement groups, respectively. Other groups demonstrated similar results with low proximal aortic reintervention rates of 6% to 13% regardless of whether the root was repaired or replaced. ^{, ,} However, aortic root diameter of >4.5 cm at the time of the primary operation is independently associated with late proximal aortic reintervention.

The need for late reoperation is more common in DeBakey type I dissections than type II dissection, largely driven by the need for distal aortic reinterventions. Freedom from distal aortic reintervention is 72% to 96% at 5 years and 62% to 88% at 10 years. ^{, , , , , , , , ,} Strategies to perform more extensive repair of the distal aorta during the initial operation, such as total arch replacement, elephant trunk, antegrade stent-graft, and FET, have been performed to try to reduce the incidence of distal reinterventions. Interestingly, although distal aortic remodeling is better with more extensive arch procedures, most studies have found no difference in the need for late distal aortic reoperations. ^{, , , , , ,}