Vascular > Aorticaneurysm

Aortic Aneurysm:

View images of aortic aneurysm

Clinical:

The aortic annulus is a virtual ring surrounding the ventriculo-aortic junction just below the lowest insertion points of the aortic valve [39]. The sinuses of valsalva are the outward bulge of the aortic root associated with each of the three aortic valve cusps [39]. The aortic root is defined as the part of the ascending aorta that contains the aortic valve, annulus, and sinuses- this is the region from the ventriculoaortic junction (aortic valve ring) to the sinotubular junction [17,27]. The sinotubular junction is the slight waist-like narrowing between the aortic root and the tubular portion of the ascending aorta [39]. The tubular portion of the ascending aorta begins above the sinuses of valsalva, at the sinotubular junction and extends to the origin of the right innominate (brachiocephalic) artery [17,19].  The aortic arch extends from the right brachiocephalic artery to the attachement of the ligamentum arteriosum [17]. From the ligamentum arteriosum to the diaphragmatic hiatus is the decending thoracic aorta [17].

Aortic aneurysms can be classified as either fusiform or saccular (a focal out-pouching of the wall). An aortic aneurysm has been defined as segmental dilatation of  ≥ 50% of the full thickness of the vessel involving any segment from the aortic root to the abdomninal aorta [43]. The normal diameter of the mid-ascending aorta should always be less than 4 cm, and that of the descending aorta no more than 3 cm [17]. Thoracic aortic measurements greater than 4 cm are considered consistent with an aeurysm [39]. The risk of rupture increases with the size of the aneurysm [17,19]. The reported risk is 0% if less than 4 cm, 16% for aneurysms between 4 to 5.9 cm, and 31% if 6 cm or more [43]. The risk for rupture when the aneurysm is greater than 5.5 cm in diameter is generally perceived to exceed the risk of operation [39].

Although thoracic aortic aneurysms expand at a slower rate than abdominal aortic aneurysms, surgical repair is contemplated when the aneurysm reaches a diameter of 5.5 cm (and for descending thoracic aneurysms greater than 6.5 cm) [17,28]. An annual growth rate of greater than 1cm [17] or a diameter greater than 4.5 cm with an increase of at least 0.5 cm in the preceding 6 months are other accepted indications for surgical repair [17,19]. Although, other authors indicate that surgical repeair is recommended in patients with an aneurysm that grows more than 0.5 cm in one year [28]. Rapid aneurysm growth (more than 0.5-1 cm per year) is also a consideration for elective repair, even if the absolute size criteria has not been met [39]. Earlier intervention is recommended in patients with Marfans syndrome (between 4.5-5 cm) or bicuspid aortic valves (more than 4 cm due to risk of dissection) [17,28,39]. 

In symptomatic patients, aneurysms are repaired regardless of size [28].

Marfan syndrome:

Marfan syndrome is an autosomal dominant connective tissue disorder caused by mutations in the gene (FBN1) that encodes fibrillin-1 [39]. Approximately 25% of cases result from a sporadic mutation of the FBN1 gene [39]. Classically, Marfan syndrome results in a tulip-shaped configuration to the aortic root (annuloaortic ectasia) with dilatation of the aortic annulus and sinuses of valsalva, and effacement of the sinotubular junction [39]. Dilatation of the aortic annulus results in aortic insufficiency in 15-44% of patients [39].

Ehlers-Danlos syndrome, vascular type:

Ehlers-Danlos syndrome, vascular type (Type IV) is a rare autosomal dominant disorder that results from mutations in the gene (COL3A1) that encodes type III procollagen [39]. Excessive tissue fragility predisposes patients to vascular complications including aortic aneurysm, dissection, and rupture [39].

Surgical repair:

Prior to surgical repair of ascending thoracic aortic aneurysms it is important to document if the aneurysm involves the aortic arch or extends to the inominant artery. In such cases hypothermic circulatory arrest will be necessary for the procedure. This entails cooling the patient systemically to below 19 degrees Celsius, placing the patient in the Trandelenburg position, and stopping the cardiopulmonary bypass circuit. Hypothermic circulatory arrest increases the complexity, length, and mortality associated with surgery. It is also used for some patients with severe aortic calcification where clamp placement leads to an increased risk for stroke due to thromboembolic phenomena, in patients with fragile aortic tissue (Marfan's) where clamping may result in aortic laceration, and in patients undergoing repeat aortic surgery [1].

The mortality rate for elective surgical repair of thoracic aortic aneurysms can be as high as 7-12% [15]. The two most common techniques for surgical repair are interposition graft and inclusion graft [17]. After the affected segment has been excised, an interposition graft is sewn end-to-end and vascular branches such as the coronary arteries are reimplanted [17]. An inclusion graft is inserted into the aortic lumen and the native aorta is wrapped around the synthetic graft, leaving a potential space between the native aorta and the graft that may thrombose (or even show persistent blood flow that would not require intervention in the absence of hemodynamic instability) [17,28]. Inclusion grafts are not commonly performed because of improved surgical techniques with interposition grafts [28]. The synthetic grafts are most commonly composed of polyethylene (Dacron) and are slightly hyperattenuating relative to the native aortic wall on non-contrast imaging, but appear hypoattenuating relative to the contrast opacified aortic lumen [28].

A supracoronary grafting is indicated in patients with an ascending aortic aneurysm or atherosclerotic origin and normal sinuses of Valsalva [28]. With this technique, the cononary ostia are preserved, which minimizes the risk for pseudoaneurysm, stenosis, thrombosis, and kicking at the cononary anastamosis site [28]. Simultaneous placement of a supracononary aortic graft and an aortic valve is known as the Wheat procedure [28]. One complication associated with supracoronary grafting is the develoment of dissection or aneurysm of the native aorta proximal to the graft- particularly in patients with Marfan syndrome or annuloaortic ectasia [28].

The Bentall procedure is performed for patients with both aortic valvular disease and dilatation of the sinuses of valsalva whose aortic root walls are too vulnerable to allow suturing of the proximal end of the aortic prosthesis [28]. In the procedure, the native aortic root and aortic valve are replaced with a composite graft that consists of both ascending aorta and aortic valve grafts- the cononary arteries are then anastamosed to the graft [28]. Because of the risk of pseudoaneurysm formation at the conronary anastamosis, a modified Bentall procedure (button Bentall or Carrel patch) was dveloped in which a "button" of of the aorta encircling the coronary ostia is removed with the coronary artery, facilitating implantation of the coronary artery to the graft [28]. A potential complication of the Bentall and modified procedures is formation of a pseudoaneurysm at the distal aortic anastamosis [28].

The Cabrol procedure is an alternative to the modified Bentall procedure in patients with aortic dissection, annuloaortic ectasia, or atherosclerotic aneurysm in whom the button Bentall cannot be performed due to severe atherosclerosis of the ascending aorta (which precludes good-quality buttons) or severe proximal coronary artery disease [28]. In this procedure, a composite aortic root and aortic valve graft and a prosthetic conduit anastamose the cononary ostia to the aortic graft in a side-to-side manner [28]. The normal post operative appearance of a rtroaortic conduit may mimick that of an intimal flap related to a dissection [28]. Complications of the Cabrol procedure include anastomotic leak, cononary graft insufficiency from kinking or intimal hyperplasia, acute graft thrombosis, and endocarditis [28].

Biologic grafts are used for repair in the Ross procedure [28]. The Ross procedure is performed in young patients with a dilated aortic root and an aortic valve condition [28]. In the procedure, the native aortic root and aortic valve are replaced with the patient's own pulmonary valve and proimxal pulmonary artery [28]. A synthetic or biologic pulmonary graft is then performed [28]. Advantages of the Ross procedure include improved hemodynamics, a lower risk for endocarditis, lower thrombogenicity and decreased need for anticoagulation, and an allowance for growth potential in children [28]. The most frequently reported complication is aneurysmal dilatation of the aortic root, but aortic dissection and pseudoaneurysm at the proximal or distal anastomotic sites has also been described [28].

Anortic valve-sparing procedure is indicated in patients with an aneurysm at the level of the sinuses of Valsalva, with or without coexisting aortic valvular insufficiency, and in patients with aneurysms that invovle the sinotubular junction, but with essentially normal aortic valve leaflets [28]. In the procedure, the aneurysmal aortic is removed to the level of the annulus, with the aortic valve left intact and the sinuses of Valsalva reconstructed with a Dacron graft [28]. Because the native valve is left intact, there is no need for long-term anticoagulation therapy [28]. The procedure is especially attractive in Marfan syndrome patients [28]. Aortic insufficiency is the most frequent cited complication of valve-sparing procedures [28].

Aneurysms or dissections that involve the aortic arch are repaired with the elephant trunk procedure [28]. The elephant trunk procedure consists of two stages [28]. In the first stage, the ascending aorta and aortic arch are removed and replaced with a graft that is inserted into the descending aorta where it is left unattached and floats freely [28]. The great vessels are anastomosed to the graft [28]. In the second stage, a second graft replaces the descending aorta and is anastomsed to the original graft [28]. Alternatively, fixation of the original distal portion of the graft can be achieved by deploying an endograft- a hybrid elephant trunck procedure [28]. Spinal cord ischemia and paraplegia are potential complications of the procedure [28].

Aortic root surgical complications:

Aortic root pseudoaneurysm: Aortic root pseudoaneurysm is a rare complication (less than 0.5% of patients) [30]. Mediastinitis and graft infection are the most common risk factors for the formation of a postoperative aortic root pseudoaneurysm [30]. Other risk factors include underlying aortic wall disease (Marfan syndrome), dissection of the native aorta, and excessive use of biologic glue [30]. The most common location is at the graft anasatomsis site, followed by the coronary artery anastomosis site, aortotomy site, aortic cannulation site, and needle vent site [30]. Many patients present with acute symptoms such as chest pain, heart failure, and sepsis, but some patients can be relatively asymptomatic [30]. The lesion carries a high risk for rupture [30].

Coronary ostial aneurysm: A coronary ostial aneurysm can develop at the coronary artery reimplantation site- especially in patients with underlying connective tissue disorders such as Marfan syndrome or Loeys-Dietz syndrome (a recently described connective tissue disorder) [30]. Coronary ostial aneurysms can develop in up to 43% of patients with Marfan syndrome and are thought to devlop as a result of perioperative stretch of the weakened coronary ostial wall [30].

Mediastinitis/graft infection: The incidence of mediastinitis following cardiac surgery is reported to be between 0.4-5% [30]. A small amount of fluid or gas may be seen for several days or weeks after removal of mediastinal drains [30]. The presence of abnormally large amounts of low-attenuation material surrounding the aortic graft or increasing fluid and soft tissue infiltration on serial scans should raise the suspicion for mediastinitis [30]. Persistent (longer than 6 weeks), new, or increasing perigraft air may indicate infection with a gas-producing organism or a fistula with the adjacent bronchus or esophagus [28].

Sternal dehiscence: Sternal dehiswcence and sternal wound infection are serious complications that are seen in 1-7% of patients who have undergone cardiac surgery [30]. Risk factors include obesity, lung disease, diabetes, history of prior chest wall radiaiton, renal disease, steroid use, and reoperation [30]. Sternal dehiscence may occur alone or in association with mediastinitis [30]. CT findings include displacement of sternal wires, sternal erosion, or a cleft/sepration of the sternotomy site [30].

Perigraft seroma: A perigraft seroma is a late complication of polytetrafluoroethylene and polyester fiber grafts [30]. The pathogenesis involves both failure of graft incorporation into the native vessel wall and increased graft porosity [30]. Fluid between the open aortic graft and the sac wall is a normal finding on imaging in the period immediately following surgery [30]. However, after 3 months any perigraft hematoma or fluid should have resolved [30].

Etiologies for thoracic aortic aneurysms include:

1- Atherosclerotic vascular disease:

Atherosclerosis is the cause of about 70% of all thoracic aortic aneurysms [17]. Atherosclerotic aneurysms can involve any portion of the thoracic aorta, but most commonly descending thoracic aorta [17] and typically produce a fusiform enlargement involving a long segment of the vessel. About 28% of patients with thoracic aortic aneurysms will also have an AAA [17]. Atherosclerotic aneurysms of the ascending aorta typically spare the sinotubular junction and aortic valve function until late in the disease process. Most thoracic aortic aneurysms are asymptomatic. When symptoms do occur, they are typically related to rupture, dissection, or compression of adjacent structures. The treatment for descending thoracic aortic aneurysms is surgical resection and replacement with prosthetic graft. Mortality rates of up to 50% have been reported in cases of emergent repair, and about 12% in elective cases. Paraplegia occurs in 5-10% of patients. Translumenal endovascular stent grafting offers an alternative method of therapy. The aneurysm must be at least 2-3 cm from the origin of the left subclavian artery to ensure that the stent does not cover the orifice of this vessel. To limit exclusion of intercostal arteries the length should be kept to a minimum. Mortality from the procedure has been reported to be about 15%, and paraplegia occurs in 4% of patients [3].

A hyperattenuating cresentic rim if seen on CT of a large abdominal aortic aneurysm is a specific sign of impending rupture [18].

On MR spin echo images, the wall of the vessel is thickened and irregular secondary to the presence of sclerotic plaque. Areas of signal void correspond to wall calcifications. Thrombus adherent to the wall of the aneurysm may be difficult to distinguish from plaque, although thrombus typically has a smooth interface with the vessel lumen.

2- Marfan's disease / Ehlers-Danlos:

Marfan's syndrome is inhereted as an autosomal dominant disorder with high penetrance, but expression is highly variable. The disorder has been linked to a fibrillin gene defect on chromosome 15 (FBN1 gene mutation that encodes for fibrillin-1) [4,33]. Marfan syndrome is a multisystem disorder that affects the cardiovascular, ocular, and skeletal systems [33]. The major manifestations include ectopia lentis, aortic root aneurysm or dissection, and dural ectasia [33]. Surgical intervention is indicated when the aortic root dimeter exceeds 5 cm, or when the aneurysm growth exceeds 1 cm/year [33].

Ehlers-Danlos syndrome (EDS) is a group of clinically and genetically heterogeneous heritable connective tissue disorders [26]. There are six types of EDS currently recognized [26]. The vascular type is a rare, autosomal-dominant disorder resulting from a mutation in the COL3A1 gene encoding for type III procollagen synthesis [26]. The more common vascular complications with EDS include aortic aneurysm (but without predilection for the aortic root), dissection, or rupture of medium-size abdominal arteries (iliac, renal, and mesenteric) [33]. Excessive tissue fragility predisposes patients with vascular EDS to premature arterial, intestinal, or uterine rupture during labor [26]. Patients also have thin ntranslucent skin and a characteristic facial appearance (thin pinched nose, thin lips, tight skin, hollow cheeks, and prominent staring eyes due to decreased subcutaneous adipose tissue) [33]. Complications are rare during childhood, but more than 80% of patients will have at least one complication by the age of 40 years [26]. Because of the risk of dissection, conventional angiography is generally contraindicated in EDS patients [33].

Both Marfan's and Ehlers-Danlos are associated with cystic medial necrosis that results in weakening of the aortic wall typically resulting in aneurysms of the ascending aorta. Annuloaortic ectasia is characterized by dilated sinuses of Valsalva with effacement of the sinotubular junction producing a pear-shaped aorta that tapers to a normal aortic arch and the condition is most commonly associated with Marfans syndrome [17]. Associated valvular dysfunction is also common secondary to dilatation of the aortic root. Other causes of annuloaortic ectasia include idiopathic (about 1/3'd of cases), homocystinuria, and osteogenesis imperfecta [17].Endovascular stent-grafts are generally not recommended in the treatment of aortic aneurysm in patients with connective tissue diseases because they have a higher risk of endoleaks, reinterventions, and disease progression compared to the general population [33].

On MR imaging, there is dilatation of the aortic root associated with complete effacement of the sinotubular junction (remember, this is not seen in atherosclerotic aneurysms until late). When viewed in an oblique coronal section this produces an "onion bulb" or "pear-shaped" appearance to the aortic root and this is considered to be characteristic of the disorders. Cine gradient images can be used to demonstrate regurgitant flow associated with valvular dysfunction.

3- Aortitis:

a) Non-infectious Aortitis: Takayasu's (pulseless disease) and temporal arteritis (giant cell arteritis) are the two most common arteritides to involve the aorta. Takayau's more commonly involves the aorta. Both disorders affect women most commonly- Takayasu's affecting women in their teens to thirties, and temporal arteritis affecting older women. Both aneurysm and stenosis are formation are common. Involvement of the aortic root is also common when there is aneurysmal dilatation and hence, regurge is also seen. The disorders typically produce associated thickening of the aortic wall.

b) Infectious Aortitis (also referred to as Mycotic aneurysm): The most common organisms are Staphylococcus (older males), Streptococcus, Pneumococcus, or Salmonella (younger or immune compromised patients). Etiologies include post-aortic or coronary artery bypass surgery. Prognosis is grim in the absence of antibiotic or surgical treatment. Mycotic aneurysms are usually saccular and contain eccentric thrombus [17]. CT and MR findings indicative of an infectious aortic aneurysm include wall thickening (with or without nodularity), periaortic inflammatory changes resulting in thickening of the periaortic tissues, perianeurysmal gas, and a saccular aneurysm (although, fusiform aneurysms can also occur).

Syphilis is a sexually transmitted disease caused b the spirochete T palladium [23]. Tertiary syphilis can involve the cardiovascular system, typically 10-20 years after the initial infection [23,41]. Syphilitis aortitis is felt to be an inflammatory response to T palladium and causes focal destruction of the media due to an endarteritis of the vasa vasorum with loss of elastic and smooth muscle fibers and scarring leading to aortic dilatation and aneurysms [17,23,41]. Syphilitic aortitis is reported to occur in 70-80% of all cases of untreated syphiltic infection and characteristically involves the ascending aorta (60% of cases) followed by the aortic arch (30% of cases) [23,41]. Aortic aneurysms are detected clinically in only 5-10% of patients - most commonly (50%) involving the asceding aorta, followed by the aortic arch (35%), and descending aorta (15%) [41]. The majority of the are saccular, but up to one-third can be fusiform [41]. Syphilitis aneurysms are at high risk for rupture (up to 40% of cases) [17]. On plain film, "pencil-line" fine calcifications within the wall of the vessel are considered classic. [23].Other complications include aortic insufficiency (seen in 20-30% of patients with syphilitic aortitis) and coronary ostial stenosis (seen in 20-26% of patients) [41].

4- Aortic stenosis:

Post-valvular dilatation of the ascending aorta is seen in association with aortic stenosis. There is relative preservation of the aortic root and sinotubular junction and the dilatation is usually limited to the mid ascending aorta where the post-stenotic flow effects are most pronounced.

5- Aortic insufficiency:

Insufficiency may also result in dilatation of the ascending aorta- likely related to the "water-hammer" effect. Dilatation in these cases is more likely to extend into the transverse arch, and there is less preservation of the aortic root and sinotubular junction.

Abdominal aortic aneurysm:

Abdominal aortic aneurysms are defined as dilatation of the abdominal aorta greater than 50% of the normal proximal segment or a diameter greater than 3 cm [37]. The most accurate measurements of the aneurysm diameter are obtained orthogonal to a center line through the aorta [35]. An AAA is defined by its location relative to the renal arteries [37]. An infrarenal AAA arises at least 10 mm below the renal arteries, a juxta renal AAA extends to the renal arteries, and a suprarenal AAA invovles the renal arteries and extends superiorly [37]. The risk of rupture increases with increasing diameter [37].

Abdomninal aortic aneurysms are more common than TAAs and occur in approximately 5% of screened males over 65 years of age and are often defined as dilatation ≥ 3 cm [45]. Concomitant abdominal aortic aneurysms occur in more than a quarter of patients with TAAs [43]. Abdominal aortic aneurysms expand at a rate of 2-4 mm per year when smaller than 4 cm, 2-5 mm per year when they are between 4-5 cm, and 3-7 mm per year when larger than 5 cm [9]. The risk for rupture of an abdominal aortic aneurysm is between 10-20% when it reaches 5-6 cm, and increases to 30-50% when it equals or exceeds 8 cm [19]. 

Series have shown that about 40% of aneurysm with diameters larger than 5 cm will ruture over a 5 year period [38]. The rupture risk has been reported as 1-3% per year at a diameter of 4-5 cm (other authors suggest less than or equal to 1% for a diameter of 5.5 cm or less [43]), 6-11% per/yr between 5-7 cm (other authors suggest 9% for diameter 5.5-5.9 cm and 10% for diameter 6-6.9 cm [43]), and 20-33% per year when equal to or greater than 7 cm [37,43]. Most abdominal aortic aneurysms grow 1-4 mm per year, and rupture risk versus oeprative risk is blanaced at a 5.0-5.5 cm threshold for intervention [35]. Abdominal aortic aneurysms smaller than 5.5 cm are usually followed with serial imaging at 6 month to 3 year intervals - a 12 month interval is recommended for aneurysms between 4-4.9 cm and 3 year surveillance for those 3.0-3.9 cm [44].

Surgical thresholds for aneurysm repair varying depending on the location of the aneurysm, but most surgeons will electively repair typical fusiform abdominal aortic aneurysms that exceed 5.4 cm in greatest diameter or an aneurysm size that is 2.5 times the normal aortic diameter [16,35,37]. Surgical repair is also indicated for aneurysms that enlarge more than 5-7 mm within 6 months or 1 cm or more within one year [35]. Other authors suggest guidelines generally recommend elective surgical repair for AAA greater than 5-5.5 cm or expansion of more than 5-10 mm over a 6- to 12 month period [43]. Maximum cross sectional aneurysm diameter, the thickness/extent/volume of intralumenal thrombus, and a rapid increase in thrombus area are independently associated with greater risk for more rapid aneurysm growth [44].

Risk factors for rupture include active tobacco use, uncontrolled hypertension, prior cardiac or renal transplant, and female gender [43]. CT signs that are suggestive of impending rupture include a hyperattenuating cresent sign, wall irregularity, a new saccular outpouching/penetrating ulcer, the draped aorta sign, and a periaortic hematoma [35]. The hyperattenuating cresent sign refers to a perilumenal curvilinear area of hyperattenuation (higher than intralumenal blood at unenhanced CT) within the wall or thrombus of the aorta [35]. Ruptured anueyrsms have been shown to contain less mural thrombus and thrombus calcification compared with more stable aneurysms [35]. Decreasing thrombus volume with progressive enlargement of the flow lumen or new eccentric outpouching of the lumen likely indicated lysis of thrombus and is another risk factor for rupture [35]. The draped aorta sign is an indication of contained rupture and refers to the posterior aortic wall closely following or "draping" along the contour of the adjacent vertebral body [35]. The aorta may also appear indistinct from the vertebral body or psoas muscle, with loss of the periaortic fat planes [35].

Endovascular stent grafting:

Endovascular stent grafting is an alternative to surgical repair primary applied to the treatment abdominal aortic aneurysms and for thoracic aortic aneurysms in patients who are poor surgical candidates [15,16]. Endovascular repeair is best suited for infrarenal AAAs and a 1.5 cm landing zone of normal anatomy is required for infrarenal fixation [37]. A short aneurysmal neck will result in radial force exerted over a smaller area resulting in a greater risk of inadequate seal, distal stent migration, and type 1 endoleak [37]. Suprarenal fixation requires a bare metallic stent component to extend above the fabric-covered stent graft [37]. The junction between the bare metallic stent and stent graft is placed just below the renal arteries- this allows perfusion to the superior mesenteric and renal arteries [37]. Tortuous AAA with proximal neck angles of less than 120 degrees pose a challange for proper delivery and deployment of the device [37]. Other factors of the proximal nexk that affect proper seating of the device include excessive calcification or thrombus (more than 2 mm thick or more than 50% circumferential involvement) and diameter of the proximal neck (more than 28 mm) [37]. A minimal iliac artery outer diameter of 7 mm is needed for device delivery [37]. Other authors suggest hostil neck configurations include a diameter of > 32 mm (which can result in proximal seal or fixation failure), a length < 15 mm (which can result in seal zone failure), angulation > 60 degrees (which can result in incomplete circumferential wall apposition, and a conical configuration (which can result in seal zone failure) [45].

Immediately after endovascular stent placement, CTA imaging may show aortic wall thickening and low density periaortic fluid [16].

Generally, aneurysms will decrease in size following successful endograft repair, however, a slight increase in size of the anuerysm sac may sometimes be seen on the first post-operative scan [16]. As long as no endoleak is identified, conservative management and careful followup can be performed [16]. The left subclavian artery may occasionally be occluded by the stent in order to achieve a minimum of 2 cm length of non-disease aorta for stent anchorage [16]. In these cases, retrograde flow from the left vertebral artery provides perfusion to the left arm [16]. Prior to occlusion of the vessel, cerebral arterial supply should be evaluated to ensure adequate posterior fossa circulation.

For repair of thoracic aortic aneurysms, patients with endovascular stent grafts have been suggested to have a lower prevalence of spinal cord ischemia, a lower prevalence of renal and respiratory insufficiency, and a shorter hospital stay [15]. Patient survival at two years is similar for open repair and stent graft patients [15]. The prevalence of endoleak for thoracic aortic aneurysms has been reported to be 6% at one year, and 9% at two years [15].

Complications of endovascular stent graft include: Endoleaks, stent collapse, stent migration, pseudoaneurysm formation, dissection, aortic perforation, kinking, thrombosis, and coverage of branch vessels [15,16]. Undersizing of the endograft is associated with an increased risk for endoleak or stent migration [24]. A certain degree of oversizing has been shown to be beneficial by providing improved fixation and sealing, however, excessive oversizing can contribute to endograft infolding or dilatation with subsequent device migration [24]. Generally, it is recommended that the range of oversizing be 10-20% of the preoperative aortic diameter at the aneurysm neck [24]. Some authors have suggested the use of ECG-gated CT imaging to measure the neck of the aortic aneurysm as the size of the aorta varies with systole versus diastole [24].

1- Endoleak- Endoleak  is the most common complication of stent graft repair. An endoleak is defined as blood flow external to the stent-graft and inside the aneurysm sac [13]. Long-term surveillance of patients following stent graft repair of AAA is required as endoleaks can be both and early and late complication of the procedure [14]. Leak can occur in up to 45% of patients (8% to 45% [7,29]; 15-52% of abdominal aortic aneurysms [12,14]; and up to 29% of thoracic aortic aneurysms [16]). Endoleaks are more consistently identified by multiphasic helical CT than conventional angiography [5,6]. This is because endoleaks have variable flow rates and are often detected at variable times following contrast administration [13]. Typically for the CT evaluation of endoleak, non-contrast, arterial phase, and late-phase images are obtained. Endoleaks seen only on delayed phase images may be more likely to close spontaneously [14].

MR imaging may be superior to CT for the detection of endoleak [11]- however, there are certain limitations to MR. Patients with stainless steel stent grafts should not undergo MR imaging because of the risk of migration or deformation of the graft by the strong magnetic field and extensive artifact associated with this type of stent [13]. Elgiloy stents can also obscure the vessel lumen [13]. Stents composed of nitinol are generally more suited to MR imaging [13].

There are 5 types of endoleaks [7]:

Type 1: The leak occurs at the graft insertion sites (ends of the graft) due to an inadequate seal between the stent graft and the aortic wall (i.e.- there is a separation between the stent graft and the native arterial wall [20]). The can be further classified as type Ia (proximal end of the graft) or type Ib (distal) [13]. These leaks result in elevated sac pressure and a continued risk for rupture (1% per year) [32,34]. Type I endoleaks are the most common to occur after endovascular repair of thoracic aortic aneurysms (they account for 40% of all endoleaks involving the thoracic aorta) [13,16]. Patients with severe angulation at the neck of the aneurysm are at an increased risk to develop proximal perigraft endoleaks [14,34]. These leaks usually appear as broad-based collections directly adjacent to the prosthesis [12]. Large circumferential perigraft collections are indicative of dislocation of the stent-graft or insufficient length a tube endoprothesis [12]. Type I endoleaks are repaired immediately following diagnosis by securing the graft attachment sites with angioplasty balloons, extending the stent coverage with additional stents, or stent graft extensions [13,16,17].

Type 2: The leak occurs when there is retrograde inflow into the aortic sac via a patent branch vessel and it is the most common type of endoleak (observed in 17-23% of patients, up to 30%) [10,12,14,25,31,36,37]. Type II endoleaks can also impart systemic or near systemic pressure within the excluded zone of the aneurysm due to the retrograde flow via the branch vessel and result in continued aneurysm sac expansion [32,35,40]. In type IIA endoleaks (simple endoleak), there is a single feeding branch vessel, while two or more feeding branch vessels indicate a Type IIB endoleak (complex endoleak) [16,31,36]. An endoleak detected within 90 days after EVAR is defined as an early endoleak, and one detected after 90 days is defined as a late endoleak [36]. A transient endoleak will resolve spontaneously within 6 months, and the endoleak is considered persistent if it lasts more than 6 months [40].

For abdominal aortic aneurysms, typical sources include the inferior mesenteric artery and the lumbar arteries [13,14,36], other potential sources include the median sacral artery or even accessory renal arteries [36]. For thoracic aneurysms, feeding vessels include bronchial and intercostal arteries, a patent ductus arteriosus, and the subclavian arteries [16]. For abdominal aortic aneuysms- ventral collections without direct connection to the endoprosthesis are supplied by the inferior mesenteric artery (persistent inflow from the IMA is responsible for 45-85% of AAA endoleaks [31]), dorsolateral collections are supplied by the lumbar or median sacral artery [13]. Retrograde endoleaks are unavoidable with current endovascular techniques [8]. The risk for type 2 endoleak is increased with increasing patent side branch vessels [7,31]. Other risk factors for a persistent endoleak include early appearance of the endoleak on the final operative angiogram (within 6 seconds) and high attenuation of the leak on the first post operative CT scan [40]. For abdominal endografts, the diameter of the IMA does not seem to necessarily be associated with an increased risk for endoleak [31].

The clinical importance and management of Type 2 endoleaks is not clear. Type II endoleaks (particularly small leaks- less than 15 mm) that have a stable or decreasing aneurysm sac size can be treated conservatively and followed with serial CT evaluation as they have a high rate of spontaneous resolution and a low risk of rupture (more than half of type II endoleaks will spontaneously resolve within the first 6 months) [10,12,13,14]. However, this type of leak (even small leaks) is often associated with failure of the aneurysm to decrease in size and it may actually increase due to persistent pressurization of the aneurysm sac [31]. Treatment should be performed if the feeding vessel is large, if there is significant contrast enhancement in the excluded aortic lumen, if the sac diameter grows by more than 1 cm over 1 year, or the excluded aortic lumen demonstrates progressive enlargement [16,29,45]. An endoleak cavity diameter measuring more than 1.42 cm has been suggestive of a greater likelihood for eventual surgical intervention [25]. Other factors associated with a higher risk for aneurysm sac enlargement include a higher number of feeding vessels (complex endoleak) and if the largest feeding vessel was 4 mm or more in diameter (a 91% risk for aneurysm sac enlargement) [36].

Treatment involves embolization of the culprit vessel near its communication with the aneurysm sac to block the retrograde flow of blood [13]. Unfortunately, coil embolization for IMA related endoleaks can fail in up to 80% of cases [31]. Preoperative embolization of the IMA has been introduced to reduce the risk of type II endoleak, but this is time consuming and expensive and places the patient at additional risk [31].

Type 3 leaks occur due to a structural failure of the stent graft including component disconnection, fabric tears/fracture of the metallic skeleton, and disintegration of graft material. Junctional dehiscence results from a defect between two adjacent or overlapping stents and often occurs early following technically complex stent procedures [16]. Type III endoleaks are currently fairly unusual, but may become more common during long-term followup [13]. Type 3 endoleaks are treated immediately with a stent graft extension because they represent a direct communication systemic arterial blood with the aneurysm sac [13,17].

Type 4 leaks occur due to transgraft flow due to graft wall porosity. This is an exceedingly rare endoleak and are self limited [12,13]. It is identified at the time of implantation as a blush on the post implant angiogram when patients are fully anticoagulated [13]. These endoleaks require no specific intervention other than normalization of the coagulation profile [13].

Type 5 or "endotension"- no leak is visible radiographically, but the aneurysm continues to grow [5]. This may be because the blood flow is undetectable by standard imaging, because of pressure transmission through the fabric, or serous ultrafiltrate across the endograft fabric [45]. Scanning the graft in both the arterial and delayed phases is important to make sure that a subtle leak is not missed. Type 5 endoleaks carry a long-term risk for sac rupture [35]. Repair is indicated if the sac diameter increases by more than 1 cm [45].

About 18% of leaks will only be seen on arterial phase images, while about 3% will only be seen on delayed exams. Note that gas may be seen in the aneurysm sac immediately following stent deployment and should not be considered pathologic when scans are performed at that time. For thoracic aortic endografts, a "bird-beak" configuration (defined as an incomplete apposition of the proximal endograft with a wedge-shaped gap between the device and the aortic wall) is associated with a markedly increased risk for Type Ia or IIa endoleak [21].

2- Graft thrombosis: Partial, peripheral, or semicirular thrombosis is seen in 3-19% of stents [10]. Graft occlusion is rare [6].

3- Graft kinking: Kinking occurs when large aneurysms shrink/shorten after stent grafting [13]. The kinking may not be detected on transaxial images, but can be demonstrated on MIP or MPR images. Kinking is in turn associated with graft migration, thrombosis, and endoleak [13].

4- Graft migration: Occurs due to poor attachment of the stent to the aortic wall [16]. Migration of 5 mm or more is considered substantial and stent graft position with respect to a constant anatomic landmark should be recorded during followup imaging [13].

5- Shower or peripheral embolism: Shower embolism occurs in 4-17% of cases and is generally fatal [6]. Peripheral embolism can lead to organ or limb ischemia [10].

6- Colonic necrosis (abdominal aortic stent grafting)

7- Aortic dissection (2%) [10].

8- Vascular perforation

9- Pseudoaneurysm associated with graft infection: In the abdominal aorta, more than 5 mm of perigraft soft tissue between the aneurysm wall and the graft is abnormal and may suggest infection [22].

10- Stent collapse- predisposing factors are poor stent attachment and oversizing of the stent [16]. On CT there is narrowing of the endolumenal stent diameter and displacement of the stent from the vessel wall [16]. This complication requires urgent surgical intervention when there is significant narrowing of the aortic lumen [16].

11- Suture breaks and metal-ring fractures: AneuRx stent grafts were the most widely deployed stent graft up until 2012 when it was replaced by a newer design [34]. The graft was constructed from self-expanding nickel-titanium (nitinol) and woven polyester graft material [34]. The diamond shaped nitinol segments are laser cut from a single piece of nitinol tubing [34]. As a result the grafts are predisposed to two types of mechanical failure- fracture of the metallic stent rings and breakage of the polyester sutures that connect adjacent rings [34]. Suture breaks and metal-ring fractures are associated with type I (due to graft migration) and III (due to component separation) endoleaks [34]. Major suture breaks and metal-ring fractures occur most frequently at the junction between the main body and the limbs of the bifurcated graft [34].

12- Post endograft repair aortic rupture: The rate of post endograft repair aortic rupture ranges from 0.4 % to 1.1% with the time to rupture ranging from 3 days to 85 months [35]. Risk factors for post endograft instability include graft migration more than 5mm, graft kinking or fracture, and persistent endoleaks [35].

13- Renal infarct: Renal infarction can be seen in up to 26% of patients following stent graft repair [42]. Often (up to 39% of cases) this is the result of intentional exlcusion of a small accessory renal artery [42]. However, up to 61% can be related to embolic phenomena [42]. Other causes include a flow limiting renal artery dissection [42].

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