Imaging Aortic Aneurysm and Dissection

This article discusses the radiographic imaging of aortic aneurysms and aortic dissection. The most common modalities include Ultrasound, CT, and Interventional Radiology. The article also includes pre and post endograph stent imaging.

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Aortic Aneurysm and Dissection

Written by Nicholas Joseph Jr. RT(R)(CT) B.S. M.S


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Anatomy of the Aorta

Pathophysiology of AAA

Summary Points




Aortic aneurysm is defined as a local dilatation of the aorta that exceeds its normal diameter by greater than fifty-percent. Aneurysm of the aorta can occur anywhere along its length, in the thoracic, abdomen, or along its bifurcation into the common iliac arteries. Aortic aneurysms occur most commonly in the abdomen and are called abdominal aortic aneurysm (AAA). About 90% of abdominal aneurysms occur below the renal arteries (infrarenal). Abdominal aortic aneurysm occurs most commonly in Caucasian males between the age of 65 and 75 years, and is especially higher in smokers. Most aneurysms are asymptomatic, therefore, are discovered on radiographs taken for other reasons. Nonetheless, aortic aneurysm is the 15th leading cause of death in the United States. Symptoms of an aneurysm include noncardiac chest pain, flank pain, abdominal pain, back pain, groin pain, or a pulsating abdominal mass. The infrarenal aorta is about 2cm in diameter, so a dilatation greater than 3 cm is considered to be an aneurysm. An aneurysm that is less than 5 cm is closely watched with routine periodic computed tomography (CT). Treatment does not usually occur until the dilatation is greater than 5 cm or becomes symptomatic. The greatest complication of aneurysm is the risk of rupture. The mortality rate for AAA rupture is about 90% so large or symptomatic AAA’s are treated. The operative mortality is also high (reported to be nearly 40%). Because clinical symptoms are often vague, imaging for aortic aneurysm and dissection is a fairly common study in radiology. This article investigates radiographic imaging of the aorta for AAA including pre and post endograph studies, 3D CT aorta imaging, maximum intensity projection (MIP), aorta ultrasound, magnetic resonance imaging (MRI), and interventional angiography of the aorta.

Cross-sectional anatomy of the aorta

To fully understand what an aortic aneurysm is and how it is treated one must have a basic knowledge of the histology of the aorta and elastic arteries. The function of the arterial system is to distribute nutrient and oxygen rich blood from the heart to the capillary beds of the body. It is the heart that provides the pumping action in the form of a pulsatile wave to the most distal parts of the arterial tree. Basically, with each contraction of the ventricles blood is propelled into the proximal aorta causing expansion of the arterial wall to receive the blood volume. Subsequently, there is recoil of the aorta initiate in its wall propagating the blood volume along its course. This action maintains blood pressure continually with each ejection fraction from the ventricles. Expansion and recoil of the aorta is a function of elastic tissue within its wall and throughout the arterial system. Elastic tissue should not be confused with smooth muscle within its wall, which has the function of varying the diameter of the vessel, thus amount of blood flow to tissues.

To accomplish its functions arteries have varying amounts of elastic fibers and smooth muscle in their walls. The basic structure of an artery does conform to common characteristics. However, there are three distinct types of arteries in the arterial system: elastic arteries, muscular arteries, and arterioles. Elastic arteries are mainly distribution vessels. The aorta is the major elastic artery of the body. Others include the subclavian, common carotid, innominate, and pulmonary arteries. Muscular arteries branch from elastic arteries, for examples the radial and ulnar arteries. The terminal branches of the arterial tree are the arterioles, which supply capillary beds. The main difference in the three types is the amount of elastic and smooth muscle in them. Elastic arteries have more elastic fibers, which gradually decreases distally along muscular arteries and smooth muscle increases.

These two light micrographs show both a vein (left) and a muscular artery (right). Notice that the main difference in these two structures is the thickness of their smooth muscle layers, or tunica media layer. The yellow arrow (left) points to the circular muscle of the vein and a blue arrow (right) show the same muscle layer in an artery, which is thicker. The tunica media of the aorta, which is an elastic artery contains relatively little smooth muscle and lots of elastin and collagen fibers.

The structure of the aorta may appear quite simple under a light microscope; however, its structure and physiology is very complex. Light microscopy reveals three layers of the aortic wall called tunics: tunica adventitia, tunica media, and tunica intima. The outermost layer is the tunica adventitia, which is composed of connective tissue that holds the vessel to other structures reducing free movement. Small blood vessels, called the vasa vasorum, supply oxygen and nutrient needs of the aorta can also be seen permeating the adventitia. The middle layer called the tunica media is the thickest and contains large amounts of elastic proteins. Light microscopy of the aorta shows a broad thick tunica media composed of fenestrated sheets of elastin separated by collagen and scattered smooth muscle cells. The strongly elastic architecture of the tunica media is responsible for the elastic recoil properties of the aorta. The tunica intima is the innermost layer of the aorta and forms the lining of the lumen over which blood flows.

The layers of the aorta are seen on this light micrograph. The tunica adventitia (A) is the outermost layer of the aorta composed of loose connective tissue. The broad thick tunica media (M) is the middle layer of the aorta wall consisting of elastin and collagen fibers. The tunica intima (I) is seen as a thin layer that lines the lumen. A white arrow points to the dense organized structure of the tunica intima. The intima is composed of a single layer of endothelial cells supported on a thin layer of connective tissue. The intimal connective tissue also contains myointimal cells that accumulate lipids with aging producing atherosclerosis.
These two high powered micrographs of the tunica media show dense fibers of collagen and elastin its structure. The left micrograph shows the typical structure with standard H & E staining. Using a van Gieson staining technique we can clearly see the elastin (E) and collagen (C) fibers, right image. These collagen and elastic fibers are fenestrated with small amounts of smooth muscle (yellow). It is the elastin and collagen that gives the aorta its recoil properties. Ironically, it is also this elastic property that is compromised in aortic aneurismal disease. Loss of elastin causes dilation of the aorta, whereas loss of collagen is the main cause of rupture

Gross Anatomy of the Aorta


The aorta is a systemic vessel whose function is to deliver oxygenated blood from the left heart to the body’s tissues. For descriptive purposes the aorta is described as the thoracic aorta (portion above the diaphragm in the thoracic cavity), and the abdominal aorta (that portion below the diaphragm in the abdominal cavity). There are many primary and secondary arterial branches from the thoracic aorta including the brachiocephalic artery, common carotid arteries, subclavian and vertebral arteries, coronary arteries, bronchial arteries, and intercostal arteries. The thoracic artery is described along its course as having three sections: ascending, arch, and descending aorta.

The ascending aorta commences at the aortic orifice of the left ventricle. The ascending portion of the aorta is about 5 cm in length before arching backwards over the pulmonary vessels to descend in the thorax just to the left of the spine as the descending thoracic aorta. The normal diameter of the ascending aorta is about 3 cm. At its origin the aortic valve has three cusps and three small dilatations called the aortic sinuses. The only branches from the ascending aorta are the right and left coronary arteries. The coronary arteries give off multiple branches along their course to supply the heart with oxygenated blood.

These two coronal CT images demonstrate the origin of the ascending aorta at the left ventricle. The aortic annulus (yellow arrow) is seen on the left CT image and the ascending aorta (red arrow) is seen on the right CT image. The proximal aorta is divided into ascending, arch, and descending portions for descriptive purposes.
These two 3D volume rendered CT images demonstrate the proximal aorta and coronary arteries that arise from it. At its origin the aortic valve has three cusps and three small dilatations called aortic sinuses (yellow arrow). The only branches from the ascending aorta are the right and left coronary arteries (red arrows) are seen on the right CT image. The dotted red line marks the beginning of the ascending aorta, which has three branches.

The arch of the aorta is so named because it courses over the pulmonary trunk and vessels. The aortic arch give off three branches: the innominate artery, left common carotid artery, and left subclavian artery. The innominate artery (or brachiocephalic trunk) supplies blood to the right upper extremity, the head and neck, and thorax. It is the first branch of the aortic arch where it emerges then shortly divides into the right common carotid artery that supplies the head and neck, and right subclavian artery that supplies the head and right upper extremity. There is no brachiocephalic artery for the left side of the body since the left common carotid, and the left subclavian arteries come directly off the aortic arch. The left common carotid artery also supplies the head and neck, and the left subclavian artery supplies the head and neck, thorax, and left upper extremity. The usual branches of the subclavian arteries are the vertebral artery, internal thoracic artery, thyrocervical trunk, costocervical trunk, and dorsal scapular artery. It then becomes the axillary artery that supplies the upper extremity giving off numerous branches such as the brachial, ulnar, and radial arteries.

These two 3D volume rendered CT images demonstrate the three branches of the aortic arch. The first branch is the brachiocephalic trunk (yellow arrow), which takes oxygenated blood to the right side of the body, head, and neck. The second branch is the left common carotid artery (red arrow), and the third branch is the left subclavian artery (blue arrow). These branches can also be seen from the superior view on the right image.
These two radiographs demonstrate the entire proximal aorta and structures it arches over in the mediastinum. The sagittal CT image on the right shows the aortic arch (AA) as it curves over mediastinal structures such as the pulmonary trunk (blue arrow) and primary bronchi. The branches of the aortic arch are clearly identifiable on the proximal aorta angiograph on the left. The brachiocephalic trunk is seen at the yellow arrow and the red arrow identifies the left subclavian artery. The left common carotid artery (blue arrow) is also seen arising from the aortic arch. Right and left coronary arteries (orange arrows) are seen arising from the ascending aorta on the angiogram on the left.

Within the thorax the aorta descends giving off numerous branches before entering the abdomen through the aortic hiatus. The branches from the thoracic aorta are small and difficult to see with conventional CT imaging; however, they can be seen with direct catheterization angiography. Branches of the thoracic aorta include: bronchial arteries,mediastinal arteries, esophageal arteries, pericardial arteries, superior phrenic artery, and numerous posterior intercostal and subcostal arteries. The posterior intercostal arteries are given off along the posterior length of the thoracic aorta and supply the intercostal muscles between the ribs.

These two aortagrams radiographs show some of branches from the thoracic aorta including posterior intercostal branches (yellow arrows). The thoracic aorta gives off numerous branches to thoracic structures such as the esophagus, intercostal muscles, and diaphragm. Bronchial arteries that supply the lungs with oxygen rich blood also arise from the thoracic aorta.

The abdominal aorta begins as it enters the abdomen through the diaphragm at the T12 level and bifurcates at L4 into the right and left common iliac arteries. The abdominal aorta is the major blood supplier to the abdomen and gives rise to arteries in three vascular planes: the anterior midline plane, lateral plane, and posterolateral planes. Aortic aneurysm or dissection can affect not just the aorta but branches from the aorta that supply abdominal structures. Therefore, it is important for the radiographer to have a general understanding of these branches and the structures they supply. Aneurysms do occur in branches from the aorta, for example, in the common iliac arteries and even in the renal arteries and others. Because small nonsymptomatic aneurysms are followed radiographically to early detect changes in diameter, it is important to have a working knowledge of vessels branching from the aorta.


The major arteries to the gut rise as unpaired single vessels from the anterior midline of the aorta. These branches are the celiac, superior mesenteric (SMA), and inferior mesenteric arteries (IMA). The celiac artery, also known as the celiac trunk, gives rise to arteries that supply the liver, stomach, esophagus, spleen, duodenum, and pancreas. The distributions of the celiac artery are unique in that there are no other blood channels that can supply oxygenated blood if it is surgically ligated. Furthermore, the celiac artery does not have a counterpart celiac vein that returns deoxygenated blood to the heart. Blood is returned via the portal venous system. An example of this is the splenic and hepatic veins that return blood for detoxification to the liver and then to the inferior vena cava (IVC). Celiac artery aneurysms are extremely rare; in fact less than 200 have ever been reported worldwide in literature. However, rupture rate when it occurs is reported to be nearly 90%; advances in diagnostic imaging and early surgical intervention have reduced the rupture rate to 7% in recent years. Early recognition and intervention is directly related to radiological imaging of the abdomen for other reasons.


The superior mesenteric artery also arises from the anterior plane of the aorta just below the celiac trunk at about L1 in the adult. It supplies the upper digestive tract with the exception of the stomach, which is supplied by the celiac artery. It provides oxygenated blood to the lower part of the duodenum through two-thirds of the transverse colon and part of the pancreas. Branches of the superior mesenteric artery include the inferior pancreaticoduodenal artery, middle colic artery, right colic artery, intestinal arteries (to ileum and jejunum), and ileocolic artery. Occlusion of the SMA causes intestinal ischemia with up to 80% of cases results in death. Aneurysms of the SMA or its branches are also uncommon, but are often lethal when they occur.

These two sagittal CT images show the celiac artery (yellow arrow) and superior mesenteric artery (red arrow) at their origins from the anterior plane of the abdominal aorta. There are three arteries that originate from the aorta in the anterior plane: the celiac artery, SMA, and IMA. These three vessels supply the gut from the stomach to the rectum as well as the liver, gallbladder, pancreas, spleen, and esophagus.
This volume rendered CT image shows the aorta and some of its major abdominal branches. The abdominal aorta originates from just below the diaphragm and bifurcates at the common iliac arteries. The celiac trunk (yellow arrow) is seen just above the superior mesenteric artery (white arrow). The celiac artery supplies structures developed from the foregut and the superior mesenteric artery supplies midgut structures. This image was obtain in the late arterial phase as the renal outline is seen and the left renal vein is seen as the SMA passes over it.
These two selective superior mesenteric arteriogram radiographs demonstrate its distribution to the intestines. The radiograph on the right demonstrates the SMA using digital subtraction techniques to remove bone densities in the field of view. The SMA distributes oxygenated blood to the duodenum, pancreas, and portions of the small and large intestines. Aneurysms involving the SMA are rare; however, they are most often fatal when discovered. There are several modalities in radiology that can image the aorta including CT, MRI, and ultrasound.

The inferior mesenteric artery also supplies part of the large intestine beginning at the left colic (splenic) flexure and distally to include the rectum. There are anastomoses between the superior and inferior mesenteric arteries forming the marginal artery so that the entire gut is supplied by these two branches. The IMA forms arcades that supply the entire lower gut. Branches of the superior and inferior mesenteric vessels permeate the bowel as they course within the mesentery to which the bowel is attached to the posterior abdominal wall.

These two radiographs are selections from an inferior mesenteric arteriogram showing its distribution to the left colic (splenic) flexure and distally to include the rectum. Arcades formed by the inferior mesenteric artery and the marginal artery that lines the border with the bowel is also seen. Branches that course within the mesentery to remote regions of the bowel are also seen. Perfusion of the mucosa is seen as radiopaque contrast media reach smaller distal vessels.

Pathophysiology of AAA

Aortic aneurysm is a long progressive disease that spans many years before becoming problematic. It affects 5-9% of the population over age 65 and is seen most commonly in smokers, those with coronary artery disease, peripheral occlusive atherosclerotic disease, and pulmonary emphysema. There are other poorly understood factors that may also interplay, such as lack of exercise, genetic predisposition, history of aortic inflammatory change, male gender, aging, and a few others. Smoking is the risk factor most strongly associated with abdominal aortic aneurysms, followed by age, hypertension, hyperlipidemia, and atherosclerosis. The concern with aortic aneurysm is the associated risk from rupture, and that aortic aneurysms are generally asymptomatic. What makes survival of AAA high is that risk of rupture is related to increases in growth of the dilation. A degraded segment of the aorta that is likely to rupture can be detected with imaging studies, but because AAA is generally asymptomatic it may not be discovered before rupture. Therefore, it is important that research differentiates the causes of aortic degradation that could lead to early detection and advance treatments for aortic aneurysm when it is small. Our current understanding of the pathophysiology of AAA is showing promise of potential early treatments. This discussion focuses on what is currently know about aortic aneurysms and dissections, how to properly image the aorta, and treatments for aneurysms when discovered.

While much is known, a significant amount of new knowledge about aortic aneurysm is needed in order to bridge a rather large gap in promising therapies and lack of current efficacy in treating aortic aneurysmal disease. The current standard for diagnosis of aortic aneurysm disease and treatment is centered on external measurement of its diameter. This is an incomplete strategy that only treats symptomatic aortic aneurysms regardless of size, and large ones symptomatic or asymptomatic that is greater than 6 cm. The problem is that the risks of treating small aneurysms far outweigh the benefit and are therefore not treated. Neither is there treatment to reverse progression of the disease, clearly, at the early stages when small is the most practical approach. We know that the pathology of segmental abdominal aortic degradation involves a complex process in which the connective tissue of the aorta undergoes destructive remodeling processes. As an aneurysm enlarges attention is given to its risk of rupture; however, more emphasis on fundamental molecular processes such as mural inflammation and remodeling of the aorta is needed. Furthermore, studies to date that provide direct insight into human AAA are from human aortic tissue samples taken from surgical aortic repair. While this has provided great understanding about the pathogenesis of the disease, most of this data on human specimens is related to “end stage” disease. Information about the progression of the disease in terms of its beginning and progression to small currently non treated aneurysms is lacking or is dependent on animal models. While we will discuss some conclusions of these models, keep in mind that different models have their strengths and weaknesses, but none have reproduced all aspects of what is known about human aortic aneurysms.

The red lines on these two CT 3D surface views of the infrarenal aorta demonstrate a normal diameter aorta (left) and a dilated aneurysm (right). Treatment of aortic aneurysm is currently based on its size; however, research is ongoing to understand the pathophysiology of aneurysms so that treatment of small aneurysms can be made available. Notice in the comparison CT images the red lines are the same measurement, which shows the relative increase in size of the aorta at the aneurismal site.

It appears that contributing factors to aortic wall weakening are many including inflammation, but lack of exercise, and genetics also appear to play a role. As we have discussed, the strength of the aortic wall lies in the elastin and collagen structure of its extracellular matrix. Consequently, conditions that degrade these structural proteins weaken the aortic wall and allow aneurysms to develop. Regardless of the cause AAA is a disease in which segmental erosion of elastic properties of the aorta and remodeling of the elastic components of the aortic wall do occur. Researchers agree on at least four factors that have been identified in experimental models: 1) chronic inflammation within the outer aortic wall, 2) increase proteases that degrade the wall matrix, 3) destruction of the wall matrix proteins elastin and collagen, 4) and depletion of smooth muscle cells. These factors constitute the cellular basis for aortic aneurysm and it inability to undergo natural self-repair. The initial cause of aortic aneurysm is not known; however, recruitment of inflammatory cells into the tunica media and tunica adventitia appears to be a crucial early step. Furthermore, degradation of the matrix wall releases chemotaxis agents that attract inflammatory cells further amplifying the inflammatory effect. It is hoped that being able to provide medical intervention at this stage may prevent aneurysm growth. However, detection of early stage localized aortic inflammatory changes is again problematic as it is asymptomatic. Therefore, some researchers are seeking a blood factor that can indicate early aortic inflammation, much like the PSA (prostate specific antigen) test can indicate prostate enlargement.

There is histological evidence of inflammatory infiltration into the aortic aneurysmal wall, and such inflammation has been implicated in the degradation of the extracellular matrix. Matrix metalloproteinases (MMPs) are enzymes that are produced by smooth muscle and inflammatory cells. They were first discovered over three decades ago by Goross and Lapiere in anuran tadpole and have been extensively studied in humans. For example, over 20 types have been reported and more are being currently classified. Their role in female reproductive tissues at puberty and throughout menopause is a well-documented area of human study. Several of these proteinases participate in abdominal aortic aneurysm formation. Indeed, certain of the matrix metalloproteinases can degrade elastin and collagen. In addition, tissue inhibitor metalloproteinase (TIMP) an inhibitor of collagenase has been identified. The levels of some matrix metalloproteinases are significantly elevated in the walls of aneurysms compared with controls. In addition, several other proteinases, including plasminogen activators, serine elastases, and cathepsins, may also contribute to the formation of aneurysms.

Animal experiments have been able to reproduce an increase in proteases that degrade the matrix wall. Pancreatic proteolytic enzymes injected into the aortic wall will produce local aortic aneurysm. A similar response seen in naturally occurring AAA is seen in a matter of days using protease infusion techniques. This model shows that pathogenesis of aortic aneurysm may involve aortic wall infusion by mononuclear macrophages, increased elastolytic matrix metalloproteineases, and destruction of the medial elastic lamellae. This animal model of aortic aneurysm demonstrates the pathogenesis of the disease and allow for experimental pharmaceutical trials to reduce the inflammatory response. While this is a good model for understanding aortic aneurysm there is a lack of efficacious targeted pharmaceuticals to treat aortic inflammatory response.

This sagittal CT image shows an abdominal aortic aneurysm. The aneurismal sac (yellow arrow) encloses a chronic inflammatory process that can be duplicated in experimental animal models. In the early stages of the disease there is an infiltration of mononuclear macrophages, MMPs, and destruction of the medial elastic lamellae that results in dilatation of the aorta.

The rennin-angiotensin system seems to also play a role in the development of abdominal aortic aneurysms. Well documented experiments with mice models show that angiotension II causes suprarenal aortic aneurysms. The exact human implications to mice research have not been elucidated because it is impractical to measure angiotension II concentrations in human blood. This is because angiotensin II has a half-life of in the circulation of about 30 seconds, and in human tissue an average of 15-30 minutes. Angiotension polypeptides also have a short half-life in human blood although rennin-angiotension polypeptides have been detected in human aneurismal tissue. Furthermore, the enzyme chymase, which can convert angiotension I to angiotension II, is found in aneurismal tissue and in mast cells taken from the aortic adventitia. The assumption is that an imbalance in the rennin-angiotension system may contribute to pathological AAA growth, or it may be part of a larger pathway for developing aneurysms.

Inflammation is a key component in the initiation, development, and growth of aneurysms. With that said, we know that inflammation is a complex process in which the body identifies an assault such as injury or infection and initiates an effective response to contain or repair it. What naturally follows is a series of responses designed to repair and promote healing so that ultimately damage is arrested and the assault is returned to homeostasis. There are many examples in human pathology where inflammation causes damage to the host, for example rheumatoid arthritis. It has been shown that chronic inflammatory changes do play a role in the pathology of aortic aneurysms. The absolute etiology of aortic aneurysms is not known, but it is clear that inflammation plays a pivotal role in the process. Understanding the role of inflammation may help provide treatment for small aneurysms before they grow to become problematic. Current literature documents a significant amount of research into the role of substances called matrix metalloproteinases (MMPs) found in the aortic wall contributing to degradation of the extracellular matrix.

You may not have heard of matrix metalloproteinases; however, researchers have been studying them since their discovery in tadpoles in the early 1940,s. The early position was that they only function in degrading extracellular matrix, a negative role. It has now been shown that MMPs also function in regulating the inflammatory response. Their role extends into wound healing, cancer metastasis, and they have been implicated in some types of arthritis. Our classical understanding of MMPs is that the only human disease they are known to cause is a type of vanishing bone chronic arthritic disease. So with all the new information about the role of MMPs there suggests more research is needed to determine the role of MMPs as causative or promoter of aortic aneurysms.

Some aortic aneurysms have an intraluminal thrombus which has been shown that the thickness of the thrombus increases the risk of aneurysm expansion and rupture. Intraluminal thrombus formation is also a source of proteolytic activity that degrades the aortic wall weakening it. Thrombus formation is an importance finding since thrombus is found in most large diameter aortic aneurysms needing repair. Follow up studies on patients with known abdominal aortic aneurysms indicate that the size of thrombus growth is a more reliable indicator of rupture risk than is size of the aneurysm itself. In the absence of intraluminal thrombus, most aneurysms do not rupture. When computed tomography demonstrates leakage of contrast media into the thrombus a diagnosis of aortic rupture can be made. For this reason it is desired by researchers to understand the role of developing thrombus in aortic aneurysm and its relationship to rupture. There are distinct dynamic processes occurring in the wall of the aorta and in the thrombus. Comparing the aorta wall segment covered by thrombus to the wall segment not covered by thrombus reveals significantly more elastin degradation and inflammation in the aneurysm wall covered by thrombus. Furthermore, mediators of proteolytic activity and inflammation are more abundant in the thrombus and its interface with the aortic wall, which is where rupture is likely to occur.

These two axial CT images demonstrate the aorta filled with intravenous contrast agent. The image on the left shows a small aneurysm of the aorta without intraluminal thrombus. On the right, a large aneurysm having a sizable intraluminal thrombus is seen. A yellow arrow points to the aortic wall covered by thrombus, which is where increased inflammation is seen and degradation of matrix elastin and collagen is seen in histological sections.
In some patients able to undergo CT scan the “crescent” sign has been demonstrated, which shows leakage of contrast into the thrombus (yellow arrows). Theoretically, blood leakage into the thrombus from the thrombus covered wall of the aneurysm is a prerequisite for rupture. Current research deciphering the relationship between thrombus formation and its effect on the aneurysm wall is making progress. Proteolytic activity in the thrombus promotes degradation of the aortic wall while factors causing medial degradation of the aortic wall weaken it. Combined, these conditions cause the aortic aneurysm to rupture.

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