Abdominal aortic aneurysm

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]

Synonyms and keywords: Abdominal aneurysm, aortic; aortic aneurysm, abdominal; AAA; triple A

An abdominal aortic aneurysm is a localized dilatation of the abdominal aorta, that exceeds the normal diameter of the abdominal aorta by more than 50%. The normal diameter of an aorta depends on the patient’s age, sex, height, weight, race, body surface area, and baseline blood pressure. On average, the normal diameter of the infrarenal aorta is 2 cm, and therefore a true AAA measures 3.0 cm or more. Aortic ectasia is a mild generalized dilatation (<50% of the normal diameter of ≤ 2.9 cm) that is due to age-related degenerative changes in the vessel walls.

The etymology of the word aneurysm comes from the Greek word for “dilatation”. Abdominal aortic aneurysm as a medical condition has been recognized since ancient times, but was not been successfully treated until the early part of the 20th century. In 1923, Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the first successful aortic ligation on a human. In 1949, Albert Einstein was operated on by Rudolf Nissen by wrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. In 1951, Charles Dubost performed the first AAA repair using a homograft. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (nylon). In 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy. In 1980, Parodi et al described an endovascular repair.

The normal diameter of one’s aorta depends on the patient’s age, sex, height, weight, race, body surface area, and baseline blood pressure. On average, the normal diameter of the infrarenal aorta (where abdominal aortic aneurysms are located) is 2 cm. Therefore an abdominal aortic aneurysm is defined as a dilation of 3.0 cm or more.

An abdominal aortic aneurysm is to be distinguished from aortic ectasia which is defined as a mild generalized dilatation (<50% of the normal diameter of ≤ 2.9 cm) that is due to age-related degenerative changes in vessel wall.

The aorta below the renal arteries, also known as the infrarenal aorta, is the location of 90% of abdominal aortic aneurysms. Other possible locations are suprarenal and pararenal. The aneurysm can extend to include one or both of the iliac arteries.

Aneurysms are usually classified by their shape:

Most common type seen in the infrarenal aorta and are diffuse and circumferential.

Involve only a portion of the circumference, with a characteristic outpouching of the vessel wall.

The underlying pathophysiology of abdominal aortic aneurysm involves genetic influences, smoking, hypertension, hemodynamic influences and underlying atherosclerosis. In rare instances infection, arteritis, and connective tissue disorders may play a role.

The most common cause of an AAA is atherosclerosis.

An abdominal aortic aneurysm should be differentiated from other causes of abdominal pain such as acute cholecystitis, gastrointestinal bleeding, perforated peptic ulcer, ischemic bowel, nephrolithiasis, pyelonephritis, appendicitis, cholelithiasis, large bowel obstruction, small bowel obstruction, pancreatitis, musculoskeletal pain, myocardial infarction, and urinary tract infection.

Abdominal aortic aneurysm is the 13th leading cause of death in the US. Abdominal aortic aneurysms are more common in developed countries. Elderly, caucasian males who are smokers are at higher risk for developing an abdominal aortic aneurysm.

The most significant modifiable risk factor for the development of an abdominal aortic aneurysm is smoking which increases the risk of aneurysm development 8 fold.

Advanced age and family history are the strongest non-modifiable risk factors for the development of an abdominal aortic aneurysm.

Hypercholesterolemia and hypertension are risk factors as well.

Caucasian race is associated with a higher incidence of AAA when compared to non Caucasian race.

An increased rate of expansion of abdominal aortic aneurysm is related to systolic hypertension, wide pulse pressure, and ongoing smoking.

The risk of abdominal aortic aneurysm rupture is proportional to the size and rate of growth of the aneurysm. Abdominal aortic aneurysms greater than 5 cm diameter or those that grow faster than 1 cm per year have a significantly increased risk of rupture and are indications for elective operative repair. Advanced age, female gender, hypertension, active smoking, outpouchings, and mural thrombus are also risk factors for abdominal aortic aneurysm rupture.

Approximately 16% of large abdominal aortic aneurysms (diameter > 5.5 cm) rupture, causing 9,000 AAA-related deaths in the United States per year^[1]. Several studies have shown that screening can drastically reduce the aneurysm rupture rate by 45-49% for men older than 60, and reduce AAA-related mortality by 21-68%. In a landmark study randomizing 67,800 men, (The Multicenter Aneurysm Screening Study) aneurysm-related mortality was 53% lower in the screening group as compared with control patients^[2][3]. The United States Preventive Services Task Force (USPSTF) recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in any man aged 65 to 75 who has ever smoked. The USPSTF makes no recommendation for or against screening for AAA in men aged 65 to 75 who have never smoked. The USPSTF recommends against routine screening for AAA in women.

Abdominal aortic aneurysms expand slowly over time. An aortic aneurysm can progress to a ruptured abdominal aortic aneurysm, which is a medical emergency associated with an extremely high mortality. Serious complications can also occur as a result of an aortic dissection, such as myocardial infarction, shock, stroke, kidney failure, and arterial emboli. A ruptured AAA carries an overall mortality rate approaching 75%, which is much higher than the mortality rate of 2-6% in those patients who underwent elective surgical repair. Approximately 16% of large AAAs (diameter >5.5 cm) rupture, causing 9,000 AAA-related deaths in the United States per year^[1]. Several studies have shown that screening can drastically reduce the aneurysm rupture rate by 45-49% for men older than 60, and reduce AAA-related mortality by 21-68%. The outcome is usually good if an experienced surgeon repairs the aneurysm before it ruptures. Rupture of an abdominal aortic aneurysm is associated with a 60% to 90% mortality before the patient reaches a hospital. It is associated with a 30% to 80% operative mortality among those patients who survive long enough to undergo surgery.

Given that smoking increases the risk of abdominal aortic aneurysm development, a smoking history should be obtained in elderly men. If a male over the age of 65 has a history of smoking, they should undergo ultrasonography to screen for an abdominal aortic aneurysm. Abdominal aortic aneurysms are usually asymptomatic until they expand or rupture. Spontaneous abdominal pain in a patient with a pulsatile epigastric mass or a known AAA may signal rupture into the retroperitoneum or leakage within the aneurysm wall. If a patient does develop symptoms, the risk of rupture is quite high, which is why symptoms are considered an indication for surgery. Pain is the most common symptomatic manifestation of AAA.

Physical examination has a low sensitivity in the detection of small abdominal aortic aneurysms (29-61% for abdominal aortic aneurysms 3.0-3.9 cm in diameter) but has a sensitivity of 76-82% to detect those abdominal aortic aneurysms that are 5.0 cm or larger that may warrant repair. It is easier to detect a pulsatile mass in thin patients and those who do not have tense abdomens. Contrary to popular belief, gentle palpation of abdominal aortic aneurysms is safe, and does not precipitate rupture.

Plain abdominal radiographs are obtained in patients with abdominal complaints before the diagnosis of AAA has been made. It is very difficult to evaluate patients with AAA using plain radiographs, because aortic wall calcification is seen in less than half of the cases with AAA. However, plain radiographs may be helpful when an aneurysmal aorta appears normal on angiogram, due to thrombus within the sac.

Abdominal ultrasound is the standard imaging modality to detect and follow the progression of an abdominal aortic aneurysm. When performed by an expert, it has a sensitivity and specificity close to 100% and 96%, respectively. Abdominal ultrasound can also detect mural thrombus, iliac artery aneurysms, and free peritoneal blood. Patients should fast before examination to optimize image quality.

Although CT scanning provides detailed anatomic information and is valuable in planning abdominal aortic aneurysm repair, it is not used as a screening tool given the potential nephrotoxicity associated with the dye load, the cost, and the exposure to radiation.

MRI might be a better soft tissue visualizer than ultrasonography and CT, but its limitations limit its usage as a screening tool and as a diagnostic tool during emergencies like ruptured AAA. However its advantages makes it a good alternative in AAA patients with poor renal function and in elective preoperative evaluation of unruptured AAA^[4].

Angiography is an alternative less often used imaging method for visualization of an abdominal aortic aneurysm. Angiography is helpful in determining anatomy of aorta precisely. It can be used preoperatively in case of suspected suprarenal or thoracic aortic aneurysm, femoral or popliteal aneurysm, renal artery stenosis, unexplained renal insufficiency, occlusive ilio-femoral disease, or visceral ischemia.

Risk factor modification, such as smoking cessation, management of hypertension, and lipid lowering are essential in reducing the risk of development and the rate of progression of abdominal aortic aneurysms.

Indications for operative repair of an abdominal aortic aneurysm include the presence of symptoms such as back pain, the presence of a rupture or contained rupture, an abdominal aortic aneurysm diameter greater than 5.5 cm, a rate of expansion of greater than 1 cm in one year, and an inflammatory or infectious etiology. Open surgical repair is favored in young patients as an elective procedure, the presence of an expanding aneurysm, symptomatic aneurysm, or ruptured aneurysm. An endovascular repair (EVAR) is favored in older patients and high risk patients or those unfit for open repair. Risk factors for postoperative morbidity and mortality include extensive atheromatous disease, mural calcification, thrombosis, juxtarenal extension of the aneurysm and the presence of inflammatory changes.

Smoking cessation and blood pressure management are two strategies to reverse modifiable risk factors for the development, progression, and rupture of an abdominal aortic aneurysm.

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Hardik Patel, M.D. Ramyar Ghandriz MD[2]

The etymology of the word aneurysm comes from the Greek word for “dilatation”. Abdominal aortic aneurysm as a medical condition has been recognized since ancient times, but was not been successfully treated until the early part of the 20th century. In 1923, Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the first successful aortic ligation on a human. In 1949, Albert Einstein was operated on by Rudolf Nissen by wrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. In 1951, Charles Dubost performed the first AAA repair using a homograft. In 1953, Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (nylon). In 1962, Javid and Creech reported the technique of endoaneurysmorrhaphy. In 1980, Parodi et al described an endovascular repair.

• The first historical accounts regarding abdominal aortic aneurysm date from Ancient Rome, more precisely from the 2nd century AD, when Greek surgeon Antyllus tried to treat an abdominal aortic aneurysm with proximal and distal ligature, along with central incision and evacuation of thrombotic material from the aneurysm.^[1]

• However, attempts to treat the AAA surgically were unsuccessful until 1923. In that year, Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the first successful aortic ligation on a human.^[2]

• Other methods that were successful in treating an AAA included wrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. Albert Einstein was operated on by Rudolf Nissen with use of this technique in 1949, and survived five years after the operation.^[3]

• Charles Dubost performed the first AAA repair using a homograft.^[4]

• Blakemore and Voorhees repaired a ruptured AAA using a Vinyon-N graft (nylon). ^[5]
• Later, they were replaced by Dacron and polytetrafluoroethylene (PTFE).
• Silk sutures were banned because of degeneration, in favor of braided Dacron, polyethylene, and PTFE sutures, all of which retain tensile strength.

• Javid and Creech reported the technique of endoaneurysmorrhaphy, which dramatically reduced mortality.^[6]

• Parodi et al described an endovascular repair using a large Palmaz stent and unilateral aortofemoral and femorofemoral crossover Dacron grafts.^[7]

CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ;Associate Editor(s)-in-Chief: Ramyar Ghandriz MD[2]

Aneurysms are usually classified by their shape. Abdominal aorta aneurysm is classified by their location as suprarenal or infrarenal. size of the aneurysm is another important criteria that may indicate the need for surgery, so they may be classified by their size in many textbooks.

• They are the most common type of aneurysm seen in the infrarenal aorta.
• They are diffuse and circumferential.^[1]

• Involve only a portion of the circumference, with a characteristic outpouching of the vessel wall.^[2].

• Determined by ultrasonography, where as it manifest the best maintenance method^[3]:
• Small aneurysm (<5.5 cm) needs close follow ups.
• If during follow ups, an aneurysm growth in size was rapid, surgery is required.
• Pronounced aneurysm (>5.5 cm) needs surgical repair via graft placement or endovascular stent placement.

CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2] Ramyar Ghandriz MD[3]

The underlying pathophysiology of abdominal aortic aneurysm involves genetic influences, smoking, hypertension, hemodynamic influences and underlying atherosclerosis. In rare instances infection, arteritis, and connective tissue disorders may play a role.

• The most striking histopathological changes of aneurysmatic aorta are seen in tunica media and intima. ^[1]
• Changes indicated include an accumulation of lipids in foam cells( a kind of macrophage), extracellular free cholesterol crystals, calcifications, ulcerations, ruptures of the layers, and thrombosis.^[2]
• There is an adventitial inflammatory infiltrate.
• The degradation of tunica media in proteolytic manners,is the basic process of abdominal aortic aneurysm initial phase. ^[3]
• Matrix metalloproteinases role in Abdominal aortic aneurysm has been shown by some researchers.^[4]
  • This leads to elimination of elastin from the media, rendering the aortic wall more susceptible to the influence of the blood pressure.
• Inflammation is another condition which plays a role in abdominal aortic aneurysm development.^[5]

• The aortic wall has a specific arrangement of structural proteins that give it both strength and elasticity.
• The composition of the extracellular matrix protein in the media may change with age or in response to other conditions, therefore resulting in subsequent destruction of the elastic lamella, rendering the aorta less able to withstand the force of systolic pressure.
• The infra-renal aorta is more prone to develop aneurysms than other segments for the following reasons:^[6]

  • It is the segment that must expand the most during systole and contract the most during diastole.
  • It has a thinner wall, and has fewer vasa vasora than the thoracic aorta.
  • It is more prone to atherosclerosis, a proposed nidus for aneurysmal dilatation.

• Patients with abdominal aortic aneurysms (AAA) also have atherosclerosis in the aorta and other arteries, suggesting that aneurysmal disease may be part of a larger spectrum of vascular disease, and that atherosclerosis actually promotes AAA formation.
• In atherosclerotic AAA, inflammatory cells infiltrate into the vessel wall and may secrete specific matrix metalloproteinases (MMPs).^[7]

  • The different types of MMPs play diverse roles via complex interactions that eventually lead to degradation of the structural media proteins, and subsequently to aneurysmal dilatation.

• There are significantly fewer smooth muscle cells in human AAA tissues than in normal or atherosclerotic nonaneurysmal aortic tissue.

  • This decrease in smooth muscle cells in suspected to be secondary to apoptosis, therefore suggesting a role for focal cell apoptosis in the pathogenesis of AAA.

• There is likely a genetic component to the development of an abdominal aortic aneurysm. A familial pattern of inheritance is most notable in males.^[8]
• It has been postulated that a variant of alpha 1-antitrypsin deficiency may play a small role.
• It has also been postulated that there is a pattern of X-linked mutation, which would explain the lower incidence in heterozygous females.

• Smoking appears to be a critical environmental influence on the development of an abdominal aortic aneurysm.^[9]

• Abdominal aortic aneurysm is a focal degenerative process with a predilection for the infrarenal aorta.
• More than 90 % of abdominal aortic aneurysms occur in the infrarenal location.
• The higher incidence of abdominal aortic aneurysms in the infrarenal region may be due to differences between the infrarenal and the thoracic aorta with respect to histologic and mechanical characteristics. ^[10]
• The diameter progressively decreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a smaller proportion of elastin.
• The mechanical tension in the abdominal aortic wall is therefore higher than in the thoracic aortic wall.
• The elasticity and distensibility also decline with age, which can result in gradual dilatation of the segment.
• Higher intraluminal pressure in patients with arterial hypertension markedly contributes to the progression of the pathological process.^[11]

• Although abdominal aortic aneurysms are frequently involved with atherosclerosis, the exact role of atherosclerosis in the pathophysiology of abdominal aortic aneurysms remains unclear at this time.

Other causes of the development of abdominal aortic aneurysm include:

• Arteritis
• Connective tissue disorders (e.g. Marfan syndrome, Ehlers-Danlos syndrome)
• Cystic medial necrosis
• Infection
• Trauma

Abdominal aortic aneurysms are associated with a high prevalence of systemic atherosclerosis:

• 23%-86% have coronary artery disease
• 3%-20% have cerebrovascular disease
• 12%-42% have peripheral arterial disease

Images shown below are courtesy of Professor Peter Anderson DVM PhD and published with permission © PEIR, University of Alabama at Birmingham, Department of Pathology

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2] Ramyar Ghandriz MD[3]

The most common cause of abdominal aortic aneurysm is atherosclerosis.

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.^[1]

• Abdominal trauma
• Bacteremia
• Gastrointestinal perforation
• Vertebral osteomyelitis

• Abdominal trauma^[1]
• Atherosclerosis^[2]
• Marfan syndrome^[3]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Hardik Patel, M.D. Ramyar Ghandriz MD[3]

An abdominal aortic aneurysm should be differentiated from other causes of abdominal pain such as acute cholecystitis, gastrointestinal bleeding, perforated peptic ulcer, ischemic bowel, nephrolithiasis, pyelonephritis, appendicitis, cholelithiasis, large bowel obstruction, small bowel obstruction, pancreatitis, musculoskeletal pain, myocardial infarction, and urinary tract infection.

• A patient becomes symptomatically after abdominal aortic rupture, so the differentiation is according to the rupture which causes acute abdomen signs and symptoms.
• Non-symptomatic AAA is diagnosed through abdominal ultrasound with no other differentials.
• In a patient with a suspected abdominal aortic aneurysm, the following conditions also need to be considered:^[1]

• • Acute cholecystitis
  • Gastritis and peptic ulcer disease
  • Gastrointestinal bleeding
  • Ischemic bowel
  • Diverticulitis
  • Nephrolithiasis
  • Pyelonephritis
  • Appendicitis
  • Cholelithiasis
  • Large bowel obstruction
  • Small bowel obstruction
  • Pancreatitis
  • Musculoskeletal pain
  • Myocardial infarction
  • Urinary tract infection in women

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Aarti Narayan, M.B.B.S [3]

Abdominal aortic aneurysm is the 13th leading cause of death in the US. Abdominal aortic aneurysms are more common in developed countries. Elderly, caucasian males who are smokers are at a higher risk for developing an abdominal aortic aneurysm.

• The incidence of abdominal aortic aneurysms increases after age 60 and peaks in the seventh and eighth decades of life.^[1]

• The prevalence among males over 60 years is 2000-6000/100,000.^[2]

• Abdominal aortic aneurysms (AAA) is a disease of the elderly, and is the 10th leading cause of death in older men in the United States.^[3]
• An individual’s risk of AAA increases by 6% per decade of life
• Rupture of the AAA occurs in 1-3% of men aged 65 or more with an associated mortality rate of 70-95%.^[4]
• AAA tends to cluster in families, therefore affecting younger members of families in the absence of traditional acquired risk factors.

• Abdominal aortic aneurysm is 5 times more common in men than women.^[5]

• The disease tends to affect older Caucasian males and is 3.5 times more common in Caucasian men than in African-American men.^[6]

• In the US, the incidence of abdominal aortic aneurysm is 2-4% in the adult population.^[7]

• Abdominal aortic aneurysm is uncommon in individuals of African, African American, Asian and Hispanic heritage.^[8]

• The frequency of abdominal aortic aneurysm is much higher in smokers than in non-smokers (8:1).^[9]

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Vishnu Vardhan Serla M.B.B.S. [3] Ramyar Ghandriz MD[4]

The most significant modifiable risk factor for the development of an abdominal aortic aneurysm is smoking which increases the risk of aneurysm development 8 fold. Advanced age and family history are the strongest non-modifiable risk factors for the development of an abdominal aortic aneurysm. Hypercholesterolemia and hypertension are risk factors as well. Both diabetes mellitus and being of African American descent appear to be associated with a lower incidence of abdominal aortic aneurysm. Caucasians report a higher incidence of AAA when compared to the non Caucasians. An increased rate of expansion of abdominal aortic aneurysm is related to systolic hypertension, wide pulse pressure, and ongoing smoking. The risk of abdominal aortic aneurysm rupture is proportional to the size and rate of growth of the aneurysm. Abdominal aortic aneurysms greater than 5 cm diameter or those that grow faster than 1 cm per year have a significantly increased risk of rupture and are indications for elective operative repair. Advanced age, female gender, hypertension, active smoking, outpouchings, and mural thrombus are also risk factors for abdominal aortic aneurysm rupture.

• The strongest independent acquired risk factor for AAA is smoking. In a study by Wilmink et. al, it is shown that current smokers are 7.6 times more likely to manifest an abdominal aortic aneurysm than non smokers. Risk of developing abdominal aortic aneurysm increases related to increase in smoking duration, but amount of cigarettes smoked per day did not provide any further information.^[1][2]
• Most important non-reversible risk factors are advanced age and family history. There is an increased risk of developing abdominal aortic aneurysm by 2 to 5 folds with family history,compared to normal society^[3][4][5].
• The prevalence of abdominal aortic aneurysms among first-degree relatives diagnosed with abdominal aortic aneurysms increases to 15-29%, compared with 2% among relatives of controls.^[6]
• Male sex
• Caucasian race
• Genetic factors like genetic polymorphism and presence of HLA-DRB 1 alleles B1*0404 and HLA-DRB1 alleles B1*15^[7]
• Hypertension
• Known atherosclerotic disease – coronary artery disease, cerebrovascular disease, peripheral artery disease
• Hypercholesterolemia
• Chronic obstructive pulmonary disease

Cardiovascular risk factors tend to cluster in certain patients:

• Men who smoke and are hypertensive have an incidence of abdominal aortic aneurysm that is 2-5 times than those of the general population.
• Similarly, women over the age of 60 with cardiovascular risk factors are 2-3 times more likely to develop aneurysmal disease.
• Both diabetes mellitus and being of African American descent appear to be associated with a lower incidence of abdominal aortic aneurysm.

• In small abdominal aortic aneurysm (3-5.4 cm), the expansion rate appears to be proportional to the initial diameter.^[8]
• Independent of the initial diameter of the aneurysm, other factors related to rapid expansion of an abdominal aortic aneurysm are:

• Systolic hypertension
• Wide pulse pressure
• Ongoing smoking

C-reactive protein levels have also been found to be elevated in larger aneurysms, however they do not appear to be linked to rapid expansion.^[9]

The risk of rupture is proportional to the size and rate of growth of the aneurysm. Aneurysms greater than 5 cm diameter or those that grow faster than 1 cm per year have a significantly increased risk of rupture and are indications for elective operative repair.^[10][11] In the UK small aneurysm trial, important independent variables were identified with abdominal aortic aneurysm rupture:

• Female sex
• Increased diameter of the abdominal aortic aneurysm
• Current smoker
• Mean blood pressure
• Increased age
• Forced expiratory volume in 1 second
• Size at diagnosis is one of the best predictors of rupture.
• The risk increases substantially when the diameter exceeds 6 cm in men and 5 cm in women.
• Small aneurysms can rupture as well, and are threefold more likely to rupture in women.
• Localized outpouchings seems to increase the aneurysm’s vulnerability for rupture.
• It has been suggested that the aneurysm growth and rupture correlate with the growth of the aneurysm’s mural thrombus: the part of the aneurysm wall that is covered with thrombus has been shown to be thinner and showed focal anoxia, inflammation, apoptosis of the smooth muscle cells, and a more degraded extracellular matrix than wall segments not covered by the thrombus.

• (Compilation of 2005 and 2011 ACCF/AHA Guideline Recommendations) : A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines^[12]

Template:WH Template:WS CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Caitlin J. Harrigan [2]; Vishnu Vardhan Serla M.B.B.S. [3] Ramyar Ghandriz MD[4]

Approximately 16% of large abdominal aortic aneurysms (diameter > 5.5 cm) rupture, causing 9,000 AAA-related deaths in the United States per year. Several studies have shown that screening can drastically reduce the aneurysm rupture rate by 45-49% for men older than 60, and reduce AAA-related mortality by 21-68%. In a landmark study randomizing 67,800 men, (The Multicenter Aneurysm Screening Study) aneurysm-related mortality was 53% lower in the screening group as compared with control patients. The United States Preventive Services Task Force (USPSTF) recommends one-time screening for abdominal aortic aneurysm (AAA) by ultrasonography in any man, aged 65 to 75 who has ever smoked. The USPSTF makes no recommendation for or against screening for AAA in men aged 65 to 75 who have never smoked. The USPSTF recommends against routine screening for AAA in women.

• Patients with abdominal aortic aneurysms (AAAs) are often asymptomatic, with the first clinical event often being fatal or life-threatening.^[1]
• Due to this apparent “detection gap,” between the asymptomatic disease and clinically apparent disease screening may be of benefit.^[2]
• AAAs are usually asymptomatic during this “detection gap”, with the possibility of as many as one in three rupturing if left untreated.^[3]
• A ruptured AAA carries an overall mortality rate approaching 75%, with a mortality rate of 2-6% in those patients who underwent elective surgical repair.^[4]
• Approximately 16% of large AAAs (diameter >5.5 cm) rupture, causing 9,000 AAA-related deaths in the United States per year.
• Several studies have shown that screening can drastically reduce the aneurysm rupture rate by 45-49% for men older than 60, and reduce AAA-related mortality by 21-68%.

• In the largest population-based screening study to date, the Multi center Aneurysm Screening Study (MASS) randomized 67,800 men (age 65-74) equally to either a group that received an ultrasound screening for AAA or a control group. ^[3][2]
• In the screening group, men with an abdominal aorta larger than 3 cm in diameter were followed with serial ultrasounds for a mean duration of 4.1 years.
• When the aneurysm reached 5.5 cm, grew more than 1 cm/year or became symptomatic, it was repaired surgically.
• The aneurysm-related mortality was 53% lower in the screening group.
• However, despite the relative risk reduction in the MASS trial, there were 65 AAA-related deaths in the intervention group (absolute risk of 0.19%), and 113 AAA-related deaths in the control group (absolute risk 0.33%).

It is estimated that abdominal aortic aneurysm screening is as cost-effective as mammography for breast cancer detection as well as therapeutic interventions such as coronary artery bypass graft surgery with a cost of $11,285 per quality adjusted life year saved.^[5]

• Physical examinations may detect large AAAs, but is not specific or sensitive enough to detect smaller ones.^[6]
• The cornerstone of AAA screening is ultrasonography. It is available in almost every medical center and many physician offices.
• Abdominal aortic ultrasonography is fast, inexpensive, safe and well-tolerated by most patients
• It is highly accurate with 95% sensitivity and 100% specificity for AAAs.^[7]
• The most important limitations of ultrasonography are:

• Operator dependence
• Reduced accuracy in those patients with bowel gas, periaortic disease and those patients who are obese.
• These limitations present less of an issue for highly experienced sonographers, and in accredited, validated, high-volume institutions.

• Computed tomography (CT) and magnetic resonance angiography are accurate for diagnosing AAA, but are less often used as a first-degree screening modality because of the lack of availability, and the risks and side-effects of iodinated contrasts for CT.

• Screening using ultrasonography causes no serious side effects, and is therefore ethically acceptable.^[8]
• Several studies have shown that screening for AAAs and diagnosing asymptomatic small aneurysms in clinical practice were not associated with long-term emotional or psychological stress to patients.^[9]
• A simple screening ultrasound test costs approximately $500, for which Medicare usually reimburses $160.
• Lack of insurance coverage raises the ethical dilemma of AAA screening being available only to the elite who can afford it.

• Small, asymptomatic AAAs (3-5.5 cm) may serve as a marker for vascular disease elsewhere, thus finding one provides good reason to aggressively start to modify risk factors.

• Periodic ultrasonographic surveillance is recommended for aneurysms smaller than the repair cutoff.
• If an abdominal aortic aneurysm is 4 to 5.4 cm then surveillance ultrasounds can be obtained every 6 to 12 months.
• If an abdominal aortic aneurysm is 3 to 4 cm then surveillance ultrasounds can be obtained every 2 to 3 years.
• However, definite and unified parameters for appropriate surveillance intervals have not yet been determined because clinical trials have enrolled heterogeneous populations and used different standards for diagnosis and management.
• In general, older men may need more frequent follow-up scans, as men older than 70 years have three times the rate of progression than younger men.
• Aneurysm diameters determined by ultrasound may vary up to 0.5 cm, which should be considered when recommending optimal times for rescanning and repair.

Clinical practice guidelines^[10] and systematic review^[11] by the United States Preventive Service Task Force in 2014 stated:

• “The USPSTF recommends 1-time screening screening for AAA with ultrasonography in men aged 65 to 75 years who have ever smoked.”
• “The USPSTF recommends that clinicians selectively offer screening for AAA in men aged 65 to 75 years who have never smoked”
• “The USPSTF concludes that the current evidence is insufficient to assess the balance of benefits and harms of screening for AAA in women aged 65 to 75 years who have ever smoked”
• “The USPSTF recommends against routine screening for AAA in women who have never smoked.”

The projected benefit of screening is:^[12]

• Number needed to invite to prevent one death is 175 – 225.

http://www.uspreventiveservicestaskforce.org/uspstf/uspsaneu.htm

CME Category::Cardiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

An aortic aneurysm can progress to a ruptured abdominal aortic aneurysm, which is a medical emergency associated with an extremely high mortality. Serious complications can also occur as a result of an aortic dissection, such as myocardial infarction, shock, stroke, kidney failure, and arterial emboli. A ruptured AAA carries an overall mortality rate approaching 75%, which is much higher than the mortality rate of 2-6% in those patients who underwent elective surgical repair. Approximately 16% of large AAAs (diameter >5.5 cm) rupture, causing 9,000 AAA-related deaths in the United States per year. Several studies have shown that screening can drastically reduce the aneurysm rupture rate by 45-49% for men older than 60, and reduce AAA-related mortality by 21-68%.

Abdominal aortic aneurysms expand slowly over time. It is for this reason that ultrasound surveillance is recommended. The risk for rupture of an aneurysm depends on several factors^[1]:

• Size of an aneurysm
  • Risk of rupture increases greatly once the size of aneurysm reaches 5.5 cm.
• Rate of expansion
  • If the rate of expansion exceeds 1 cm per year, this is an indication for surgery.
  • Growth tends to be more rapid in smokers than non-smokers.
• Gender
  • The risk of rupture is higher in women than in men.^[2]

When an abdominal aortic aneurysm ruptures, it is a true medical emergency. Aortic dissection occurs when the innermost lining of the artery tears and blood leaks into the wall of the artery. This most commonly occurs in the aorta within the chest. Complications include:

• Aortic rupture: Once an aneurysm has ruptured, it presents with a classic pain–hypotension-mass triad. The pain is classically reported in the abdomen, back or flank. It is usually acute, severe and constant, and may radiate through the abdomen to the back. The diagnosis of an abdominal aortic aneurysm can be confirmed at the bedside by the use of ultrasound. Rupture is indicated by the presence of free fluid in potential abdominal spaces, such as Morrison’s pouch, the splenorenal space, subdiaphragmatic spaces and peri-vesical spaces. A contrast-enhanced abdominal CT scan is needed for confirmation. Only 10-25% of patients survive a rupture due to large pre and post-operative mortality. Annual mortality from ruptured abdominal aneurysms in the United States alone is about 15,000.
• Acute aortic occlusion
• Aortocaval or aortoduodenal fistulae
• Arterial embolism
• Disseminated intravascular coagulation
• Heart attack
• Hypovolemic shock
• Kidney failure
• Stroke

The outcome is usually good if an experienced surgeon repairs the aneurysm before it ruptures.

Rupture of an abdominal aortic aneurysm is associated with a 60% to 90% mortality before the patient reaches a hospital. It is associated with a 30% to 80% operative mortality among those patients who survive long enough to undergo surgery.

CME Category::Cardiology