Wikipedia - Abdominal Aortic Aneurysm (CHECKED)

6/15/15, 22:15Abdominal aortic aneurysm - Wikipedia, the free encyclopedia

Page 1 of 17https://en.wikipedia.org/wiki/Abdominal_aortic_aneurysm

Abdominal aortic aneurysm

CT reconstruction image of an abdominal aortic aneurysm (white arrows)Classification and external resources

ICD-10 I71.3(http://apps.who.int/classifications/icd10/browse/2015/en#/I71.3),I71.4(http://apps.who.int/classifications/icd10/browse/2015/en#/I71.4)

ICD-9 441.3 (http://www.icd9data.com/getICD9Code.ashx?icd9=441.3), 441.4(http://www.icd9data.com/getICD9Code.ashx?icd9=441.4)

OMIM 100070 (http://omim.org/entry/100070)DiseasesDB 792 (http://www.diseasesdatabase.com/ddb792.htm)MedlinePlus 000162

(http://www.nlm.nih.gov/medlineplus/ency/article/000162.htm)eMedicine med/3443 (http://www.emedicine.com/med/topic3443.htm)

emerg/27 (http://www.emedicine.com/emerg/topic27.htm#)radio/1 (http://www.emedicine.com/radio/topic1.htm#)

MeSH D017544 (https://www.nlm.nih.gov/cgi/mesh/2015/MB_cgi?field=uid&term=D017544)

Abdominal aortic aneurysmFrom Wikipedia, the free encyclopedia

Abdominal aortic aneurysm(AAA),[1] also known as a triple-a,is a localized enlargement of theabdominal aorta such that thediameter is greater than 3 cm or morethan 50% larger than normal.[2] Theyusually cause no symptoms exceptwhen ruptured.[2] Occasionally theremay be abdominal, back or legpain.[3] Large aneurysms cansometimes be felt by pushing on theabdomen.[3] Rupture may result inpain in the abdomen or back, lowblood pressure or a brief loss ofconsciousness.[2][4]

AAAs occur most commonly in thoseover 50 years old, in men, and amongthose with a family history.[2]Additional risk factors includesmoking, high blood pressure, andother heart or blood vesseldiseases.[5] Genetic conditions withan increased risk include Marfansyndrome and Ehlers-Danlossyndrome. AAAs are the mostcommon form of aortic aneurysm.[6]Approximately 85 percent occurbelow the kidneys with the rest eitherat the level of or above thekidneys.[2] In the United Statesscreening males with ultrasound whoare between 65 and 75 year old andhave a history of smoking isrecommended.[7] In the UnitedKingdom screening all men over 65is recommended.[2] Australia has no guideline on screening.[8] Once an aneurysm is found, further ultrasoundsare typically done on a regular basis.[3]

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Not smoking is the single best way to prevent the disease. Other methods of prevention include treating highblood pressure, treating high blood cholesterol and not being overweight. Surgery is usually recommendedwhen an AAA's diameter grows to >5.5 cm in males and >5.0 cm in females.[2] Other reasons for repair includethe presence of symptoms and a rapid increase in size.[3] Repair may be either by open surgery or endovascularaneurysm repair (EVAR).[2] As compared to open surgery, EVAR has a lower risk of death in the short term anda shorter hospital stay but may not always be an option.[2][9][10] There does not appear to be a difference inlonger term outcomes between the two.[11] With EVAR there is a higher need for repeat procedures.[12]

AAAs affect between 2% and 8% of males over the age of 65. Rates among women are four times lower. Inthose with an aneurysm less than 5.5 cm the risk of rupture in the next year is less than 1%. Among those withan aneurysm between 5.5 and 7 cm the risk is about 10% while for those with an aneurysm greater than 7 cmthe risk is about 33%. Mortality if ruptured is 85% to 90%.[2] During 2013, aortic aneurysms resulted in152,000 deaths up from 100,000 in 1990.[13] In the United States AAAs resulted in between 10,000 and 18,000deaths in 2009.[6]

Contents1 Signs and symptoms

1.1 Aortic rupture2 Causes3 Pathophysiology4 Diagnosis

4.1 Classification5 Prevention6 Screening7 Management

7.1 Conservative7.2 Medication7.3 Surgery7.4 Rupture

8 Prognosis9 Epidemiology10 History11 Society and culture12 Research

12.1 Risk assessment12.2 Experimental models12.3 Prevention and treatment

13 References14 External links

Signs and symptoms

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Drawing of an abdominal aorticaneurysm.

The vast majority of aneurysms are asymptomatic. However, asabdominal aortic aneurysms expand, they may become painful and leadto pulsating sensations in the abdomen or pain in the chest, lower back,or scrotum.[14] The risk of rupture is high in a symptomatic aneurysm,which is therefore considered an indication for surgery. Thecomplications include rupture, peripheral embolization, acute aorticocclusion, and aortocaval (between the aorta and inferior vena cava) oraortoduodenal (between the aorta and the duodenum) fistulae. Onphysical examination, a palpable abdominal mass can be noted. Bruitscan be present in case of renal or visceral arterial stenosis.[15]

Aortic ruptureThe signs and symptoms of a ruptured AAA may includes severe pain inthe lower back, flank, abdomen or groin. A mass that pulses with theheart beat may also be felt.[4] The bleeding can leads to a hypovolemicshock with low blood pressure and a fast heart rate. This may lead tobrief passing out.[4]

The mortality of AAA rupture is up to 90%. 6575% of patients die before they arrive at hospital and up to 90%die before they reach the operating room.[16] The bleeding can be retroperitoneal or into the abdominal cavity.Rupture can also create a connection between the aorta and intestine or inferior vena cava.[17] Flank ecchymosis(appearance of a bruise) is a sign of retroperitoneal bleeding, and is also called Grey Turner's sign.[15][18]

Aortic aneurysm rupture may be mistaken for the pain of kidney stones, muscle related back pain.[4]

CausesThe exact causes of the degenerative process remain unclear. There are, however, some hypotheses and well-defined risk factors.[19]

Tobacco smoking: Greater than 90% of people who develop a AAA have smoked at some point in theirlife.[20]Alcohol and hypertension: The inflammation caused by prolonged use of alcohol and hypertensive effectsfrom abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is alsoconsidered a long-term cause of AAA.Genetic influences: The influence of genetic factors is high. AAA is 4-6 times more common in malesiblings of known patients, with a risk of 20-30%.[21] The high familial prevalence rate is most notable inmale individuals.[22] There are many hypotheses about the exact genetic disorder that could cause higherincidence of AAA among male members of the affected families. Some presumed that the influence ofalpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis ofX-linked mutation, which would explain the lower incidence in heterozygous females. Other hypothesesof genetic etiology have also been formulated.[15] Connective tissue disorders, such as Marfan syndrome

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A plate from Gray's Anatomy withyellow lines depicting the mostcommon infrarenal location of theAAA.

and Ehlers-Danlos syndrome, have also been strongly associated with AAA.[17] Both relapsingpolychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.[23]Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of theAAA are frequently affected heavily. However, this hypothesis cannot be used to explain the initial defectand the development of occlusion, which is observed in the process.[15]Other causes of the development of AAA include: infection, trauma, arteritis, cystic medial necrosis (m.Erdheim).[17]

PathophysiologyThe most striking histopathological changes of aneurysmatic aorta areseen in tunica media and intima. These include accumulation of lipids infoam cells, extracellular free cholesterol crystals, calcifications,thrombosis, and ulcerations and ruptures of the layers. There is anadventitial inflammatory infiltrate.[17] However, the degradation oftunica media by means of proteolytic process seems to be the basicpathophysiologic mechanism of the AAA development. Someresearchers report increased expression and activity of matrixmetalloproteinases in individuals with AAA. This leads to elimination ofelastin from the media, rendering the aortic wall more susceptible to theinfluence of the blood pressure.[15] Others reports have suggested theserine protease granzyme B may contribute to aortic aneurysm rupturethrough the cleavage of decorin leading to disrupted collagenorganization and tensile strength of the adventitia.[24][25] There is also areduced amount of vasa vasorum in the abdominal aorta (compared tothe thoracic aorta); consequently, the tunica media must rely mostly ondiffusion for nutrition which makes it more susceptible to damage.[26]

Hemodynamics affect the development of AAA. It has a predilection for the infrarenal aorta. The histologicalstructure and mechanical characteristics of infrarenal aorta differ from those of the thoracic aorta. The diameterdecreases from the root to the bifurcation, and the wall of the abdominal aorta also contains a lesser proportionof elastin. The mechanical tension in 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 ofthe pathological process.[17] Suitable hemodynamics conditions may be linked to specific intraluminal thrombus(ILT) patterns along the aortic lumen, which in turn may affect AAA's development.[27]

DiagnosisAn abdominal aortic aneurysm is usually diagnosed by physical exam, ultrasound, or CT. Plain abdominalradiographs may show the outline of an aneurysm when its walls are calcified. However, this is the case in lessthan half of all aneurysms. Ultrasonography is used to screen for aneurysms and to determine the size of anypresent. Additionally, free peritoneal fluid can be detected. It is noninvasive and sensitive, but the presence of

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bowel gas or obesity may limit its usefulness. CT scan has a nearly 100% sensitivity for aneurysm and is alsouseful in preoperative planning, detailing the anatomy and possibility for endovascular repair. In the case ofsuspected rupture, it can also reliably detect retroperitoneal fluid. Alternative less often used methods forvisualization of the aneurysm include MRI and angiography.

An aneurysm ruptures if the mechanical stress (tension per area) exceeds the local wall strength; consequently,peak wall stress (PWS)[28] and peak wall rupture risk (PWRR)[29] have been found to be more reliableparameters than diameter to assess AAA rupture risk. Medical software allows computing these rupture riskindices from standard clinical CT data and provides a patient-specific AAA rupture risk diagnosis.[30] This typeof biomechanical approach has been shown to accurately predict the location of AAA rupture.[31]

A ruptured AAA withan open arrow markingthe aneurysm and theclosed arrow markingthe free blood in theabdomen

Sagittal CT image of anAAA.

Biomechanical AAARupture risk prediction.

An axial contrastenhanced CT scandemonstrating anabdominal aorticaneurysm of 4.8 by3.8 cm

Ultrasound image of anormal abdominal aortameasuring 1.9 cm indiameter.

The faint outline of thecalcified wall of a AAAas seen on plain X-ray

Abdominal aorticaneurysms (3.4 cm)

Classification

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Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysmis usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm).[32] If theouter diameter exceeds 5.5 cm, the aneurysm is considered to be large.[33] A ruptured AAA is a clinicaldiagnosis involving the presence of the triad of abdominal pain, shock and a pulsatile abdominal mass. If theseconditions are present, indicating AAA rupture, no further clinical investigations are needed before surgery.[34]

PreventionSmoking cessationTreatment of hypertension

ScreeningThe U.S. Preventive Services Task Force recommends a single screening ultrasound for abdominal aorticaneurysm in males age 65 to 75 years who have a history of smoking.[7] There is an estimated number neededto screen of approximately 850 people.[35] It is unclear if screening is useful in women aged 65 to 75 who havesmoked and they recommend against screening in women who have never smoked.[7]

Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm.[36] In thosewhose aorta is between 3.0 and 3.9 cm this should be every three years, if between 4.0 and 4.4 cm every twoyear, and if between 4.5 and 5.4 cm every year.[36]

In the United Kingdom one time screening is recommended in all males over 65 years of age.[2]

ManagementThe treatment options for asymptomatic AAA are conservative management, surveillance with a view toeventual repair, and immediate repair. There are currently two modes of repair available for an AAA: openaneurysm repair (OR), and endovascular aneurysm repair (EVAR). An intervention is often recommended if theaneurysm grows more than 1 cm per year or it is bigger than 5.5 cm.[20] Repair is also indicated forsymptomatic aneurysms.[37]

ConservativeConservative management is indicated in patients where repair carries a high risk of mortality and in patientswhere repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smokingcessation.

Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceedsthe risk of rupture. As an AAA grows in diameter the risk of rupture increases. Surveillance until the aneurysmhas reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to earlyintervention.[38][39]

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Abdominal aortic endoprosthesis, CTscan, original aneurysm marked inblue.

MedicationNo medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomaticAAAs.[2] Blood pressure and lipids should however be treated per usual.[32]

SurgerySurgery for an abdominal aortic aneurysm is known as AAA surgery or AAA repair.

The threshold for repair varies slightly from individual to individual, depending on the balance of risks andbenefits when considering repair versus ongoing surveillance. The size of an individual's native aorta mayinfluence this, along with the presence of comorbidities that increase operative risk or decrease lifeexpectancy.[37] Evidence; however, does not support repair if the size is between 4 cm and 5.5 cm.[40]

Open repair

Open repair is indicated in young patients as an elective procedure, or in growing or large, symptomatic orruptured aneurysms. The aorta must be clamped off during the repair, denying blood to the abdominal organsand sections of the spinal cord; this can cause a range of complications. It is essential to make the critical part ofthe operation fast, so the incision is typically made large enough to facilitate the fastest repair. Recovery afteropen AAA surgery takes significant time. The minimums are a few days in intensive care, a week total in thehospital and a few months before full recovery.

Endovascular repair

Endovascular repair first became practical in the 1990s and although it isnow an established alternative to open repair, its role is yet to be clearlydefined. It is generally indicated in older, high-risk patients or patientsunfit for open repair. However, endovascular repair is feasible for only aproportion of AAAs, depending on the morphology of the aneurysm.The main advantages over open repair are that there is less peri-operative mortality, less time in intensive care, less time in hospitaloverall and earlier return to normal activity. Disadvantages ofendovascular repair include a requirement for more frequent ongoinghospital reviews, and a higher chance of further procedures beingrequired. According to the latest studies, the EVAR procedure does notoffer any benefit for overall survival or health-related quality of lifecompared to open surgery, although aneurysm-related mortality islower.[41][42][43][44] In patients unfit for open repair, EVAR plusconservative management was associated with no benefit, morecomplications, subsequent procedures and higher costs compared toconservative management alone.[45] Endovascular treatment forparaanastomotic aneurysms after aortobiiliac reconstruction is also a possibility.[46]

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AAA Size (cm) Growth rate (cm/yr)[48] Annual rupture risk (%)[49]3.0-3.9 0.39 04.0-4.9 0.36 0.5-55.0-5.9 0.43 3-156.0-6.9 0.64 10-20>=7.0 - 20-50

RuptureIn those with aortic rupture of the AAA, treatment is immediate surgical repair. There appears to be benefits toallowing permissive hypotension and limiting the use of intravenous fluids during transport to the operatingroom.[47]

PrognosisAlthough the current standard ofdetermining rupture risk is basedon maximum diameter, it is knownthat smaller AAAs that fall belowthis threshold (diameter5.5 cm) may remainstable.[50][51] In one report, it wasshown that 1024% of rupturedAAAs were less than 5 cm indiameter.[51] It has also been reported that of 473 non-repaired AAAs examined from autopsy reports, therewere 118 cases of rupture, 13% of which were less than 5 cm in diameter. This study also showed that 60% ofthe AAAs greater than 5 cm (including 54% of those AAAs between 7.1 and 10 cm) never experiencedrupture.[52] Vorp et al. later deduced from the findings of Darling et al. that if the maximum diameter criterionwere followed for the 473 subjects, only 7% (34/473) of cases would have succumbed to rupture prior tosurgical intervention as the diameter was less than 5 cm, with 25% (116/473) of cases possibly undergoingunnecessary surgery since these AAAs may never have ruptured.[52]

Alternative methods of rupture assessment have been recently reported. The majority of these approachesinvolve the numerical analysis of AAAs using the common engineering technique of the finite element method(FEM) to determine the wall stress distributions. Recent reports have shown that these stress distributions havebeen shown to correlate to the overall geometry of the AAA rather than solely to the maximumdiameter.[53][54][55] It is also known that wall stress alone does not completely govern failure as an AAA willusually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be moreaccurate if both the patient-specific wall stress is coupled together with patient-specific wall strength. A non-invasive method of determining patient-dependent wall strength was recently reported,[56] with more traditionalapproaches to strength determination via tensile testing performed by other researchers in the field.[57][58][59]Some of the more recently proposed AAA rupture-risk assessment methods include: AAA wall stress;[28][60][61]AAA expansion rate;[62] degree of asymmetry;[55] presence of intraluminal thrombus (ILT);[63] a rupturepotential index (RPI);[64][65] a finite element analysis rupture index (FEARI);[66] biomechanical factors coupledwith computer analysis;[67] growth of ILT;[68] geometrical parameters of the AAA;[69] and also a method ofdetermining AAA growth and rupture based on mathematical models.[70][71]

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The post-operative mortality for an already ruptured AAA has slowly decreased over several decades butremains higher than 40%.[34] However, if the AAA is surgically repaired before rupture, the post-operativemortality rate is substantially lower: approximately 1-6%.[72]

EpidemiologyThe occurrence of AAA varies by ethnicity. In the United Kingdom the rate of AAA in Caucasian men olderthan 65 years is about 4.7%, while in Asian men it is 0.45%.[73] It is also less common in individuals ofAfrican, and Hispanic heritage.[2] They occur four times more often in men than women.[2]

There are at least 13000 deaths yearly in the U.S. secondary to AAA rupture.[2] The peak number of new casesper year among males is around 70 years of age, the percentage of males affect over 60 years is 2-6%. Thefrequency is much higher in smokers than in non-smokers (8:1), and the risk decreases slowly after smokingcessation.[74] In the U.S., the incidence of AAA is 2-4% in the adult population.[15]

Rupture of the AAA occurs in 1-3% of men aged 65 or more, the mortality is 70-95%.[33]

HistoryThe first historical records about AAA are from Ancient Rome in the 2nd century AD, when Greek surgeonAntyllus tried to treat the AAA with proximal and distal ligature, central incision and removal of thromboticmaterial from the aneurysm. However, attempts to treat the AAA surgically were unsuccessful until 1923. Inthat year, Rudolph Matas (who also proposed the concept of endoaneurysmorrhaphy), performed the firstsuccessful aortic ligation on a human.[75] Other methods that were successful in treating the AAA includedwrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of theaneurysm. Albert Einstein was operated on by Rudolph Nissen with use of this technique in 1949, and survivedfive years after the operation, though he eventually died when the aneurysm ruptured.[76] Endovascularaneurysm repair was first performed in the late 1980s and has been widely adopted in the subsequent decades.Endovascular repair was first used for treating a ruptured aneurysm in Nottingham in 1994[77]

Former presidential candidate Bob Dole had an abdominal aortic aneurysm in 2001 and was treated surgicallyby vascular surgeon Kenneth Ouriel. The operation was successful. In 1993, country music singer ConwayTwitty died from AAA, and actor George C. Scott also died of an Abdominal Aneurysm.[78]

Society and cultureIn 2001 former presidential candidate Bob Dole underwent surgery for an abdominal aortic aneurysm in whicha team of surgeons led by Doctor Kenneth Ouriel inserted a stent graft:

Ouriel said that the team inserted a Y-shaped tube through an incision in Dole's leg and placed itinside the weakened portion of the aorta. The aneurysm will eventually contract around thestent, which will remain in place for the rest of Dole's life.[78]

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Associated Press

Actor Robert Jacks, who plays Leatherface in Texas Chainsaw Massacre: The Next Generation died from anabdominal aneurysm on August 8, 2001, just one day shy of his 42nd birthday. His father also died from thesame cause when Robert was a child.

ResearchRisk assessmentThere have been many calls for alternative approaches to rupture-risk assessment over the past number of years,with many believing that a biomechanics-based approach may be more suitable than the current diameterapproach. Numerical modelling is a valuable tool to researchers allowing approximate wall stresses to becalculated, thus revealing the rupture potential of a particular aneurysm. Experimental models are required tovalidate these numerical results, and provide a further insight into the biomechanical behaviour of the AAA. Invivo, AAAs exhibit a varying range of material strengths[79] from localised weak hypoxic regions[80] to muchstronger regions and areas of calcifications.[81]

Experimental modelsExperimental models can now be manufactured using a novel technique involving the injection-moulding lost-wax manufacturing process to create patient-specific anatomically correct AAA replicas.[82] Work has alsofocused on developing more realistic material analogues to those in vivo, and recently a novel range of silicone-rubbers was created allowing the varying material properties of the AAA to be more accurately represented.[83]These rubber models can also be used in a variety of experimental testing from stress analysis using thephotoelastic method[84] to deterimining whether the locations of rupture experimentally correlate with thosepredicted numerically.[85] New endovascular devices are being developed that are able to treat more complexand tortuous anatomies.[86]

Prevention and treatmentAn animal study showed that removing a single protein prevents early damage in blood vessels from triggeringa later-stage, complications. By eliminating the gene for a signaling protein called cyclophilin A (CypA) from astrain of mice, researchers were able to provide complete protection against abdominal aortic aneurysm.[87]

Other recent research identified Granzyme B (GZMB) (a protein-degrading enzyme) to be a potential target inthe treatment of abdominal aortic aneurysms. Elimination of this enzyme in mice models both slowed theprogression of aneurysms and improved survival.[88][89]

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79. Raghavan ML, Kratzberg J, Castro de Tolosa EM, Hanaoka MM, Walker P, da Silva ES (2006). "Regional distribution ofwall thickness and failure properties of human abdominal aortic aneurysm" (http://www.jbiomech.com/article/S0021-9290(05)00478-1/abstract). J. Biomech 39 (16): 30103016. doi:10.1016/j.jbiomech.2005.10.021(https://dx.doi.org/10.1016%2Fj.jbiomech.2005.10.021). PMID 16337949(https://www.ncbi.nlm.nih.gov/pubmed/16337949).

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81. Speelman L, Bohra A, Bosboom EM, Schurink GW, van de Vosse FN, Makaorun MS, Vorp DA (2007). "Effects of wallcalcifications in patient-specific wall stress analyses of abdominal aortic aneurysms". Journal of BiomechanicalEngineering 129 (1): 105109. doi:10.1115/1.2401189 (https://dx.doi.org/10.1115%2F1.2401189). PMID 17227104(https://www.ncbi.nlm.nih.gov/pubmed/17227104).

82. Doyle BJ, Morris LG, Callanan A, Kelly P, Vorp DA, McGloughlin TM (2008). "3D reconstruction and manufacture ofreal abdominal aortic aneurysms: From CT scan to silicone model". Journal of Biomechanical Engineering 130 (3):034501. doi:10.1115/1.2907765 (https://dx.doi.org/10.1115%2F1.2907765). PMID 18532870(https://www.ncbi.nlm.nih.gov/pubmed/18532870).

83. Doyle BJ, Corbett TJ, Cloonan AJ, O'Donnell MR, Walsh MT, Vorp DA, McGloughlin TM (2009). "ExperimentalmOdelling of Aortic Aneurysms: Novel applications of Silicone Rubbers"(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757445). Medical Engineering & Physics 31 (8): 10021012.doi:10.1016/j.medengphy.2009.06.002 (https://dx.doi.org/10.1016%2Fj.medengphy.2009.06.002). PMC 2757445(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757445). PMID 19595622(https://www.ncbi.nlm.nih.gov/pubmed/19595622).

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External linksCochrane Peripheral Vascular Diseases Review Group (http://pvd.cochrane.org/welcome)

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Categories: Diseases of the aorta Vascular surgery Diseases of arteries, arterioles and capillariesDeaths from abdominal aortic aneurysm

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86. Albertini JN, Perdikides T, Soong CV, Hinchliffe RJ, Trojanowska M, Yusuf SW (Jun 2006). "Endovascular repair ofabdominal aortic aneurysms in patients with severe angulation of the proximal neck using a flexible stent-graft:European Multicenter Experience" (http://www.minervamedica.it/index2.t?show=R37Y2006N03A0245). J CardiovascSurg (Torino) 47 (3): 24550. PMID 16760860 (https://www.ncbi.nlm.nih.gov/pubmed/16760860).

87. "Study establishes major new treatment target in diseased arteries" (http://www.physorg.com/news161183060.html).U.S. News & World Report. May 10, 2009.

88. Chamberlain CM, Ang LS, Boivin WA, Cooper DM, Williams SJ, Zhao H, Hendel A, Folkesson M, Swedenborg J,Allard MF, McManus BM, Granville DJ (2010). "Perforin-Independent Extracellular Granzyme B Activity Contributesto Abdominal Aortic Aneurysm" (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808106). The American Journal ofPathology 176 (2): 10381049. doi:10.2353/ajpath.2010.090700 (https://dx.doi.org/10.2353%2Fajpath.2010.090700).PMC 2808106 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808106). PMID 20035050(https://www.ncbi.nlm.nih.gov/pubmed/20035050).

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