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利用者:加藤勝憲/腹部大動脈瘤

Abdominal aortic aneurysm
three white arrows pointing to an enlargement of the abdominal aorta
CT reconstruction image of an abdominal aortic aneurysm (white arrows)
概要
診療科 Vascular surgery
症状 None, abdominal, back, or leg pain[1][2]
発症時期 Over 50 year old males[1]
危険因子 Smoking, high blood pressure, other heart or blood vessel diseases, family history, Marfan syndrome[1][3][4]
診断法 Medical imaging (abdominal aorta diameter > 3 cm)[1]
予防 Not smoking, treating risk factors[1]
治療 Surgery (open surgery or endovascular aneurysm repair)[1]
頻度 ~5% (males over 65 years)[1]
死亡数・率 168,200 aortic aneurysms (2015)[5]
分類および外部参照情報

腹部大動脈瘤（AAA）は、腹部大動脈の直径が3cm以上、または正常の50％以上となるような局所的な拡大である。[1］時に、腹痛、背部痛、下肢痛が起こることがある［2］。 大きな動脈瘤は、時に腹部を押して感じることがある［2］。破裂すると、腹部または背部の痛み、低血圧、意識喪失が起こることがあり、しばしば死に至る［1］［3］。

Abdominal aortic aneurysm (AAA) is a localized enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal.[1] An AAA usually causes no symptoms, except during rupture.[1] Occasionally, abdominal, back, or leg pain may occur.[2] Large aneurysms can sometimes be felt by pushing on the abdomen.[2] Rupture may result in pain in the abdomen or back, low blood pressure, or loss of consciousness, and often results in death.[1][6]

AAAは、男性、50歳以上、および家族歴のある人に最も多く発症する[1]。その他の危険因子としては、喫煙、高血圧、および他の心臓疾患や血管疾患が挙げられる[4]。 リスクが増加する遺伝的疾患としては、マルファン症候群およびエーラス・ダンロス症候群が挙げられる[5]。

AAAs occur most commonly in men, those over 50 and those with a family history of the disease.[1] Additional risk factors include smoking, high blood pressure, and other heart or blood vessel diseases.[3] Genetic conditions with an increased risk include Marfan syndrome and Ehlers–Danlos syndrome.[4]

AAAは大動脈瘤の最も一般的な形態である[4]。約85％は腎臓の下に発生し、残りは腎臓の高さか上に発生する[1]。

AAAs are the most common form of aortic aneurysm. About 85% occur below the kidneys, with the rest either at the level of or above the kidneys.


AAAは大動脈瘤の最も一般的な形態である。[米国では、喫煙歴のある65～75歳の男性に腹部超音波検査によるスクリーニングが推奨されている。 英国とスウェーデンでは、65歳以上のすべての男性にスクリーニングが推奨されている。

In the United States, screening with abdominal ultrasound is recommended for males between 65 and 75 years of age with a history of smoking.[7] In the United Kingdom and Sweden, screening all men over 65 is recommended.[1][8] Once an aneurysm is found, further ultrasounds are typically done on a regular basis.[2]

他の予防法としては、高血圧の治療、高コレステロール血症の治療、過体重を避けることなどが挙げられる[1]。 手術は通常、動脈瘤の直径が男性で5.5cm以上、女性で5.0cm以上になった場合に推奨される[1]。

Abstinence from cigarette smoking is the single best way to prevent the disease.[1] Other methods of prevention include treating high blood pressure, treating high blood cholesterol, and avoiding being overweight.[1] Surgery is usually recommended when the diameter of an AAA grows to >5.5 cm in males and >5.0 cm in females.[1] Other reasons for repair include the presence of symptoms and a rapid increase in size, defined as more than one centimeter per year.[2]

修復には開腹手術と血管内動脈瘤修復術（EVAR）がある[1]。開腹手術と比較すると、EVARは短期的には死亡リスクが低く、入院期間も短いが、常に選択できるとは限らない[1][8][9]。両者の間に長期的な転帰の差はないようである[10]。

Repair may be either by open surgery or endovascular aneurysm repair (EVAR).[1] As compared to open surgery, EVAR has a lower risk of death in the short term and a shorter hospital stay, but may not always be an option.[1][9][10] There does not appear to be a difference in longer-term outcomes between the two.[11] Repeat procedures are more common with EVAR.[12]

動脈瘤は65歳以上の男性の2～8％が罹患している[1]。破裂した場合の死亡率は85％～90％である[1]。2013年中、大動脈瘤による死亡者数は168,200人で、1990年の100,000人から増加した[13][14]。米国では2009年にAAAによる死亡者数は10,000～18,000人であった[5]。

AAAs affect 2-8% of males over the age of 65.[1] They are five times more common in men.[13] In those with an aneurysm less than 5.5 cm, the risk of rupture in the next year is below 1%.[1] Among those with an aneurysm between 5.5 and 7 cm, the risk is about 10%, while for those with an aneurysm greater than 7 cm the risk is about 33%.[1] Mortality if ruptured is 85% to 90%.[1] During 2013, aortic aneurysms resulted in 168,200 deaths, up from 100,000 in 1990.[5][14] In the United States AAAs resulted in between 10,000 and 18,000 deaths in 2009.[4]

「 Ouriel said that the team inserted a Y-shaped tube through an incision in Dole's leg and placed it inside the weakened portion of the aorta. The aneurysm will eventually contract around the stent, which will remain in place for the rest of Dole's life.[15] 」

Signs and symptoms

[編集]
Abdominal aortic aneurysm location

動脈瘤の大部分は無症状である。しかし、腹部大動脈が拡張および/または破裂すると、動脈瘤は痛みを伴うようになり、腹部の脈動感や胸部、腰部、脚、陰嚢の痛みにつながることがある[16]。

Complications

[編集]

合併症としては、破裂、末梢塞栓、急性大動脈閉塞、大動脈瘤（大動脈と下大静脈の間）または大動脈十二指腸瘤（大動脈と十二指腸の間）がある。身体診察では、触知可能で拍動性の腹部腫瘤を認めることがある。腎動脈狭窄または内臓動脈狭窄の場合は、破裂がみられることがある。

The complications include rupture, peripheral embolization, acute aortic occlusion, and aortocaval (between the aorta and inferior vena cava) or aortoduodenal (between the aorta and the duodenum) fistulae. On physical examination, a palpable and pulsatile abdominal mass can be noted. Bruits can be present in case of renal or visceral arterial stenosis.[17]

AAA破裂の徴候と症状には、腰、脇腹、腹部、鼠径部の激痛が含まれる。また、心臓の拍動に伴って脈打つ腫瘤を感じることもある[3]。出血は、血圧低下と心拍数の速さを伴う血液量減少性ショックにつながり、失神を引き起こすこともある[3]。AAA破裂の死亡率は90％と高い。患者の65～75％が病院に到着する前に死亡し、最大90％が手術室に到着する前に死亡する [17] 。出血は後腹膜または腹腔内に及ぶ。破裂はまた、大動脈と腸または下大静脈の接続部を形成することもある。 [18] 脇腹の紅斑（あざのように見える）は後腹膜出血の徴候であり、グレイ・ターナー徴候とも呼ばれる [16] [19] 。

The signs and symptoms of a ruptured AAA may include severe pain in the lower back, flank, abdomen or groin. A mass that pulses with the heart beat may also be felt.[6] The bleeding can lead to a hypovolemic shock with low blood pressure and a fast heart rate, which may cause fainting.[6] The mortality of AAA rupture is as high as 90 percent. 65 to 75 percent of patients die before they arrive at the hospital and up to 90 percent die before they reach the operating room.[18] 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.[19] Flank ecchymosis (appearance of a bruise) is a sign of retroperitoneal bleeding and is also called Grey Turner's sign.[17][20]

Causes

[編集]

退行過程の正確な原因はまだ不明である。しかし、いくつかの仮説と明確に定義された危険因子が存在する[20]。

The exact causes of the degenerative process remain unclear. There are, however, some hypotheses and well-defined risk factors.[21]

  • Tobacco smoking: More than 90% of people who develop an AAA have smoked at some point in their lives.[22]
  • Alcohol and hypertension: The inflammation caused by prolonged use of alcohol and hypertensive effects from abdominal edema which leads to hemorrhoids, esophageal varices, and other conditions, is also considered a long-term cause of AAA.[要出典]
  • Genetic influences: The influence of genetic factors is high. AAA is four to six times more common in male siblings of known patients, with a risk of 20–30%.[23] The high familial prevalence rate is most notable in male individuals.[24] There are many hypotheses about the exact genetic disorder that could cause higher incidence of AAA among male members of the affected families. Some presumed that the influence of alpha 1-antitrypsin deficiency could be crucial, while other experimental works favored the hypothesis of X-linked mutation, which would explain the lower incidence in heterozygous females. Other hypotheses of genetic causes have also been formulated.[17] Connective tissue disorders, such as Marfan syndrome and Ehlers-Danlos syndrome, have also been strongly associated with AAA.[19] Both relapsing polychondritis and pseudoxanthoma elasticum may cause abdominal aortic aneurysm.[25]
  • Atherosclerosis: The AAA was long considered to be caused by atherosclerosis, because the walls of the AAA frequently carry an atherosclerotic burden. However, this hypothesis cannot explain the initial defect and the development of occlusion, which is observed in the process.[17] Another hypothesis is that plaque buildup can cause a feed-forward dysfunction in the signaling among neurons that regulate pressure in the aorta. This feed-forward process leads to an over-pressuring condition that ruptures in the aorta.[26]
  • Other causes of the development of AAA include: infection, trauma, arteritis, and cystic medial necrosis.[19]

Pathophysiology

[編集]
A plate from Gray's Anatomy with yellow lines depicting the most common infrarenal location of the AAA
3D file showing an aortic aneurysm

動脈瘤性大動脈の最も顕著な病理組織学的変化は中膜と内膜層にみられる。これらの変化には、泡沫細胞における脂質の蓄積、細胞外遊離コレステロール結晶、石灰化、血栓症、潰瘍および層の破裂が含まれる。血管内皮の炎症性浸潤がみられる。 [18] しかしながら、中膜の蛋白分解過程による分解が、AAA発症の基本的な病態生理学的メカニズムであるようである。研究者の中には、AAA患者ではマトリックスメタロプロテアーゼの発現と活性が増加していると報告している者もいる。これによって中膜からエラスチンが除去され、大動脈壁が血圧の影響を受けやすくなる。 [16] 他の報告では、セリンプロテアーゼであるグランザイムBがデコリンを切断することによって大動脈瘤の破裂に関与し、コラーゲンの組織破壊と外膜の引張強度の低下をもたらす可能性が示唆されている。[26] [27] また、腹部大動脈では（胸部大動脈と比較して）血管弓の量が減少しており、その結果、中膜は栄養補給のほとんどを拡散に頼らざるを得ず、損傷を受けやすくなっている [28] 。

The most striking histopathological changes of the aneurysmatic aorta are seen in the tunica media and intima layers. These changes include the accumulation of lipids in foam cells, extracellular free cholesterol crystals, calcifications, thrombosis, and ulcerations and ruptures of the layers. Adventitial inflammatory infiltrate is present.[19] However, the degradation of the tunica media by means of a proteolytic process seems to be the basic pathophysiologic mechanism of AAA development. Some researchers report increased expression and activity of matrix metalloproteinases in individuals with AAA. This leads to elimination of elastin from the media, rendering the aortic wall more susceptible to the influence of blood pressure.[17] Other reports have suggested the serine protease granzyme B may contribute to aortic aneurysm rupture through the cleavage of decorin, leading to disrupted collagen organization and reduced tensile strength of the adventitia.[27][28] There is also a reduced amount of vasa vasorum in the abdominal aorta (compared to the thoracic aorta); consequently, the tunica media must rely mostly on diffusion for nutrition, which makes it more susceptible to damage.[29]

血行動態はAAA発症に影響し、AAAは腎下大動脈に好発する。腎下大動脈の組織学的構造と力学的特性は胸部大動脈のそれとは異なる。直径は根元から大動脈分岐部に向かって小さくなっており、また腎下大動脈の壁はエラスチンの割合が少ない。したがって、腹部大動脈壁の機械的張力は胸部大動脈壁よりも高い。弾性と伸展性も加齢とともに低下し、その結果、大動脈は徐々に拡張する。動脈圧亢進症患者における高い管腔内圧力は、病的過程の進行に著しく寄与する。 [18] 適切な血行動態条件は、大動脈管腔に沿った特定の管腔内血栓（ILT）パターンと関連している可能性があり、ひいてはAAA発症に影響を及ぼす可能性がある。

Hemodynamics affect the development of AAA, which has a predilection for the infrarenal aorta. The histological structure and mechanical characteristics of the infrarenal aorta differ from those of the thoracic aorta. The diameter decreases from the root to the aortic bifurcation, and the wall of the infrarenal aorta also contains a lesser 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.[19] Suitable hemodynamic conditions may be linked to specific intraluminal thrombus (ILT) patterns along the aortic lumen, which in turn may affect AAA's development.[30]

Diagnosis

[編集]

腹部大動脈瘤は通常、身体診察、腹部超音波検査、またはCTスキャンによって診断される。腹部単純X線写真では、動脈瘤の壁が石灰化している場合、動脈瘤の輪郭を示すことがある。しかし、動脈瘤の輪郭がX線で確認できるのは全体の半数以下である。超音波検査は動脈瘤をスクリーニングし、存在する場合はその大きさを決定するために用いられる。さらに、遊離腹水も検出できる。超音波検査は非侵襲的で高感度であるが、腸内ガスや肥満の存在によってその有用性が制限されることがある。CTスキャンは動脈瘤に対する感度がほぼ100％であり、解剖学的構造および血管内修復の可能性を詳述する術前計画にも有用である。破裂が疑われる場合には、後腹膜液も確実に検出できる。動脈瘤を描出する方法としては、MRIや血管造影などがあるが、あまり用いられていない。

An abdominal aortic aneurysm is usually diagnosed by physical exam, abdominal ultrasound, or CT scan. Plain abdominal radiographs may show the outline of an aneurysm when its walls are calcified. However, the outline will be visible by X-ray in less than half of all aneurysms. Ultrasonography is used to screen for aneurysms and to determine their size if present. Additionally, free peritoneal fluid can be detected. It is noninvasive and sensitive, but the presence of bowel gas or obesity may limit its usefulness. CT scan has nearly 100% sensitivity for an aneurysm and is also useful in preoperative planning, detailing the anatomy and possibility for endovascular repair. In the case of suspected rupture, it can also reliably detect retroperitoneal fluid. Alternative less often used methods for visualization of an aneurysm include MRI and angiography.

その結果、ピーク壁応力（PWS）[30]、平均壁応力（MWS）[31]、およびピーク壁破裂リスク（PWRR）[32]は、AAA破裂リスクを評価するための直径よりも信頼性の高いパラメータであることが判明している。医療用ソフトウェアでは、標準的な臨床CTデータからこれらの破裂リスク指標を計算することができ、患者固有のAAA破裂リスク診断が可能である[33][34][35]。この種の生体力学的アプローチは、AAA破裂の部位を正確に予測することが示されている[34][35][36]。

An aneurysm ruptures if the mechanical stress (tension per area) exceeds the local wall strength; consequently, peak wall stress (PWS),[31] mean wall stress (MWS),[32] and peak wall rupture risk (PWRR)[33] have been found to be more reliable parameters than diameter to assess AAA rupture risk. Medical software allows computing these rupture risk indices from standard clinical CT data and provides a patient-specific AAA rupture risk diagnosis.[34][35][36] This type of biomechanical approach has been shown to accurately predict the location of AAA rupture.[35][36][37]

分類
外部リソース
（英語）
  • Ultrasound showing a previously repaired AAA that is leaking with flow around the graft[39]

Classification

[編集]
Size classification
Ectatic or

mild dilatation 		>2.0 cm and <3.0 cm[40]
Moderate 3.0 - 5.0 cm[40]
Large or severe >5.0[40] or 5.5[41] cm

腹部大動脈瘤は、その大きさと症状によって一般的に分けられている。動脈瘤は通常、大動脈の外径が3cm以上（大動脈の正常径は2cm前後）[41]、または正常径の50％以上と定義される[42]。 外径が5.5cmを超える場合、動脈瘤は大きいと考えられる[40]。60歳以上で虚脱、原因不明の低血圧、突然発症する背部痛や腹痛を経験した場合は、破裂したAAAを疑うべきである。腹痛、ショック、拍動性の腫瘤がみられるのは少数例である。 動脈瘤がわかっている不安定な人は、さらなる画像診断を行わずに手術を受けることがあるが、診断は通常、CTまたは超音波検査で確認される。

Abdominal aortic aneurysms are commonly divided according to their size and symptomatology. An aneurysm is usually defined as an outer aortic diameter over 3 cm (normal diameter of the aorta is around 2 cm),[42] or more than 50% of normal diameter.[43] If the outer diameter exceeds 5.5 cm, the aneurysm is considered to be large.[41] Ruptured AAA should be suspected in any person older than 60 who experiences collapse, unexplained low blood pressure, or sudden-onset back or abdominal pain. Abdominal pain, shock, and a pulsatile mass is only present in a minority of cases. Although an unstable person with a known aneurysm may undergo surgery without further imaging, the diagnosis will usually be confirmed using CT or ultrasound scanning.

The suprarenal aorta normally measures about 0.5 cm larger than the infrarenal aorta.[44]

Differential diagnosis

[編集]

Aortic aneurysm rupture may be mistaken for the pain of kidney stones, or muscle related back pain.[6]

Prevention

[編集]

Screening

[編集]

The U.S. Preventive Services Task Force (USPSTF) recommends a single screening abdominal ultrasound for abdominal aortic aneurysm in males age 65 to 75 years who have a history of smoking.[45] Among this group who does not smoke, screening may be selective.[45] It is unclear if screening is useful in women who have smoked and the USPSTF recommend against screening in women who have never smoked.[7][46]

In the United Kingdom the NHS AAA Screening Programme invites men in England for screening during the year they turn 65. Men over 65 can contact the programme to arrange to be screened.[47]

In Sweden one time screening is recommended in all males over 65 years of age.[1][8] This has been found to decrease the risk of death from AAA by 42% with a number needed to screen of just over 200.[46] In those with a close relative diagnosed with an aortic aneurysm, Swedish guidelines recommend an ultrasound at around 60 years of age.[48]

Australia has no guideline on screening.[49]

Repeat ultrasounds should be carried out in those who have an aortic size greater than 3.0 cm.[50] In those whose aorta is between 3.0 and 3.9 cm this should be every three years, if between 4.0 and 4.4 cm every two years, and if between 4.5 and 5.4 cm every year.[50]

Management

[編集]

The treatment options for asymptomatic AAA are conservative management, surveillance with a view to eventual repair, and immediate repair. Two modes of repair are available for an AAA: open aneurysm repair, and endovascular aneurysm repair (EVAR). An intervention is often recommended if the aneurysm grows more than 1 cm per year or it is bigger than 5.5 cm.[51] Repair is also indicated for symptomatic aneurysms. Ten years after open AAA repair, the overall survival rate was 59%.[52] Mycotic abdominal aorta aneurysm (MAAA) is a rare and life-threatening condition. Because of its rarity, there is a lack of adequately powered studies and consensus on its treatment and follow up. A management protocol on the management of mycotic abdominal aortic aneurysm was recently published in the Annals of Vascular Surgery by Premnath et al.[53]

Conservative

[編集]

Conservative management is indicated in people where repair carries a high risk of mortality and in patients where repair is unlikely to improve life expectancy. The mainstay of the conservative treatment is smoking cessation.[要出典]

Surveillance is indicated in small asymptomatic aneurysms (less than 5.5 cm) where the risk of repair exceeds the risk of rupture.[51] As an AAA grows in diameter, the risk of rupture increases. Surveillance until an aneurysm has reached a diameter of 5.5 cm has not been shown to have a higher risk as compared to early intervention.[54][55]

Medication

[編集]

No medical therapy has been found to be effective at decreasing the growth rate or rupture rate of asymptomatic AAAs.[1] Blood pressure and lipids should, however, be treated per usual.[42]

Surgery

[編集]

The threshold for repair varies slightly from individual to individual, depending on the balance of risks and benefits when considering repair versus ongoing surveillance. The size of an individual's native aorta may influence this, along with the presence of comorbidities that increase operative risk or decrease life expectancy. Evidence, however, does not usually support repair if the size is less than 5.5 cm.[51]

Open repair

[編集]

Template:Vascular diseases開腹修復術は、若年患者や、成長期、症候性動脈瘤や破裂した大きな動脈瘤に適用される。修復中は大動脈をクランプしなければならず、腹部臓器や脊髄の一部への血液が遮断されるため、さまざまな合併症を引き起こす可能性がある。これはさまざまな合併症を引き起こす可能性がある。手術の重要な部分を素早く行うことが不可欠であるため、切開は通常、最も早く修復できるように十分な大きさに行われる。AAA開腹手術後の回復にはかなりの時間がかかる。最低でも集中治療室で数日、合計で1週間入院し、完全に回復するまでには数カ月かかる。

Abdominal aortic endoprosthesis, CT scan, original aneurysm marked in blue

血管内修復術は1990年代に初めて実用化され、現在では開腹修復術の代替術として確立しているが、その役割はまだ明確に定義されていない。血管内修復術は一般に、高齢でリスクの高い患者や開腹修復に適さない患者に適応される。しかし、血管内修復が可能なのは動脈瘤の形態によってはAAAsの一部に限られる。開腹手術と比較した主な利点は、周術期死亡率が低いこと、集中治療室での治療期間が短いこと、入院期間が短いこと、通常の活動への復帰が早いことである。血管内修復術の不利な点としては、病院での継続的な検査がより頻繁に必要となること、さらに必要な処置が増える可能性が高くなることなどが挙げられる。最新の研究によると、EVAR手技は開腹手術と比較して、動脈瘤関連死亡率は低いものの、全生存期間や健康関連QOLの点で利点はない [55][56][57][58] 。

Endovascular repair first became practical in the 1990s and although it is now an established alternative to open repair, its role is yet to be clearly defined. It is generally indicated in older, high-risk patients or patients unfit for open repair. However, endovascular repair is feasible for only a portion 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 hospital overall and earlier return to normal activity. Disadvantages of endovascular repair include a requirement for more frequent ongoing hospital reviews and a higher chance of further required procedures. According to the latest studies, the EVAR procedure does not offer any benefit for overall survival or health-related quality of life compared to open surgery, although aneurysm-related mortality is lower.[56][57][58][59]

開腹修復に適さない患者では、EVARと保存的管理の併用は、保存的管理単独と比較して、有益性がなく、合併症が多く、その後の処置や費用が高くなることと関連していた[59]。 大動脈吻合部再建後の傍吻合部動脈瘤に対する血管内治療も可能性がある[60]。 2017年のコクランレビューでは、破裂したAAAに対する血管内修復と開腹修復の転帰に最初の1ヵ月間は差がないという暫定的なエビデンスが見出された[61]。


In patients unfit for open repair, EVAR plus conservative management was associated with no benefit, more complications, subsequent procedures and higher costs compared to conservative management alone.[60] Endovascular treatment for paraanastomotic aneurysms after aortobiiliac reconstruction is also a possibility.[61] A 2017 Cochrane review found tentative evidence of no difference in outcomes between endovascular and open repair of ruptured AAA in the first month.[62]

Rupture

[編集]

In those with aortic rupture of the AAA, treatment is immediate surgical repair. There appear to be benefits to allowing permissive hypotension and limiting the use of intravenous fluids during transport to the operating room.[63]

Prognosis

[編集]
AAA Size (cm) Growth rate (cm/yr)[64] Annual rupture risk (%)[65]
3.0–3.9 0.39 0
4.0–4.9 0.36 0.5–5
5.0–5.9 0.43 3–15
6.0–6.9 0.64 10–20
>=7.0 - 20–50

Although the current standard of determining rupture risk is based on maximum diameter, it is known that smaller AAAs that fall below this threshold (diameter<5.5 cm) may also rupture, and larger AAAs (diameter>5.5 cm) may remain stable.[66][67] In one report, it was shown that 10–24% of ruptured AAAs were less than 5 cm in diameter.[67] It has also been reported that of 473 non-repaired AAAs examined from autopsy reports, there were 118 cases of rupture, 13% of which were less than 5 cm in diameter. This study also showed that 60% of the AAAs greater than 5 cm (including 54% of those AAAs between 7.1 and 10 cm) never experienced rupture.[68] Vorp et al. later deduced from the findings of Darling et al. that if the maximum diameter criterion were followed for the 473 subjects, only 7% (34/473) of cases would have died from rupture prior to surgical intervention as the diameter was less than 5 cm, with 25% (116/473) of cases possibly undergoing unnecessary surgery since these AAAs may never have ruptured.[68]

Alternative methods of rupture assessment have been recently reported. The majority of these approaches involve 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 have been shown to correlate to the overall geometry of the AAA rather than solely to the maximum diameter.[69][70][71] It is also known that wall stress alone does not completely govern failure as an AAA will usually rupture when the wall stress exceeds the wall strength. In light of this, rupture assessment may be more accurate if both the patient-specific wall stress is coupled together with patient-specific wall strength. A noninvasive method of determining patient-dependent wall strength was recently reported,[72] with more traditional approaches to strength determination via tensile testing performed by other researchers in the field.[73][74][75] Some of the more recently proposed AAA rupture-risk assessment methods include: AAA wall stress;[31][76][77] AAA expansion rate;[78] degree of asymmetry;[71] presence of intraluminal thrombus (ILT);[79] a rupture potential index (RPI);[80][81] a finite element analysis rupture index (FEARI);[82] biomechanical factors coupled with computer analysis;[83] growth of ILT;[84] geometrical parameters of the AAA;[85] and also a method of determining AAA growth and rupture based on mathematical models.[86][87]

The postoperative mortality for an already ruptured AAA has slowly decreased over several decades but remains higher than 40%.[88] However, if the AAA is surgically repaired before rupture, the postoperative mortality rate is substantially lower, approximately 1-6%.[89]

Epidemiology

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The occurrence of AAA varies by ethnicity. In the United Kingdom, the rate of AAA in Caucasian men older than 65 years is about 4.7%, while in Asian men it is 0.45%.[90] It is also less common in individuals of African, and Hispanic heritage.[1] They occur four times more often in men than in women.[1]

There are at least 13,000 deaths yearly in the U.S. secondary to AAA rupture.[1] The peak number of new cases per year among males is around 70 years of age, and the percentage of males affected over 60 years is 2–6%. The frequency is much higher in smokers than in non-smokers (8:1), and the risk decreases slowly after smoking cessation.[91] In the U.S., the incidence of AAA is 2–4% in the adult population.[17]

Rupture of the AAA occurs in 1–3% of men aged 65 or more, for whom the mortality rate is 70–95%.[41]

History

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The first historical records about AAA are from Ancient Rome in the 2nd century AD, when Greek surgeon Antyllus tried to treat the AAA with proximal and distal ligature, central incision and removal of thrombotic material from the aneurysm. 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.[92] Other methods that were successful in treating the AAA included wrapping the aorta with polyethene cellophane, which induced fibrosis and restricted the growth of the aneurysm. Endovascular aneurysm 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.[93]

Society and culture

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Theoretical physicist Albert Einstein underwent an operation for an abdominal aortic aneurysm in 1949 that was performed by Rudolph Nissen, who wrapped the aorta with polyethene cellophane. Einstein's aneurysm ruptured on April 13, 1955. He declined surgery, saying, "I want to go when I want. It is tasteless to prolong life artificially. I have done my share, it is time to go. I will do it elegantly." He died five days later at age 76.[94]

Actress Lucille Ball died April 26, 1989, from an abdominal aortic aneurysm. At the time of her death, she was in Cedars-Sinai Medical Center recovering from emergency surgery performed just six days earlier because of a dissecting aortic aneurysm near her heart. Ball was at increased risk as she had been a heavy smoker for decades.[95]

Musician Conway Twitty died in June 1993 from an abdominal aortic aneurysm at the age of 59, two months before the release of what would be his final studio album, Final Touches.[要出典]

Actor George C. Scott died in 1999 from a ruptured abdominal aortic aneurysm at age 71.[要出典]

In 2001, former presidential candidate Bob Dole underwent surgery for an abdominal aortic aneurysm in which a team led by vascular surgeon Kenneth Ouriel inserted a stent graft:[15]

「 Ouriel said that the team inserted a Y-shaped tube through an incision in Dole's leg and placed it inside the weakened portion of the aorta. The aneurysm will eventually contract around the stent, which will remain in place for the rest of Dole's life.[15] 」

— Associated Press

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

Actor Tommy Ford died of abdominal aneurysm in October 2016 at 52 years old.[96]

Gary Gygax, co-creator of Dungeons and Dragons, died in 2008 from an abdominal aortic aneurysm at the age of 69.

Research

[編集]

Risk assessment

[編集]

There 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 diameter approach. Numerical modeling is a valuable tool to researchers allowing approximate wall stresses to be calculated, thus revealing the rupture potential of a particular aneurysm. Experimental models are required to validate these numerical results and provide a further insight into the biomechanical behavior of the AAA. In vivo, AAAs exhibit a varying range of material strengths[97] from localised weak hypoxic regions[98] to much stronger regions and areas of calcifications.[99]

Finding ways to predict future AAA growth is seen as a research priority.[100]

Another related line of research is utilizing mathematical decision modeling (e.g., Markov decision processes) to determine improved treatment policies. Initial results suggest that a more dynamic policy could provide benefits, although such claims have not been clinically verified.[101][102]A study recently showed that aneurysms can be accurately predicted as to whether they are stable (lacking repair or intervention), requiring repair, or at risk of rupture from scans years prior to any event based on a machine-learning based classification tool.[103]

Experimental models

[編集]

Experimental 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.[104] Work has also focused 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.[105] These rubber models can also be used in a variety of experimental situations, from stress analysis using the photoelastic method[106] New endovascular devices are being developed that are able to treat more complex and tortuous anatomies.[107]

Prevention and treatment

[編集]

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

Other recent research identified Granzyme B (GZMB) (a protein-degrading enzyme) to be a potential target in the treatment of abdominal aortic aneurysms. Elimination of this enzyme in mice models both slowed the progression of aneurysms and improved survival.[108][109]

Preclinical Research

[編集]

The mechanisms that lead to AAA development are still not completely understood at a cellular and molecular level. In order to better understand the pathophysiology of AAA, it is often necessary to use experimental animal models. It is often questioned how well do these models translate to human disease. Even though there is no animal model that exactly represents the human condition, all the existing ones focus on one different pathophysiological aspect of the disease. Combining the results from different animal models with clinical research can provide a better overview of the AAA pathophysiology. The most common animal models are rodents (mice and rats), although for certain studies, such as testing preclinical devices or surgical procedures, large animal models (pig, sheep) are more frequently used. The rodent models of AAA can be classified according to different aspects. There are dissecting models vs non-dissecting models and genetically determined models vs chemically induced models. The most commonly used models are the angiotensin-II infusion into ApoE knockout mice (dissecting model, chemically induced), the calcium chloride model (non-dissecting, chemically induced) and the elastase model (non-dissecting, chemically induced model).[110][111] A recent study has shown that β-Aminopropionitrile plus elastase application to abdominal aorta causes more severe aneurysm in mice as compared to elastase alone.[112]

References

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[編集]
分類
外部リソース
（英語）

[[Category:男性の健康]] [[Category:医療翻訳プロジェクト]] [[Category:血管外科学]] [[Category:未査読の翻訳があるページ]]

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