Abstract：
UNASSIGNED: Most abdominal aortic aneurysms (AAAs) are small with low rupture risk (<1%/y) when diagnosed but slowly expand to ≥55 mm and undergo surgical repair. Patients and clinicians require medications to limit AAA growth and rupture, but drugs effective in animal models have not translated to patients.
UNASSIGNED: Use models that simulate human AAA tissue pathology, growth patterns, and rupture; focus on the clinically relevant outcomes of growth and rupture; design studies with the rigor required of human clinical trials; monitor AAA growth using reproducible ultrasound; and perform studies in both males and females.
UNASSIGNED: The aortic adventitial elastase oral β-aminopropionitrile model has many strengths including simulating human AAA pathology and modeling prolonged aneurysm growth. The Ang II (angiotensin II) model performed less well as it better simulates acute aortic syndrome than AAA. The elastase plus TGFβ (transforming growth factor-β) blocking antibody model displays a high rupture rate, making prolonged monitoring of AAA growth not feasible. The elastase perfusion and calcium chloride models both display limited AAA growth.
UNASSIGNED: Use models that simulate human AAA tissue pathology, growth patterns, and rupture; focus on the clinically relevant outcomes of growth and rupture; design studies with the rigor required of human clinical trials; monitor AAA growth using reproducible ultrasound; and perform studies in both males and females.
UNASSIGNED: The aortic adventitial elastase oral β-aminopropionitrile model has many strengths including simulating human AAA pathology and modeling prolonged aneurysm growth. The Ang II (angiotensin II) model performed less well as it better simulates acute aortic syndrome than AAA. The elastase plus TGFβ (transforming growth factor-β) blocking antibody model displays a high rupture rate, making prolonged monitoring of AAA growth not feasible. The elastase perfusion and calcium chloride models both display limited AAA growth.
摘要：
■大多数腹主动脉瘤（AAAs）在诊断时很小，破裂风险低（<1％/y），但缓慢扩张至≥55mm并接受手术修复。患者和临床医生需要药物来限制AAA的生长和破裂，但是在动物模型中有效的药物尚未转化为患者。
■使用模拟人类AAA组织病理学的模型，增长模式，和破裂;专注于生长和破裂的临床相关结果;设计具有人体临床试验所需的严格性的研究;使用可重复超声监测AAA生长;并在男性和女性中进行研究。
■主动脉外膜弹性蛋白酶口服β-氨基丙腈模型具有许多优点，包括模拟人类AAA病理学和建模延长的动脉瘤生长。AngII（血管紧张素II）模型的表现较差，因为它比AAA更好地模拟急性主动脉综合征。弹性蛋白酶加TGFβ（转化生长因子-β）阻断抗体模型显示出较高的破裂率，使得长期监测AAA增长不可行。弹性蛋白酶灌注和氯化钙模型均显示出有限的AAA生长。
■使用模拟人类AAA组织病理学的模型，增长模式，和破裂;专注于生长和破裂的临床相关结果;设计具有人体临床试验所需的严格性的研究;使用可重复超声监测AAA生长;并在男性和女性中进行研究。
■主动脉外膜弹性蛋白酶口服β-氨基丙腈模型具有许多优点，包括模拟人类AAA病理学和建模延长的动脉瘤生长。AngII（血管紧张素II）模型的表现较差，因为它比AAA更好地模拟急性主动脉综合征。弹性蛋白酶加TGFβ（转化生长因子-β）阻断抗体模型显示出较高的破裂率，使得长期监测AAA增长不可行。弹性蛋白酶灌注和氯化钙模型均显示出有限的AAA生长。
