Abdominal Aortic Aneurysm: Evolving Controversies and Uncertainties

Abstract

Abdominal aortic aneurysm (AAA) is defined as a permanent dilatation of the abdominal aorta that exceeds 3 cm. Most AAAs arise in the portion of abdominal aorta distal to the renal arteries and are defined as infrarenal. Most AAAs are totally asymptomatic until catastrophic rupture. The strongest predictor of AAA rupture is the diameter. Surgery is indicated to prevent rupture when the risk of rupture exceeds the risk of surgery. In this review, we aim to analyze this disease comprehensively, starting from an epidemiological perspective, exploring etiology and pathophysiology, and concluding with surgical controversies. We will pursue these goals by addressing eight specific questions regarding AAA: (1) Is the incidence of AAA increasing? (2) Are ultrasound screening programs for AAA effective? (3) What causes AAA: Genes versus environment? (4) Animal models: Are they really relevant? (5) What pathophysiology leads to AAA? (6) Indications for AAA surgery: Are surgeons over-eager to operate? (7) Elective AAA repair: Open or endovascular? (8) Emergency AAA repair: Open or endovascular?

Keywords: AAA; abdominal aortic aneurysm; animal models; endovascular aortic repair; indication for AAA surgery; risk factors; rupture AAA.

Fig. 1

Prevalence of abdominal aortic aneurysm according to age and gender in 6,836 men and women aged 25 to 83 years analyzed in 1994 to 1995 in the city of Tromsø, Norway. Note the sharp rise of the prevalence in men after 60 years of age. (Reproduced with permission from Singh et al. 255 ).

Fig. 2

( A ) Linear correlation between number of cigarettes smoked and AAA mortality in the United States. (Reproduced with permission from Lederle. 45 ) ( B ) Historical and contemporary AAA prevalence rates compared with time trends in smoking in the Swedish population. Again, a linear correlation between smoking and AAA prevalence is evident. (Reproduced with permission from Svensjö et al. 256 ) AAA, abdominal aortic aneurysm.

Fig. 3

Linear regression revealing the positive association between temporal trends in (A) male and (B) female mean systolic blood pressure and AAA mortality. (Reproduced with permission from Sidloff et al. 54 ) AAA, abdominal aortic aneurysm.

Fig. 4

( A ) Isolation of the aorta from the left renal vein to the bifurcation. ( B ) A 5-minute type 1 porcine pancreatic elastase infusion at a pressure of 100 mm Hg for 5 minutes. ( C ) Incision is closed with a single suture and blood flow is re-established. ( D ) Aneurysm is formed 14 days after elastase infusion. (Reproduced with permission from Lysgaard Poulsen et al. 125 )

Fig. 5

Suprarenal AAA 4 weeks after Ang-II infusion in the apoE ^–/– mouse; note hemorrhage into the wall in the macroscopic (upper, arrow) and H&E section (lower; arrow). (Reproduced with permission from Gertz et al. 132 ) AAA, abdominal aortic aneurysm; Ang-II, angiotensin-II; H&E, hematoxylin and eosin.

Fig. 6

Kaplan–Meier's method to estimate all-cause mortality and AAA-related mortality in patient unfit for open surgery treated with EVAR or with no intervention. EVAR does not offer benefit in survival respect, no intervention in patient deemed unfit for open surgery. (Reproduced with permission from EVAR trial participants. 192 ) AAA, abdominal aortic aneurysm; EVAR, endovascular aortic repair.

Fig. 7

Kaplan–Meier's method to estimate survival from any cause and AAA-related survival in the very long-term follow-up in the EVAR I trial. In the first 2 years, EVAR gives an advantage in survivals, but this advantage is lost after 2 years of follow-up and after 12 years, the open repair offers an advantage in survival. (Reproduced with permission from Patel et al. 209 ) AAA, abdominal aortic aneurysm; EVAR, endovascular aortic repair.

Fig. 8

Kaplan–Meir's survival in patients with ruptured AAA treated with EVAR or open surgery. No significant difference is seen at 30, 90 days, and after 1 year of follow-up. (Reproduced with permission from IMPROVE Trial Investigators. 228 ) AAA, abdominal aortic aneurysm; EVAR, endovascular aortic repair.

Fig. 9

Abdominal aortic aneurysm: from the development to management. Smoking, family history, aging, male sex, and hypertension are the main risk factors for AAA development. VSMC apoptosis, inflammation, and proteolysis are the molecular mechanism that causes AAA. When the risk of rupture exceeds the risk of surgery, there are two options: EVAR and open surgery. (Portions of this figure are modified from Kent and Davis FM, Rateri DL, Daugherty A. Mechanisms of aortic aneurysm formation: translating preclinical studies into clinical therapies. Heart 2014;100:1498–1505.) AAA, abdominal aortic aneurysm; EVAR, endovascular aortic repair.