Estimates of rupture risk are imprecise because large numbers of patients with AAAs have not been followed without intervention. Studies conducted before the widespread application of surgical repair documented the likelihood that large AAAs would rupture. Contemporary reports have necessarily focused on the natural history of small AAAs, because larger ones are nearly always repaired when detected. Unfortunately, there are still insufficient data to develop an accurate prediction of the risk of rupture for AAA in a particular patient, which makes surgical decision making somewhat difficult. However, knowledge of available natural history data can assist these decisions.

From a hemodynamic perspective, AAA rupture occurs when the forces acting on the wall of an AAA exceed the wall-bursting strength. Laplace law indicates that the wall tension of an ideal cylinder is directly proportional to its radius and intraluminal pressure and inversely proportional to wall thickness. AAAs in humans are not ideal cylinders and have wall thickness of variable strength. Theoretically, however, Laplace law predicts that larger AAA diameter and hypertension should increase wall tension and thus increase rupture risk. Decreasing wall thickness (or strength), while difficult to measure clinically, should also theoretically increase the probability of rupture.

The simple observation that not all AAAs rupture at a specific diameter indicates that other patient-specific and aneurysm-specific variables must also influence rupture. Several studies have employed multivariate analysis to examine the predictive value of various clinical parameters on AAA rupture risk. The UK Small Aneurysm Trialists followed 2,257 patients over the 7-year period of the trial, including 1,090 randomized patients and an additional 1,167 patients who were ineligible for randomization. There were 103 documented ruptures. Predictors of rupture using proportional hazards modeling (adjusted hazard ratio in parentheses) were: female gender (3.0), initial AAA diameter (2.9 per cm), smoking status (never smokers 0.65, former smokers 0.59-both vs. current smokers), mean blood pressure (1.02 per mmHg), and FEV₁ (0.62 per L). The mean diameter for ruptures was 1 cm lower for women (5 cm) than it was for men (6 cm). This analysis confirmed early work by Cronenwett et al., who determined that larger initial AAA diameter, hypertension, and chronic obstructive pulmonary
disease (COPD) were independent predictors of rupture. By comparing patients with ruptured and intact AAAs at autopsy, Sterpetti et al. also concluded that larger initial AAA size, hypertension, and bronchiectasis were independently associated with AAA rupture. Patients with ruptured AAAs had significantly larger aneurysms (8.0 vs. 5.1 cm), more frequently had hypertension (54% vs. 28%), and more frequently had both emphysema (67% vs. 42%) and bronchiectasis (29% vs. 15%). In a review of 75 patients with AAAs managed nonoperatively, Foster et al. noted that death from rupture occurred in 72% of patients with diastolic hypertension, but in only 30% of the entire group. Among 156 patients with AAAs managed nonoperatively, Szilagyi et al. found that hypertension (>150/100 mmHg) was present in 67% of patients who experienced rupture, but in only 23% of those without rupture. Thus, in addition to AAA size, these reports strongly implicate hypertension, chronic pulmonary disease, female gender, and current smoking status as important risk factors for AAA rupture. The explanation for a causative role of hypertension is straightforward, based on Laplace law. The UK Trial was the first to demonstrate that smoking status, in addition to chronic pulmonary disease, indendently predicts rupture. This study prospectively measured pulmonary disease with the FEV₁, and documented smoking status with both self-reported status and serum cotinine (a nicotine breakdown product with a plasma half-life of 16 hours). This study suggests that smoking has a two-tiered effect in that FEV₁, which is likely a measure of duration and quantity of smoking, is related to rupture; also, current smokers were more likely to rupture than former smokers, even after adjusting for the FEV₁. Perhaps not surprisingly, the UK Trialists found that serum cotinine was a better predictor of rupture than was self-reported smoking status. Many clinicians consider the ratio of the aneurysm diameter to the adjacent normal aorta to be important in determining rupture risk. Women are known to have smaller aortas than men. Intuitively, a 4-cm AAA in a small woman with a 1.5-cm-diameter native aorta would be at greater rupture risk than a comparable 4-cm AAA in a large man with a native aortic diameter of 2.5 cm. The validity of this concept, however, has not been proven. Ouriel et al. have suggested that a relative comparison between aortic diameter and the diameter of the third lumbar vertebra may increase the accuracy for predicting rupture risk, by adjusting for differences in body size. The improvement in prediction potential was minimal, however, when compared with absolute AAA diameter and the relative risk of gender.

Although a positive family history of AAA is known to increase the prevalence of AAAs in other first-degree relatives (FDRs) it also appears that familial AAAs have a higher rupture risk. Darling et al. reported that the frequency of ruptured AAAs increased with the number of FDRs who have AAAs: 15% with 2 FDRs, 29% with 3 FDRs, and 36% with ≥4 FDRs. Women with familial aneurysms were more likely (30%) to present with rupture than men with familial AAAs (17%). Verloes et al. found that the rupture rate was 32% in patients with familial vs. 9% in patients with sporadic aneurysms, and that familial AAAs ruptured 10 years earlier (65 vs. 75 years of age). These observations suggest that patients with a strong family history of AAA may have an individually higher risk of rupture, especially if they are female. However, these studies did not consider other potentially confounding factors, such as AAA size, which might have been different in the familial group. Thus, further epidemiologic research is required to determine whether a positive family history is an independent risk factor for AAA rupture in addition to a risk factor for increased AAA prevalence.

Although rapid AAA expansion is presumed to increase rupture risk, it is difficult to separate this effect from the influence of expansion rate on absolute diameter, which alone could increase rupture risk. Two studies have reported that expansion rate was larger in ruptured than intact AAAs, but these ruptured AAAs were also larger. Other studies have found that absolute AAA diameter, rather than expansion rate, predicted rupture. One study of patients with thoracoabdominal aneurysms demonstrated that not only initial diameter, but more importantly subsequent expansion rate, were independent predictors of rupture. One recent study by Hatakeyama with 7 ruptures in 39 patients examined with serial 3-D computed tomography (CT) scans found expansion rate to be a predictor of rupture. However, Sharp and Collin recently reported 32 patients with AAA diameter expansion of 0.5 cm or more in 6 months, but still with maximum diameter <5.5 cm, who did not undergo surgery and who did not experience ruptures. Sharp and Collin noted that many patients had apparent negative expansion either directly before or after the episode of rapid expansion, which suggests that one or more of the measured diameters (all measured with ultrasound) may have been erroneous. They also noted that rapid expansion was sustained in only 11% of their patients and that the majority had expansion rates that regressed toward the population average. Thus, although far from being proven, rapid AAA expansion is frequently regarded as a risk factor for rupture and is often used as a criterion for elective repair of small AAAs. However, it would appear prudent to confirm rapid expansion with CT or magnetic resonance imaging (MRI) prior to recommending surgery for this indication alone.