Intermediate Pressure-Normalized Strain Values Are Associated With Increased Abdominal Aortic Aneurysmal Growth Rates

Abstract

Current abdominal aortic aneurysm (AAA) assessment methods rely on simple morphometric analysis of the AAA diameter and growth rate. However, evidence has shown that AAA pathology varies among patients, and morphometric analysis alone is insufficient to predict individual risk of growth. Biomechanical parameters, such as pressure-normalized aortic wall strain (εp+/PP), can provide a surrogate to vessel wall stiffness. We aimed to use our novel ultrasound elastography (USE) technique to measure ερ+/PP and correlate ερ+/PP with maximal AAA diameter and growth rate in the largest clinical trial to date. Our USE algorithm uses a finite element mesh overlayed on a 2D axial view of the user-defined AAA wall at the point of maximum diameter to track frame-to-frame displacements over a full cardiac cycle to measure ερ+/PP. ερ+/PP and growth rate were assessed between small and large AAAs based on a diameter of ≥5 cm. Patients with AAA were then separated into terciles based on ερ+/PP values of 0.0251 and 0.038 to assess differences in the AAA diameter and growth rate. Mann-Whitney U and Kruskal-Wallis tests were used to assess differences as appropriate. USE analysis was conducted on 127 patients, 16 normal aortas and 111 AAAs. A total of 79 patients had at least one follow-up clinical scan used to calculate growth rate. Of the 111 aortas, 85 were classified as small and 26 as large. AAAs showed lower ερ+/PP (stiffer) compared with nonaneurysmal aortas (0.034 ± 0.017 vs 0.044 ± 0.015 %/kPa; P = .006). There was no difference in ερ+/PP or growth rate between small and large AAAs. When divided into terciles based on ερ+/PP, there was no difference in the AAA diameter. There was a statistically significant difference in growth rate between the intermediate tercile and the outer terciles (1.46 ± 2.48 vs 3.59 ± 3.83 vs 1.78 ± 1.64 mm/y; P = .014) (Fig). Our validated USE algorithm shows that AAAs are stiffer than nonaneurysmal aortas, similar to previous reports. There was no correlation between AAA diameter and ερ+/PP, indicating that AAA stiffness is independent of diameter, and diameter thresholds alone may not accurately assess future risk of growth. AAAs in the intermediate tercile of ερ+/PP values were found to have greater growth rates than the outer tercile, indicating that an intermediate range of ερ+/PP values, regardless of diameter, place patients at increased risk for AAA growth. These findings also suggest that AAA growth may be related to a failure of collagen remodeling and may be the underlying event that leads to AAA rupture.