Journal of Vascular Surgery
Volume 43, Issue 3 , Pages 570-576, March 2006

Biomechanical properties of ruptured versus electively repaired abdominal aortic aneurysm wall tissue

  • Elena S. Di Martino, PhD

      Affiliations

    • Department of Surgery, University of Pittsburgh, Pittsburgh, PA
    • Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA
    • McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA
    • ,
  • Ajay Bohra, MS

      Affiliations

    • Department of Surgery, University of Pittsburgh, Pittsburgh, PA
    • ,
  • Jonathan P. Vande Geest, BS

      Affiliations

    • Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA
    • ,
  • Navyash Gupta, MD

      Affiliations

    • Department of Surgery, University of Pittsburgh, Pittsburgh, PA
    • ,
  • Michel S. Makaroun, MD

      Affiliations

    • Department of Surgery, University of Pittsburgh, Pittsburgh, PA
    • ,
  • David A. Vorp, PhD

      Affiliations

    • Department of Surgery, University of Pittsburgh, Pittsburgh, PA
    • Department of Bioengineering, University of Pittsburgh, Pittsburgh, PA
    • McGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA
    • Corresponding Author InformationReprint requests: David A. Vorp, PhD, University of Pittsburgh, Division of Vascular Surgery, Department of Surgery and Bioengineering, Vascular Bioengineering Research Laboratory, McGowan Institute for Regenerative Medicine, Suite 200, 100 Technology Dr, Pittsburgh, PA 15219

Received 3 July 2005; accepted 30 October 2005.

Article Outline

Objective

The purpose of this study was to evaluate and compare the biomechanical properties of abdominal aortic aneurysm (AAA) wall tissue from patients who experienced AAA rupture with that of those who received elective repair.

Methods

Rectangular, circumferentially oriented AAA wall specimens (approximately 2.5 cm × 7 mm) were obtained fresh from the operating room from patients undergoing surgical repair. The width and thickness were measured for each specimen by using a laser micrometer before testing to failure with a uniaxial tensile testing system. The force and deformation applied to each specimen were measured continuously during testing, and the data were converted to stress and stretch ratio. The tensile strength was taken as the peak stress obtained before specimen failure, and the distensibility was taken as the stretch ratio at failure. The maximum tangential modulus and average modulus were also computed according to the peak and average slope of the stress-stretch ratio curve.

Results

Twenty-six specimens were obtained from 16 patients (aged 73 ± 3 years [mean ± SEM]) undergoing elective repair of their AAA (diameter, 7.0 ± 0.5 cm). Thirteen specimens were resected from nine patients (aged 73 ± 3 years; P = not significant in comparison to the electively repaired AAAs) during repair of their ruptured AAA (diameter, 7.8 ± 0.6 cm; P = not significant). A significant difference was noted in wall thickness between ruptured and elective AAAs: 3.6 ± 0.3 mm vs 2.5 ± 0.1 mm, respectively (P < .001). The tensile strength of the ruptured tissue was found to be lower than that for the electively repaired tissue (54 ± 6 N/cm2 vs 82 ± 9.0 N/cm2; P = .04). Considering all specimens, no significant correlation was noted between tensile strength and diameter (R = −0.10; P = .55). Tensile strength, however, had a significant negative correlation with wall thickness (R = −0.42; P < .05) and a significant positive correlation with the tissue maximum tangential modulus (R = 0.76; P < .05).

Conclusions

Our data suggest that AAA rupture is associated with aortic wall weakening, but not with wall stiffening. A widely accepted indicator for risk of aneurysm rupture is the maximum transverse diameter. Our results suggest that AAA wall strength, in large aneurysms, is not related to the maximum transverse diameter. Rather, wall thickness or stiffness may be a better predictor of rupture for large AAAs.

Clinical Relevance

Rupture of an abdominal aortic aneurysm is a deadly event that carries an overall mortality of more than 70%. Nonetheless, there exists no reliable criterion to determine the severity of an aneurysm. The wall of an aneurysm progressively weakens as a result of discordant repair/remodeling mechanisms, which can lead to changes in the mechanical properties of the tissue. We demonstrate here that a decrease in stiffness and an increase in thickness of the tissue (both noninvasively measurable) correlate with a decreased strength. Therefore, we believe that an improved risk prediction criterion could be drawn from our data.

 

Abdominal aortic aneurysm (AAA) is a vascular pathology that occurs primarily in the elderly.1, 2 A recent study3 reported that mortality for ruptured AAA (rAAA) is 40% or more. Degradation of extracellular matrix proteins has been indicated as a leading factor in AAA progression and rupture.4, 5, 6, 7, 8, 9, 10, 11, 12, 13 Distinctive features of aortic wall pathology associated with AAA have been described, including upregulation of proteinase enzymes (notably matrix metalloproteinase [MMP]-1, -2, -3, and -9),9, 13, 14, 15 elastin and collagen fiber breakdown,4, 6, 16 loss of elastin content,17 and collagen degradation.9, 10, 13

Rupture of AAA represents a mechanical failure of the degenerated aortic wall that occurs when its structural integrity is unable to withstand the mechanical load caused by the intraluminal blood pressure. It has been suggested that elastin loss may cause the vessel to enlarge, whereas collagen degradation may initiate wall rupture.4, 18, 19 Furthermore, the concomitant action of different MMP enzymes is seemingly needed to achieve aneurysmal wall degradation.5, 19 Despite these recent studies, the exact mechanisms that cause rupture are still unknown.

In this study, we evaluated and compared the biomechanical properties of AAA wall tissue specimens obtained from patients who experienced AAA rupture with that of those who received elective repair. We looked at intrinsic properties of the aneurysm tissue by performing mechanical tests on harvested pieces with standard techniques used in material characterization.

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Materials and methods 

Human aortic tissue specimens 

All human aortic tissue specimens were obtained according to the guidelines of our institutional review board. Segments of AAA were obtained fresh from the operating room from patients undergoing surgical repair. The specimens were all taken from the same area located across the midline on the anterior surface of the aneurysm at the point of maximum diameter (Fig 1). The aneurysm diameter was recorded from patient charts as assessed from computed tomographic scans. No bias to AAA patient selection was made with respect to age or sex. All tissue specimens were placed in saline, refrigerated at 4°C, and tested within 48 hours of procurement.20 Age and sex as reported in the patient’s clinical chart were collected for all specimens.

Tensile testing 

Rectangular specimens (approximately 2.5 cm × 7 mm) were cut in the circumferential orientation with respect to the intact aorta. The specimen width and thickness were measured for each specimen in a noncontacting fashion with a laser micrometer (Beta LaserMike, Inc, Dayton, Ohio), and length was measured with a manual caliper. The tissue specimens were placed in a previously described uniaxial tensile testing system21 and continuously wetted with saline solution at 37°C. After a short thermal equilibration period, the specimen was stretched until failure (rupture) of the tissue was reached, as the force was measured continuously. Corresponding deformation was calculated from the known strain rate of 8.5%/min, data acquisition rate (1 Hz), and specimen length previously described.21 A representative stress-stretch curve obtained from the tensile tests is shown in Fig 2.

  • View full-size image.
  • Fig 2. 

    Stress-stretch curve for one generic tensile test. UTS, Ultimate tensile strength; TMmax, maximum tangential modulus; TM100, tangential modulus corresponding to a pressure of 100 mm Hg; UStr, ultimate stretch.

Data analysis 

The Cauchy stress was calculated as the applied force normalized by the deformed cross-sectional area, and stretch was calculated as the deformed length normalized by the original length of each specimen (see Raghavan et al21 for details). The maximum tangential modulus (TMmax) was taken as the maximum slope of each stress-stretch curve; the ultimate tensile strength (UTS) was taken as the peak stress obtained before specimen failure; and the ultimate stretch (UStr) was taken as the peak stretch ratio at failure (Fig 2). A custom routine written in Mathematica (version 5.0; Wolfram Research Inc, Champaign, IL) was used to calculate the average tissue tangential modulus (TMavg) as the average of all tangential moduli computed by using a fixed window size of data points on the stress-stretch curve. The ratio between the maximum and average tangential modulus was calculated for each curve (TMmax/TMavg) to provide a quantitative indication of the nonlinearity of the stress-stretch curve. That is, as the ratio approaches the value of 1.0, TMavg approaches a value equal to TMmax, thus indicating that the stress-stretch curve is close to linear. Conversely, if the ratio is much less than 1.0, the curve is highly nonlinear. In addition, another tangential modulus (TM100) was calculated at the stress predicted by the law of Laplace corresponding to a pressure of 100 mm Hg:

(1)
where P is pressure, D is the maximum diameter of that particular aorta and t is the undeformed thickness of the specimen. All parameters used in the statistical analysis are reported in Fig 2.

Statistical methods 

The statistical package SigmaStat 3.0 (SPSS Inc, Chicago, Ill) was used for statistical analysis. A multiple t test procedure was considered for the two groups of rAAA and elective AAA (eAAA) specimens. A total of eight t tests were performed to compare differences in age, diameter, wall thickness, UTS, UStr, TMmax, TMmax/TMavg, and TM100 between the two groups with a familywise significance level set to α = .05. As is standard practice in multiple testing, the appropriate significance level at which each of the planned tests was to be conducted was determined through the Bonferroni correction, and the value of significance level to be used in each test was set to α′ = α/8 = .006.

The χ2 test of statistical significance was used to test bivariate tables, such as the male vs female population of patients. Spearman rank order correlation coefficients were used to test correlations among all variables for all aneurysm specimens (AAAs and rAAAs).

To take into account the effect of harvesting multiple specimens from the same patient and to evaluate whether the results might change if only one value for each parameter was considered for each patient, all statistical analyses were performed by first considering all specimens tested and then averaging values from multiple specimens obtained from the same patient to yield one value per patient. Data are reported as mean ± SEM.

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Results 

Twenty-six eAAA specimens were obtained from 16 patients (aged 73 ± 3 years; AAA diameter, 7.0 ± 0.5 cm). Thirteen rAAA specimens were resected from nine patients (aged 72 ± 3 years; P = not significant; AAA diameter, 7.8 cm ± 0.5; P = not significant) during repair of their rAAA. Most AAA patients were male (12/16 [60%] for AAAs and 8/9 [80%] for rAAAs; χ2 = not significant), which is consistent with findings of other reported studies.22

A significant difference was noted in wall thickness between eAAA and rAAA: 2.5 ± 0.1 mm vs 3.6 ± 0.3 mm (P < .001; Table I, Table II). The tensile strength of the rAAA tissue was found to be lower than that for the eAAA group (54.2 ± 5.6 N/cm2 vs 82.9 ± 9.1 N/cm2, respectively; P = .04; Table II). However, when the Bonferroni correction for multiple tests was applied to the significance level and the corresponding α = .006 was used, the test was nonsignificant. No difference was noted between the two groups in terms of UStr (1.54 ± 0.04 vs 1.60 ± 0.09; P = .9). TMmax and TM100 were not significantly different between the two groups, although both were lower on average for the rAAA group (TMmax: 277 ± 36 N/cm2 for eAAA vs 202 ± 32 N/cm2 for rAAA, P = .19; TM100: 235 ± 22 N/cm2 for eAAA vs 214 ± 36 N/cm2 for rAAA; P = .6; Table II). Conversely, TMmax/TMavg was higher, on average, for the rAAA group. All comparisons were performed by averaging data from specimens obtained from the same patient to yield a single value for each patient, and the results showed no difference with respect to what was found by considering each specimen separately.

Table I. Parameters used in the statistical analysis
VariableDescription
AgeAge of the patient at the time of surgery
DiameterMaximum diameter of the aneurysm
Wall thicknessThickness of the sample
TMmaxMaximum slope of the stress-stretch curve (Fig 2)
TMmax/TMavgRatio between the maximum and average slope of the stress-stretch curve (indicates the nonlinearity of the stress-stretch curve: close to 1, linear; close to 0, nonlinear)
TM100Slope of the curve at the stretch corresponding to 100 mm Hg (Fig 2)
UTSUltimate stress value at rupture (Fig 2)
UStrUltimate stretch ratio at rupture (Fig 2)

TMmax, Maximum tangential modulus; TMavg, average tissue tangential modulus; TM100, tangential modulus corresponding to a pressure of 100 mm Hg; UTS, ultimate tensile strength; UStr, ultimate stretch.

Table II. Patient data and results for eAAA and rAAA specimens
VariableeAAA specimensrAAA specimensP value
Age (y)74±273±2.76
Diameter (cm)7.0±0.57.8±0.6.34
Wall thickness (mm)2.5±0.13.6±0.3<.001⁎†
TMmax (N/cm2)315±69202±32.27
TMmax/TMavg0.53±0.010.59±0.02.13
TM100 (N/cm2)235±22214±36.6
UTS (N/cm2)82±954±6.04†
UStr1.5±0.041.6±0.09.4

Data are mean ± SEM.

TMmax, Maximum tangential modulus; TMavg, average tissue tangential modulus; TM100, tangential modulus corresponding to a pressure of 100 mm Hg; UTS, ultimate tensile strength; UStr, ultimate stretch ratio; eAAA, elective abdominal aortic aneurysm; rAAA, ruptured abdominal aortic aneurysm.

⁎ Significant difference after Bonferroni correction.

† Significant difference with significance level set to α = .05.

No correlation was found between UTS and diameter (R = −0.1; P = .55; Fig 1) or between UTS and age (R = 0.13; P = .44). UTS, however, had a positive correlation with TMmax (R = 0.76; P < .01) and a weak negative correlation with wall thickness (R = −0.42; P < .01) (Abstract) and (Fig 3, Fig 4, Fig 5).

  • View full-size image.
  • Fig 3. 

    Correlation between the diameter of the aneurysm and the ultimate tensile strength (UTS). The Spearman correlation coefficient showed no statistical significance (P = .55). The regression line is shown for all data in the plot. eAAA, elective abdominal aortic aneurysm; rAAA, ruptured abdominal aortic aneurysm.

  • View full-size image.
  • Fig 4. 

    Correlation between tissue thickness and ultimate tensile strength (UTS). The regression line is shown for all data in the plot. eAAA, elective abdominal aortic aneurysm; rAAA, ruptured abdominal aortic aneurysm.

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Discussion 

In this study, we compared the biomechanical properties of rAAA vs eAAA tissue. We found that tensile strength was on average lower for rAAA tissue, which also had significantly thicker walls than the eAAA tissue specimens (Table II). The various modulus values considered here showed no significant difference between these two groups (Table II). These results are consistent with a previous study that compared the in vivo stiffness values of eAAA vs rAAA.23 Our results also showed a significant correlation between ultimate tissue strength and tissue stiffness (Fig 5), whereas no correlation was found between ultimate tissue strength and maximum AAA diameter (Fig 3).

It is well known that extensive extracellular matrix changes are present within the AAA wall,24, 25 and these are believed to be associated with inflammatory cell infiltration and MMP activity.26, 27, 28 Petersen et al28 studied the presence and activation of MMP-2 and MMP-9 in medium rAAAs (5-7 cm) and large eAAAs (>7 cm). They found that MMP-9 was significantly higher in rAAA than eAAA tissue but that MMP-2 was significantly higher in eAAAs. Moreover, MMP-9 was negatively correlated with diameter, whereas MMP-2 was positively correlated with diameter. This suggests that MMP-2 may be involved in aneurysm enlargement, whereas MMP-9 may be involved in aneurysm rupture. Wilson et al29 demonstrated a positive correlation between tissue elastolytic activity and arterial distensibility in an aneurysm. Because the strength of an aneurysm has been linked to the continued loss of structural integrity of the elastin and collagen network, these data would suggest that a reduction in AAA wall strength is accompanied by an increased compliance. Indeed, in a subsequent study, Wilson et al30 showed that AAAs that went on to rupture tended to be more distensible compared with those that did not rupture during follow-up. These findings were corroborated by our direct measurements of aortic stiffness ex vivo. We found that both TMmax and TMavg were positively correlated with the ultimate strength, thus suggesting that AAAs that are less stiff are weaker and therefore more prone to rupture.

It is generally believed that the thickness of an AAA diminishes as the diameter increases, as would the thickness of a cylinder (or a sphere) while it enlarges under the effect of internal pressure. However, AAAs enlarge with time, and remodeling plays an important role in aneurysm progression. Although some AAA tissue walls do present, as expected, as very thin specimens, we found that, on average, the thickness of AAA tissue was 2.9 mm. Measurements performed with a manual caliper may underestimate thickness because the value is taken while the specimen is compressed. To avoid this problem, we used an optical method (laser) to measure thickness. There is variability in thickness among specimens from the same patients, and this variability is hard to measure because only two specimens per patients were obtained at most. When comparing eAAAs vs rAAAs, we found a significant difference in the specimen thickness, which may be due to the documented increased inflammatory infiltration found in the latter.31

The procedure by which specimens were collected was standardized, and the surgeon harvested only tissue samples that came from the same area (located axially at the level of the maximum diameter and circumferentially across the midline on the anterior surface of the AAA). This choice is dictated in part by surgical reasons; in fact, current surgical procedures require that the AAA wall be sutured on top of the prosthesis after AAA content is removed. Our procedure was such that it did not interfere with the standard care of the patient, and, therefore, only tissue from the anterior surface of the aorta (that the surgeon cuts before suturing the aortic wall) was available to be tested. None of the specimens was collected at the site of rupture, which is in general retroposterior. Although our procedure limits the appreciation of the regional variability of mechanical properties in AAA and prevents, for the most part, the rupture site tissue from being harvested, it provides a standardization of the site of harvest and eliminates the location of harvest from the variables to be considered in the statistical analysis.

Recognizing that the aortic wall in the presence of an aneurysm is nonhomogeneous,32 we concentrated our study on local measures of intrinsic properties of the aortic tissue in the presence of an aneurysm, such as the local stiffness and local thickness, as opposed to global measures, such as the diameter of the aneurysm. As a consequence, we chose to test multiple specimens when available. We found that thickness was inversely correlated with the local strength of the material and that stiffness was directly correlated with strength, even within the same patient. This finding further demonstrates the nonhomogeneity of the aortic wall in the presence of an aneurysm and may imply that there are changes at the local tissue level that change the mechanical properties and the thickness of the wall as the aneurysm progresses.32

The use of ex vivo aortic specimens limited our study to patients who received surgical treatment. Therefore, we cannot infer the propensity for rupture of the eAAA patients studied here, which may explain why no significant difference was found between eAAA and rAAA tangential moduli, although a significant correlation was found between the tangential modulus and strength of the tissue. However, our method allows a direct assessment of the mechanical properties of the tissue, as opposed to only estimation, as with in vivo measurements. Furthermore, in vivo measurements can not assess tissue strength; only destructive ex vivo methods can be used for that assessment.

A widely accepted indicator for risk of aneurysm rupture is the maximum transverse diameter,33, 34 but our results suggest that the AAA wall strength is not related to the maximum transverse diameter. Rupture is the final event that occurs when the tissue stress exceeds the tissue ability to sustain stress (tissue strength). Diameter is definitely a factor in wall stress in any tubular or spherical structure, because wall stress increases with diameter. Therefore, because stress is ultimately what causes rupture, it is correct to infer that larger aneurysms are more prone to rupture. Our results concern large aneurysms; in fact, there was no significant difference between the eAAA and rAAA groups in terms of diameter, and the average diameter was 7 cm. Although it is accepted that a large aneurysm is at greater risk of rupture than a smaller one, we show that factors other than diameter only could be considered and used to better discriminate the risk of rupture and could explain why, in some cases, the diameter rule fails. The recent advances in diagnostic images provide noninvasive means to estimate the stiffness of an artery and could therefore be used to add one diagnostic piece of information to the clinical decision.

In conclusion, our data suggest that aneurysm rupture is associated with aortic wall weakening, but not with wall stiffening. Moreover, our results suggest that AAA wall strength, in large aneurysms, is not related to the maximum transverse diameter. Rather, wall thickness or stiffness may be a better predictor of AAA rupture.

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Author Contributions 

Conception and design: E.S.D.M, N.G, M.S.M, D.A.V

Analysis and interpretation: E.S.D.M, J.P.V.G

Data collection: A.B, E.S.D.M

Writing the article: E.S.D.M

Critical revision of the article: D.A.V, J.P.V.G, E.S.D.M, N.G, M.S.M, A.B

Final approval of the article: E.S.D.M, J.P.V.G, A.B, N.G, M.S.M, D.A.V

Statistical analysis: E.S.D.M

Obtained funding: D.A.V

Overall responsibility: D.A.V

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The authors would like to acknowledge Isabella Verdinelli (Department of Statistics, Carnegie Mellon University) for her contribution to the statistical analysis of our data.

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 This research was funded in part by National Institutes of Health grant RO1HL060670 (D.A.V.).Competition of interest: none.Preliminary data presented at the Biomedical Engineering Society Fall meeting, Philadelphia, PA, October 13-16, 2004.

PII: S0741-5214(05)01921-X

doi:10.1016/j.jvs.2005.10.072

Journal of Vascular Surgery
Volume 43, Issue 3 , Pages 570-576, March 2006

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