| | Expansion rate of nonaneurysmatic abdominal aorta: Over 10 years of follow-up CT studiesReceived 29 May 2007; received in revised form 19 September 2008; accepted 26 September 2008. Abstract Expansion rate of the nonaneurysmatic abdominal aorta (NAA) is completely unknown. The purpose was to evaluate the expansion rate of the NAA and the factors influencing its enlargement. 114 subjects without aortic disease were entered into this retrospective study (mean age: 58.7 years). In all subjects, follow-up CT studies were obtained for more than 10 years after initial CT studies (mean: 147.0 months). The diameter of the abdominal aorta was measured at two sites (suprarenal and infrarenal abdominal aorta), and the growth rate was calculated at each site. The growth rate of NAA and the factors influencing its enlargement were evaluated. In 68 (59.6%), the suprarenal segment of NAA increased in size with a mean growth rate of 1.3 mm/10 years. In 49 subjects (43.0%), the infrarenal segment of NAA increased in size during the follow-up period with the mean growth rate of 1.0mm/10 years. The mean growth rate was significantly higher in the suprarenal segment (p=0.002). The suprarenal segment of NAA and presence of hyperlipidemia were significant risk factors for NAA enlargement. NAA enlargement is more likely to occur in the suprarenal segment than in the infrarenal segment. The presence of hyperlipidemia was also a significant risk factor for NAA enlargement. 1. Introduction  Abdominal aortic aneurysm (AAA) is one of the most frequent vascular diseases, which can progress to lethal complications such as rupture. Previously, several articles reported the growth rates of AAA, and in most cases, its diameter increases with time [1], [2], [3], [4]. Although the natural history of the nonaneurysmatic abdominal aorta (NAA) is completely unknown, various changes occur in the aortic wall with time. The loss of elasticity and aortic compliance probably accounts for the increase pulse pressure commonly seen in the elderly. Such changes occur even in normal healthy adults [5], [6], [7]. In addition, atherosclerotic changes usually occur or progress with time, however, there have been no reports on the growth rate of NAA [5]. The purpose of this study is to evaluate the growth rate of NAA using repeated computed tomography (CT) examinations, and the factors influencing its enlargement. 2. Materials and methods 2.3. Image analysis CT images were evaluated by two experienced (over 10 years of experience) cardiovascular radiologists. The diameter of the abdominal aorta was measured at two sites. One site was the orifice of the superior mesenteric artery (suprarenal site), and the other site was the middle site between the orifice of the right renal artery and the aorto-iliac bifurcation (Fig. 1). Final decisions regarding the findings were reached by consensus. The initial and final CT measurements were used to calculate changes in aortic size at the same level in each site. The largest short-axial diameter of the outer contour of the affected segment of aorta was measured (Fig. 2) [3]. The diameter was measured using direct-reading calibers from hard-copy images and corrected for the appropriate scale. The growth rate was calculated in the following manner [3]: the difference in the diameter between the initial (D1) and final (D2) measurements was divided by the time interval (T) between the two measurements: growth rate=(D2−D1)/T. 3. Results In 85 of 114 subjects (74.6%), the suprarenal or infrarenal segment of NAA increased in size, and 117 of 228 segments of NAA (51.3%) increased in size during the follow-up period (Fig. 3). In two subjects (1.8%), the infrarenal segment of NAA progressed to aneurysm formation (diameter ≥30mm and/or 1.5 times that of the expected normal diameter of the given aortic segment) (Fig. 4). Table 1 shows the mean initial diameter, final diameter, and growth rate of all subjects and decades. In each suprarenal and infrarenal segment group, there was a significant difference between the mean initial and final diameter (p<0.0001). Comparing the initial diameters of the suprarenal segments with those of the infrarenal segments, the mean diameter of the suprarenal segments was significantly higher (p<0.0001). In 68 of 114 subjects (59.6%), the suprarenal segment of NAA increased in size during the follow-up period with a mean growth rate of 1.3±2.1mm/10 years (forties; 1.1±1.5mm/10 years, fifties; 1.2±2.3mm/10 years, sixties; 1.5±1.9mm/10 years, and seventies; 1.5±2.6mm/10 years). | | |  | | Initial diameter (mm) | Final diameter (mm) | Growth rate (mm/10 years) | |
|---|
| Suprarenal segment (n=114) | 19.2±2.8 | 20.7±3.5 | 1.3±2.1 | | | Forties (n=22) | 18.2±2.7 | 19.2±2.8 | 1.1±1.5 | | | Fifties (n=36) | 18.8±2.9 | 20.1±2.6 | 1.2±2.3 | | | Sixes (n=40) | 19.5±2.9 | 21.3±4.2 | 1.5±1.9 | | | Seventies (n=16) | 20.1±2.0 | 22.6±3.6 | 1.5±2.6 | | | | | | Infrarenal segment (n=114) | 16.1±3.0 | 17.2±4.7 | 1.0±2.7 | | | Forties (n=22) | 15.9±2.7 | 16.6±2.9 | 0.7±1.0 | | | Fifties (n=36) | 15.7±3.4 | 17.4±7.3 | 1.6±4.6 | | | Sixes (n=40) | 16.2±2.6 | 17.1±2.8 | 0.7±1.1 | | | Seventies (n=16) | 17.3±3.1 | 18.4±2.7 | 0.9±1.3 | | | | |
In 49 subjects (43.0%), the infrarenal segment of NAA increased in size during the follow-up period with a mean growth rate of 1.0±2.7mm/10 years (forties; 0.7±1.0mm/10 years, fifties; 1.6±4.6mm/10 years, sixties; 0.7±1.1mm/10 years, and seventies; 0.9±1.3mm/10 years). For each suprarenal and infrarenal segments, there was no significant difference in the mean growth rate between decades. In five of 114 subjects (4.4%), the suprarenal (n=1) or infrarenal segment (n=3) of NAA decreased in size because of NAA deformity (Fig. 5). In the remaining suprarenal (n=45) or infrarenal segments (n=62) of NAA, the diameter did not change between the initial and final CT (Fig. 6). Comparing the suprarenal segments to the infrarenal segments, the mean growth rate was significantly higher in the suprarenal segment than in the infrarenal segment (p=0.002). Table 2 shows the mean growth rates in the two groups of segments divided by gender, suprarenal segment of NAA, or by the presence or absence of characteristics of age ≥60, calcification of the aortic wall, hyperlipidemia (HL) (total cholesterol of blood ≥220mg/dl), diabetes mellitus, family history of aortic aneurysm (including parents, siblings, and children), atherosclerotic disease (including atherosclerotic aneurysm and cerebrovascular disease), smoking ≥20 years, chronic renal failure, heart disease (including ischemic heart disease and heart failure), COPD, and blood pressure (BP) ≥140mmHg at the initial CT. The suprarenal segment of NAA and the presence of HL were significantly different between the two groups; their p values were 0.0414 and 0.0011, respectively. The suprarenal segment of NAA with the presence of HL had a significantly higher mean growth rate. Table 3 shows that subject characteristics (risk factors) such as age ≥60, gender, calcification of the aortic wall, diabetes mellitus, family history of aortic aneurysm, atherosclerotic disease (including atherosclerotic aneurysm, and cerebrovascular disease), smoking ≥20 years, chronic renal failure, heart disease (including ischemic heart disease and heart failure), COPD, and blood pressure (BP) ≥140mmHg at the initial CT were not significant risk factors for increased in diameter in univariate or multivariate analysis. The suprarenal segment of NAA and the presence of HL were significant risk factors for NAA enlargement as confirmed by univariate and multivariate analysis. | | | | Patient characteristics | Increase (n=117) | No increase (n=111) | Univariate | Multivariate | |
|---|
| | | | X2 | p | p | 95%CI | OR | |
|---|
| Gender, female, n (%) | 48 (41.0) | 52 (46.8) | 0.001 | 0.9713 | 0.4917 | 0.406–1.542 | 0.791 | | | Age ≥60 years, n (%) | 62 (53.0) | 50(45.0) | 1.439 | 0.2303 | 0.4281 | 0.701–2.311 | 1.273 | | | Calcification, n (%) | 71(60.7) | 73 (65.8) | 0.632 | 0.4265 | 0.3325 | 0.401–1.352 | 0.713 | | | Hyperlipidemia, n (%) | 25 (21.4) | 9 (8.1) | 7.892 | 0.005 | 0.007 | 1.401–8.441 | 3.44 | | | Diabetes mellitus, n (%) | 31 (26.5) | 35(31.5) | 0.702 | 0.402 | 0.1802 | 0.340–1.224 | 0.645 | | | Family history of AAA, n (%) | 7 (6.0) | 3 (2.7) | 1.461 | 0.2267 | 0.3969 | 0.435–8.150 | 1.883 | | | Atherosclerotic disease, n (%) | 14 (12.0) | 24 (21.6) | 3.824 | 0.0505 | 0.0691 | 0.131–1.080 | 0.376 | | | Smoking ≥20 years, n (%) | 44 (37.6) | 73 (65.8) | 0.001 | 0.9713 | 0.3472 | 0.352–1.444 | 0.713 | | | Location in suprarenal site, n (%) | 68 (58.1) | 46(41.4) | 6.338 | 0.0118 | 0.0067 | 1.240–3.815 | 2.175 | | | Chronic renal failure, n (%) | 21 (17.9) | 19 (17.1) | 0.027 | 0.8689 | 0.7939 | 0.388–2.062 | 0.895 | | | Heart disease, n (%) | 11 (9.4) | 15 (13.5) | 0.953 | 0.3289 | 0.5983 | 0.416–4.573 | 1.38 | | | COPD, n (%) | 2 (1.7) | 8 (7.2) | 4.105 | 0.0427 | 0.0813 | 0.043–1.203 | 0.227 | | | BP ≥140mmHg at initial CT, n (%) | 59 (50.4) | 53 (47.7) | 0.164 | 0.6858 | 0.5329 | 0.627–2.465 | 1.243 | | | | |
4. Discussion The term aortic aneurysm refers to the pathological dilatation of the normal aortic lumen involving one or several segments. In most AAAs, the diameter increases with time at a mean rate that is initially slow and then increases exponentially [1], [2], [3], [4]. The incidence of AAA has increased threefold in recent decades, and the disorder is more common in men than in women, with prevalence rates estimated at between 1.3% and 8.9% in men and between 1.0% and 2.2% in women [1]. AAAs are much more common than thoracic aortic aneurysms. Although it is now evident that abdominal aortic aneurysms arise as a consequence of multiple interacting factors, classically, atherosclerosis has been considered the common underlying etiology [1], [2], [3], [4], [5]. On the other hand, most of the population has no AAA during their lives, and the natural history of NAA is completely unknown. There have been no reports on the growth rate of NAA. However, it can be hypothesized that most abdominal aortas increase in size with time, because degenerative changes of the aortic wall such as loss of elasticity and aortic compliance, the atherosclerotic changes usually occur and/or progress with time [5], [6], [7]. According to this study, in 68 of 114 subjects (59.6%), the suprarenal segment of NAA increased in size. In 49 subjects (43.0%), the infrarenal segment of NAA increased in size during the follow-up period. The incidence of increased aortic diameter was not so high. These results suggest that NAAs do not always increase in size with time. According to previous reports, the infrarenal abdominal aorta is most affected by the atherosclerotic process and is similarly the most common site of AAA formation (5). Only a fraction of AAAs are suprarenal, tending to arise only as an extension of a thoracic (thoracoabdominal) aneurysm. The atherosclerotic process less often involves the thoracic aorta [5]. In contrast, our result showed that the mean growth rate was significantly higher in the suprarenal segment than in the infrarenal segment (p=0.002). The suprarenal segment of NAA was a significant risk factor for NAA enlargement as confirmed by univariate and multivariate analysis. Thus, there is a discrepancy between the expansion of NAA and the formation of AAA. These results may be explained by La Place's Law [3], [9], [10]. In this study, comparing the diameters of the suprarenal segments with those of the infrarenal segments, the mean diameter of the suprarenal segments was significantly higher. La Place's Law states that the perpendicular stress on a cylinder is directly proportional to the pressure exerted by the fluid contents and its radius, and is inversely proportional to the wall thickness. This means that the larger the diameter, the faster the growth rate at constant pressure. Therefore, these results indicate that aortic diameter is the most important risk factor for NAA enlargement, which is similar to AAA [2]. In this study, age, gender, history of atherosclerotic disease, calcification of aortic wall, hypertension, and diabetes mellitus were not significant risk factors. These factors are associated with atherosclerotic change. These results suggest that atherosclerotic changes do not always accelerate NAA expansion. Atherosclerotic disease of the aorta may produce either stenotic obstruction or aneurysmal dilatation. Why one process should predominate over the other in any given individual, however, is unknown [5]. In regards to AAA, previous reports suggested that atherosclerosis plays a minor role in AAA expansion [2], [11]. In addition, our study also showed no significant differences among the growth rates in the forties, fifties, sixties, and seventies. Multiple interacting factors may cause NAA expansion, and atherosclerosis and the loss of elasticity and aortic compliance may be included. However, this result also suggests that the loss of elasticity and aortic compliance do not always accelerate NAA expansion. In this study, the suprarenal (n=1) or infrarenal segment (n=3) of NAA decreased in size because of NAA deformity. This deformity may be due to the loss of elasticity and aortic compliance. In previous reports, there was a strong clinical association between tobacco smoking and AAA development [1], [2]. However, this study did not show that smoking was a significant risk factor, and there was a discrepancy between NAA expansion and AAA. As another important factor, cellular factors play important roles in the formation of AAA [5], [6], [7], [12], [13], [14]. In this study, HL was a significant risk factor for NAA enlargement. According to previous reports, HL causes focal activation of the endothelium in large and medium-sized arteries. The infiltration and retention of low-density lipoprotein (LDL) in the arterial intima initiate an inflammatory response in the artery wall. Oxidative and enzymatic modifications lead to the release of inflammatory lipids that induce endothelial cells to express leukocyte adhesion molecules. The modified LDL particles are taken up by scavenger receptors of macrophages, which evolve into foam cells. Monocytes recruited through the activated endothelium differentiate into macrophages. Several endogenous and microbial molecules can ligate pattern-recognition receptors on these cells, inducing activation and leading to the release of inflammatory cytokines, chemokines, oxygen and nitrogen radicals, and other inflammatory molecules and, ultimately, to inflammation and tissue damage [14]. Thus, pathological destruction of the media and its elastic tissue may contribute to NAA enlargement, but further studies are needed to clarify this tissue. As another important factor, genetic factor plays important roles in the formation of AAA [1], [5], [15], [16], [17], [18], [19]. A genetic predisposition to AAA development has been repeatedly suggested by studies of familial incidence, with up to 28% of patients with an AAA having a first-degree relative similarly affected [5], [16]. However, a family history of AAA was not a significant risk factor in this study. In two of 114 subjects, NAA progressed to AAA. Both AAAs were located in the infrarenal segment, which is the most common site of AAA formation. In this study, the differences between groups with and without AAA were not clear, because the number of subjects with AAA was too small. Multiple interacting factors may cause AAA formation, and further studies involving larger numbers of subjects are needed to clarify this issue. As a limitation of this study, the sample size was relatively small. To completely clarify the natural history of NAA, further studies addressing other factors and involving larger numbers of patients with a longer follow-up period are therefore needed. 5. Conclusion NAA does not always increase in size with time. Additionally, unlike the prevalent location for abdominal aortic aneurysms, NAA enlargement is more likely to occur in the suprarenal segment than in the infrarenal segment. The suprarenal segment of NAA and the presence of HL were significant risk factors for NAA enlargement. However, further studies are needed to completely clarify the natural history of NAA. References [1]. [1]Sakalihasan N, Limet R, Dewawe OD. Abdominal aortic aneurysm. Lancet. 2005;365:1577–1589. Abstract | Full Text |
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Dr. Takashi Mizowaki was born in Nagasaki, Japan, in 1972. He received a degree from Kagoshima University in 1997. Since 1997, he has been with Nagasaki University as a radiologist. His research interests focus on cardiovascular radiology. Dr. Eijun Sueyoshi was born in Nagasaki, Japan, in 1968. He received a degree from Nagasaki University in 1992. Since 1992, he has been with Nagasaki University as a radiologist. His research interests focus on cardiovascular radiology. Dr. Ichiro Sakamoto was born in Nagasaki, Japan, in 1958. He received a degree from Hiroshima University in 1984. Since 1984, he has been with Nagasaki University as a assistant professor in Radiology. Dr. Masataka Uetani was born in Nagasaki, Japan, in 1956. He received a degree from Hiroshima University in 1981. Since 1981, he has been with Nagasaki University as a professor and a chairman in Radiology. Department of Radiology, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852-8501, Japan  Corresponding author. Tel.: +81 95 849 7354; fax: +81 95 849 7357.
PII: S0895-6111(08)00098-0 doi:10.1016/j.compmedimag.2008.09.003 © 2008 Elsevier Ltd. All rights reserved. | |
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