Abdominal Aortic Aneurysm Expansion Rate Research Articles

Selective management of abdominal aortic aneurysms smaller than 5.0 cm in a prospective sizing program with gender-specific analysis.

We present extended follow-up findings of the Kingston prospective sizing program for patients with abdominal aortic aneurysm (AAA) smaller than 5.0 cm in diameter, with gender-specific analysis. From 1976 to 2001, 895 patients (688 men, 207 women) with AAA smaller than 5.0 cm were entered, regardless of fitness, in a prospective sizing program in which computed tomography scans were obtained every 6 months. Operations were performed in fit patients with an increase in AAA size to 5 cm (n = 190), AAA expansion greater than 0.5 cm in 6 months (n = 27), or for other reasons (n = 33). Follow-up continued until AAA rupture, surgery, death, or removal from the program. No AAA smaller than 5.0 cm ruptured during prospective follow-up. There was a statistically significant increase in expansion rate relative to size at entry, with the highest mean expansion rate of 0.52 cm/y for AAA 4.5 to 4.9 cm in diameter. There was no significant difference in AAA expansion rate between men and women. The frequency of surgery was inversely related to age at entry, but was positively related to AAA size at entry, with patients with AAA 4.5 to 4.9 cm at entry 6.8 times more likely (95% confidence interval, 4.3-10.7) to undergo surgery than those with AAA 3.0 to 3.4 cm at entry. Women were older than men at entry, and age at entry in those undergoing surgery was significantly greater in women. The study confirms the results of the United Kingdom Small Aneurysm Trial and the Aneurysm Detection and Management Study, that is, that risk for rupture is extremely unlikely with AAA smaller than 5.0 cm, which enables safe follow-up surveillance programs in both men and women with AAA smaller than 5.0 cm.

Systemic Levels of Cotinine and Elastase, but not Pulmonary Function, are Associated with the Progression of Small Abdominal Aortic Aneurysms

Objective: to study whether smoking and impaired pulmonary function are associated with the expansion of abdominal aortic aneurysms (AAA).Methods and material: seventy-nine men with small (3–5 cm), screen-detected AAA underwent a simple 5-step smoking history, measurement of the forced first second expiratory volume (FEV1), venepuncture and annual ultrasound scan for mean follow-up period of 3.5 years.Results: all but one patient had a significantly reduced FEV1 (p<0.05, Mann–Whitney). The FEV1/expected FEV1 ratio (rFEV1) was not related to AAA expansion but was negatively correlated with P-elastase-α1-antitrypsin-complexes (P-Elastase). P-Elastase was positively correlated with smoking and S-cotinine. Smoking, S-cotinine, and P-elastase were positively correlated with the mean annual AAA expansion rate but not rFEV1.Conclusion: in general, patients with AAA have impaired pulmonary function. A simple five step smoking classification is as predictive of AAA-expansion as S-cotinine. Smoking may cause elastase secretion leading to pulmonary and aortic elastin degradation but the lack of association between AAA-expansion and rFEV1 suggest that other mechanisms are important.

Macrophage migration inhibitory factor is associated with aneurysmal expansion.

Macrophage migration inhibitory factor (MIF) is an inflammatory cytokine released mainly from macrophages and activated lymphocytes. Both atherosclerosis and abdominal aortic aneurysm (AAA) are inflammatory diseases tightly linked to the function of these cells. The correlation and contribution of MIF to these human diseases remain unknown, although a recent rabbit study showed expression of this cytokine in atherosclerotic lesions. MIF immunohistochemistry was performed on tissue sections from five normal aortas, seven atherosclerotic carotids, and six AAAs. A group of 112 men with small AAAs (defined as 3 to 5 cm) was recruited at the time of diagnosis, had serum samples taken, and was followed annually for 1 to 5 years (mean, 2.9 years) and referred for surgery if the AAA exceeded 5 cm in diameter. Of this study group, 98 had serum MIF measured with an enzyme-linked immunosorbent assay and 61 had detectable levels. In human atherosclerotic and aneurysmal lesions, MIF protein colocalized in macrophages, endothelial cells, and smooth muscle cells, but normal arteries had negligible MIF expression. Furthermore, serum-MIF levels correlated significantly with annual expansion rate (r = 0.28; P =.005), persisting after adjustment for initial AAA size, smoking habits, diastolic blood pressure, ankle blood pressure index, and age. After exclusion of 38 cases with MIF levels below the detection limit, initial AAA size was also significantly correlated with the MIF levels (r = 0.42; P =.001), persisting after adjustment for similar confounders, and the correlation coefficient with expansion rate increased to 0.42 (P =.001). Highly expressed MIF in macrophages, endothelial cells, and smooth muscle cells in lesions from atherosclerosis and AAA and significant association between serum MIF level and AAA initial size and AAA expansion rate in a group of patients with AAA suggest a potential involvement of this proinflammatory cytokine in the pathogenesis of these cardiovascular diseases.

Randomized double-blind controlled trial of roxithromycin for prevention of abdominal aortic aneurysm expansion (Br J Surg 2001: 88: 1066–72)

Abstract Background Macrolide treatment has been reported to lower the risk of recurrent ischaemic heart disease. The influence of macrolides on the expansion rate of abdominal aortic aneurysms (AAAs) remains unknown. The aim was to investigate the effect of roxithromycin on the expansion rate of small AAAs. Methods A total of 92 subjects with a small AAA were recruited from two populations. One population consisted of 6339 men aged 65–73 years who were offered a hospital-based mass screening programme for AAA. From this population 66 subjects were recruited. The remaining 26 men were recruited from among 49 subjects diagnosed at interval screening for an initial aortic diameter between 25 and 29 mm. Subjects were randomized to receive either oral roxithromycin 300 mg once daily for 28 days or matching placebo, and followed for a mean of 1·5 years. Results During the first yearthe mean annual expansion rate of AAAs was reduced by 44 per cent in the intervention group (1·56 mm per year), compared with 2·80 mm per year following placebo (P = 0·02). During the second year the difference was only 5 per cent. Multiple linear regression analysis showed that roxithromycin treatment and initial AAA size were significantly related to AAA expansion when adjusted for smoking, diastolic blood pressure and immunoglobulin A level of 20 or more. Logistic regression analysis confirmed a significant difference in expansion rates above 2 mm annually between the intervention and placebo groups: odds ratio = 0·09 (95 per cent confidence interval 0·01–0·83). Conclusion In comparison to placebo, roxithromycin 300 mg daily for 4 weeks reduced the expansion rate of AAAs.

Epidemiology of aortic disease: aneurysm, dissection, occlusion

The physiological infrarenal aortic diameter varies between 12.4 mm in women an 27.6 mm in men. As defined, an aneurysmatic dilatation begins with 29 mm. According to that, 9% of all people above the age of 65 are affected by an abdominal aortic aneurysm (AAA). Compared with the female sex, the male sex predominates at a rate of about 5:1. The disease is predominant in men of the white race. In black men, black and white women the incidence of AAA is identical. 38 to 50 percent of the AAA patients (patients) suffer from hypertension, 33 to 60% from coronary, 28% from cerebrovascular and 25% from peripheral occlusive disease. The AAA expansion rate varies between 0.2 and 0.8 cm per year and is exponential from a diameter of 5 cm on. In autopsy studies, the rupture rates with AAA diameters of < 5 cm, between 5.1 and 6.9 cm, and of > 7 cm were below 5%, 39% and 65%, respectively. 70% of the AAA patients do not die of a rupture, but of a cardiac disease. Serum markers, such as metalloproteinases and procollagen peptides are significantly increased in AAA patients. Thoraco-abdominal aneurysms (TAA) make up only 2 to 5% of all degenerative aneurysms. 20 to 30% of the TAA patients are also affected by an AAA. 80% of the TAA are degenerative, 15 to 20% are a consequence of the chronic dissection--including 5% of Marfan patients--, 2% occur in case of infections and 1 to 2% in case of aortitis. The TAA incidence in 100,000 person-years is 5.9% during a monitoring period of 30 years. In case of TAA, an operation is indicated with a maximum diameter of 5.5 to 6 cm and more and, in case of a Marfan's syndrome (incidence of 1:10,000), with a maximum diameter of 5.5 cm and more. With regard to aorto-iliac occlusive diseases, there are defined 3 types of distribution. Type I refers to the region of the bifurcation itself. Type II defines the diffuse aorto-iliac spread of the disease. Type III designates multiple-level occlusions also beyond the inguinal ligament. Type I patients in most cases are female and more frequently suffer from hyperlipidaemia, while Type II patients are affected by hypertension and diabetes. Compared to Type II patients, Type I patients have a life expectancy that is 10 years higher. Type I and Type II patients often suffer from a pelvic claudication and, unlike Type III patients, are more frequently affected by arterio-arterial embolisms.

Apolipoprotein E genotype is associated with differential expansion rates of small abdominal aortic aneurysms.

The common polymorphism of the apolipoprotein E (APOE) gene is associated with differential risk of atherosclerosis; the gene could be a candidate gene in abdominal aortic aneurysms (AAA). APOE genotypes were determined in 57 men aged 65-73 years with a small AAA (30-50 mm). The patients were included in a population ultrasonographic screening programme and were followed with at least two examinations during an interval of 2-4.5 years. The AAA expansion rates in patients with four different APOE genotypes were studied, with adjustment for initial AAA size and smoking. APOE genotype was a significant determinant of AAA expansion rate (P = 0.001). The adjusted mean (95 per cent confidence interval) rate was 2.1 (1.7-2.6) mm/year in 31 men with genotype E3E3, 1.3 (0.7-1.9) mm/year in 17 men with E3E4, 3.1 (2.0-4. 1) mm/year in six men with E2E3 and 4.2 (2.7-5.6) mm/year in three men with E2E4. The mean expansion rate was 2.2 (1.5-2.8) mm/year in non-smokers and 3.0 (2.5-3.6) mm/year in smokers (P = 0.014). APOE genotype seems to influence AAA expansion rate, but the effects of the individual genotypes, in particular E3E3 and E3E4, are contradictory when compared with the effects of the genotypes on risk of atherosclerosis.

Immunoglobulin A antibodies against Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm.

The aim of this study was to examine the possible association between the progression of small abdominal aortic aneurysm (AAA) and chronic infection with Chlamydia pneumoniae. Patients from a hospital-based mass screening programme for AAA with annual follow-up (mean 2.7 years) were included. After initial interview, 139 men aged 65-73 years with a small AAA underwent examination and blood sampling. Immunoglobulin (Ig) G and IgA titres against C. pneumoniae were measured by a microimmunofluorescence test. Some 83 (95 per cent confidence interval 74-93) per cent of the men had an IgA titre of 20 or more, or an IgG titre of 32 or more. Men with an IgA titre of 20 or more had a 48 per cent higher AAA expansion rate than those with a titre of less than 20 (3.1 versus 2.1 mm/year; P < 0.05). Multiple linear and logistic regression analyses showed that an IgA titre of 20 or more was a significant independent predictor of increased AAA expansion, adjusted for known risk factors of expansion. Initial AAA size and serum total cholesterol level were also predictors of expansion. A high proportion of men with a small AAA had signs of chronic infection with C. pneumoniae. Aneurysm progression correlated with evidence of chronic C. pneumoniae infection.