Initial Abdominal Aortic Aneurysms Size Research Articles

The natural history of large abdominal aortic aneurysms in patients without timely repair.

Contemporary data on the natural history of large abdominal aortic aneurysms (AAAs) in patients undergoing delayed or no repair are lacking. In this study, we examine the impact of large AAA size on the incidence of rupture and mortality. From a prospectively maintained aneurysm surveillance registry, patients with an unrepaired, large AAA (≥5.5cm in men and ≥5.0cm in women) at baseline (ie, index imaging) or who progressed to a large size from 2003 to 2017 were included, with follow-up through March 2020. Outcomes of interest obtained by manual chart review included rupture (confirmed by imaging/autopsy), probable rupture (timing/findings consistent with rupture without more likely cause of death), repair, reasons for either no or delayed (>1year after diagnosis of large AAA) repair and total mortality. Cumulative incidence of rupture was calculated using a nonparametric cumulative incidence function, accounting for the competing events of death and aneurysm repair and was stratified by patient sex. Of the 3248 eligible patients (mean age, 83.6± 9.1years; 71.2% male; 78.1% white; and 32.0% current smokers), 1423 (43.8%) had large AAAs at index imaging, and 1825 progressed to large AAAs during the follow-up period, with a mean time to qualifying size of 4.3± 3.4years. In total, 2215 (68%) patients underwent repair, of which 332 were delayed >1year; 1033 (32%) did not undergo repair. The most common reasons for delayed repair were discrepancy in AAA measurement between surgeon and radiologist (34%) and comorbidity (20%), whereas the most common reasons for no repair were patient preference (48%) and comorbidity (30%). Among patients with delayed repair (mean time to repair, 2.6± 1.8years), nine (2.7%) developed symptomatic aneurysms, and an additional 11 (3.3%) ruptured. Of patients with no repair, 94 (9.1%) ruptured. The 3-year cumulative incidence of rupture was 3.4% for initial AAA size 5.0 to 5.4cm (women only), 2.2% for 5.5 to 6.0cm, 6.0% for 6.1 to 7.0cm, and 18.4% for >7.0cm. Women with AAA size 6.1 to 7.0cm had a 3-year cumulative incidence of rupture of 12.8% (95% confidence interval, 7.5%-19.6%) compared with 4.5% (95% confidence interval, 3.0%-6.5%) in men (P= .002). In this large cohort of AAA registry patients over 17years, annual rupture rates for large AAAs were lower than previously reported, with possible increased risk in women. Further analyses are ongoing to identify those atincreased risk for aneurysm rupture and may provide targeted surveillance regimens and improve patient counseling.

Patients on AAA Surveillance are at Greater Threat of Cardiovascular Events or Malignancy than their AAA: Outcomes of AAA Surveillance over 19 years at a Tertiary Vascular Centre

BackgroundTo analyse 19 years’ worth of data from a Major UK Vascular Centre to determine the outcome of patients after they enter abdominal aortic aneurysm (AAA) surveillance (surgery, death, discharge or transfer), this may inform interventions to improve these outcomes in the AAA surveillance population. MethodsThis was a retrospective analysis of a prospectively collected database of outcomes of every patient entered on AAA surveillance at Manchester University NHS Foundation Trust – Wythenshawe Hospital between September 2000 and June 2019. Analyses included what proportion suffered death, discharge, transfer or surgery whilst on surveillance. Multi-variate analysis was used to determine the effect of initial AAA size, age when entering surveillance and gender. Boxplots were produced in those who had already reached an outcome to determine historic median times. Causes of death/discharge were also analysed. ResultsOne thousand nine hundred fifty-one patients were identified from the databased after data cleaning and were included in the final analysis. Thirty-two percent of patients had died, 23.8% had surgery, 13.3% were discharged due to worsening/severe comorbidity, 3.1% had been transferred and 27.7% were still active in surveillance. A longer time to surgery was significantly associated with increasing age on entering surveillance OR (95% CI) 0.95 (0.94–0.96) (P < 0.001), smaller initial AAA size 4.26 (3.80–4.78) (P < 0.001) but not female gender. Impaired survival was associated with increasing age 1.06 (1.05–1.07) (P < 0.001), initial AAA size, 1.56 (1.39–1.74) (P < 0.001) and female gender 1.40 (1.18–1.67) (P < 0.001). Overall, death occurred more frequently than operative repair every year over all 15 years. Out of the deaths where cause was known (n = 401), 34.9% (n = 108) were due to cardiovascular events, 27.3% (n = 109) due to malignancy (primarily lung), and 19.3% due to respiratory disease. ConclusionsBased on this data, death, primarily due to cardiovascular events, is a more likely outcome than operative repair in patients on AAA surveillance and is associated with increasing age, increasing AAA size and female gender. A median time on surveillance of over three and a half years provides sufficient time to affect subsequent health outcomes in this population and therefore a shift of focus of AAA surveillance programmes to address cardiovascular, malignancy and respiratory disease risk is warranted.

Follow-up Compliance is Not Contingent on Insurance Provider, Race, Socioeconomic Status, or Patient Comorbidities in Abdominal Aortic Aneurysm Surveillance

Many vascular surgery patients will be lost to follow-up. We aimed to determine whether socioeconomic status (SES), insurance provider, race, or comorbidities affected the appropriate surveillance of patients with a known abdominal aortic aneurysm (AAA). Patients aged >18 years evaluated in the outpatient setting from October 2009 to January 2020 for AAAs were eligible. Race, gender, insurance status or provider, zip code, comorbidities, age, date of initial presentation, initial AAA size, AAA growth, and subsequent follow-up and imaging studies were collected. Appropriate follow-up was defined by the 2009 Society for Vascular Surgery (SVS) practice management guidelines for AAA surveillance, and a metric of >80% compliance with the guidelines was set. The median household income was obtained from the U.S. Census Bureau. Data analysis was performed using SPSS (IBM Corp, Armonk, NY). The study included 140 patients (Table). Appropriate follow-up and imaging with >80% compliance with guidelines was achieved for 64% of the patients. Aneurysm growth at follow-up had occurred in 94 patients; 59 had undergone repair, 3 of which were emergent. Finally, 35% of patients were ultimately lost to follow-up, even if initially compliant. Mortality was 20%. SES, race, insurance provider, and all comorbid conditions did not significantly affect compliance with appropriate follow-up or loss to follow-up. Rigorous follow-up of patients with AAAs is indicated by the SVS guidelines. Previous studies have identified several at-risk groups for diminished follow-up in vascular pathologies. For surveillance of known AAAs, only 64% of patients achieved 80% compliance with the SVS guidelines for follow-up and 35% of patients were lost to follow-up. No single factor, including insurance provider, SES, race, or comorbidities, significantly contributed to either loss to follow-up or noncompliance with SVS guidelines. Many patients experienced AAA growth and had ultimately required intervention, warranting further study into the explanations for inappropriate/loss to follow-up. Additional education of patients and practitioners alike regarding appropriate follow-up (including improved medical record automation) has the potential to improve surveillance and should also be strongly considered.TablePatient demographicsDemographicPatients, No.Sex Male101 Female39Race White106 Black33 Hispanic0 Asian0 Other1Insurance status Yes133 No6Insurance provider Private28 Medicare101 Medicaid4SES Poor/near poor15 Lower middle class80 Middle class41 Upper middle class4Comorbidity CAD/MI72 CHF21 COPD37 CVA30 PVD31 CKD/ESRD31 DM30 Cancer47CAD, Coronary artery disease; CHF, congestive heart failure; CKD, chronic kidney disease; COPD, chronic obstructive pulmonary disease; CVA, cerebrovascular accident; DM, diabetes mellitus; ESRD, end-stage renal disease; MI, myocardial infarction; PVD, peripheral vascular disease; SES, socioeconomic status. Open table in a new tab

Temporal Changes in Intraluminal Thrombus Volume Within Abdominal Aortic Aneurysms: Implications for Planning Endovascular Aneurysm Sealing

Purpose: To explore whether or not there are temporal changes in the abdominal aortic aneurysm (AAA) and intraluminal thrombus (ILT) volumes between planning and implantation of the endovascular aneurysm sealing (EVAS) device and how these changes influence lumen volume. Methods: A retrospective review was conducted of 51 AAA patients (mean age 76±7.1 years; 36 men) in whom 2 serial preoperative computed tomography angiograms (CTAs) had been performed within 1 to 18 months before fenestrated endovascular repair. The 2 preoperative CTAs were analyzed to identify changes in total sac, ILT, and lumen volumes. Results: Over a median 7.0 months (interquartile range 4, 10), 46 (90%) of 51 AAAs increased in volume between the 2 CTAs. ILT volume increased in 44 aneurysms. In contrast, lumen volume increased in 31 and decreased in 20 AAAs. There was a strong correlation between changes in AAA volume and ILT volume (rs=0.859, p<0.001), which remained significant after adjustment for initial volumes (rs=0.815; p<0.001). There was no correlation between the time interval separating the 2 CTAs and changes in AAA volume (rs=0.115; p=0.421), changes in ILT volume (rs=0.084; p=0.599), or changes in lumen volume (rs=0.060; p=0.676). The AAA growth rate (defined as the change in AAA size/days between CTAs) showed a weak correlation with ILT volume (rs=0.272, p=0.054), which disappeared after adjustment for initial AAA size (rs=−0.002, p=0.991). Between the 2 CTAs, 12 aneurysms crossed the new <1.4 Nellix maximum aorta/lumen diameter ratio. Conclusion: As AAAs grow, the increase in aortic volume is largely occupied by additional ILT formation, with minimal change in lumen volume. These changes may alter the suitability of the aneurysm for the Nellix device and could have implications for EVAS planning and device deployment.

Biomarkers of AAA progression. Part 1: extracellular matrix degeneration

Abdominal aortic aneurysm (AAA) is an important health problem. Elective surgical treatment is recommended on the basis of an individual's risk of rupture, which is predicted by AAA diameter. However, the natural history of AAA differs between patients and a reliable and individual predictor of AAA progression (growth and expansion rates) has not been established. Several circulating biomarkers are candidates for an AAA diagnostic tool. However, they have yet to meet the triad of biomarker criteria: biological plausibility, correlation with AAA progression, and prediction of treatment effect on disease outcome. Circulating levels of markers of extracellular matrix degeneration, such as elastin peptides, aminoterminal propeptide of type III procollagen, elastase-alpha1-antitrypsin complexes, matrix metalloproteinase 9, cystatin C, plasmin-antiplasmin complexes and tissue plasminogen activator, have been correlated with AAA progression and have biological plausibility. Although studies of these markers have shown promising results, they have not yet led to a clinically applicable biomarker. In future studies, adjustment for initial AAA size, smoking history and the measurement error for determination of AAA size, among other variables, should be taken into account. A large, prospective, standardized, follow-up study will be needed to investigate multiple circulating biomarkers for their potential role in the prediction of AAA progression, followed by a study to investigate the effect of treatment on the circulating levels of biomarkers.

The role of aortic neck dilation and elongation in the etiology of stent graft migration after endovascular abdominal aortic aneurysm repair with a passive fixation device

Endovascular repair of abdominal aortic aneurysm (AAA) is complicated by the potential for stent graft migration over time. Factors including the type of fixation, initial proximal fixation length, and dilation and elongation of the infrarenal aortic neck may contribute to device migration. We sought to determine when device migration is a real phenomenon with actual device movement that compromises aneurysm exclusion. Computed tomographic (CT) scans and computer reconstructions of all patients undergoing endovascular AAA repair with a passive fixation device at our institution from June 1996 to October 2004 were retrospectively reviewed. The distance from the distal renal artery to the proximal end of the stent graft at the time of initial deployment was determined for each patient. Migration was defined as a distance increase greater than 5 mm in the follow-up period; proximal fixation length, aortic neck enlargement and elongation, and neck angle were then measured. Data were further analyzed with respect to AAA growth, development of endoleak, AAA rupture, and the need for reintervention. A total of 308 patients with endovascular AAA repairs using a passive fixation device had complete postoperative imaging data sets; 48 patients (15.6%) with stent graft migration of 5 mm or more were identified, and 25 (8.1%) of these had a migration of 10 mm or more. Seventeen (35.4%) of 48 migration patients had a total loss of the proximal seal zone (loss patients); their average migration distance was 17.7 +/- 12.0 mm, with a mean neck shortening of 13.6 +/- 14.2 mm, and the average proximal fixation length loss was 14.0 +/- 7.6 mm. Those 31 patients with an intact proximal seal zone (nonloss patients) showed an average migration of 9.4 +/- 3.7 mm, with a mean neck lengthening of 9.6 +/- 8.4 mm and an average proximal fixation length change of 0.7 +/- 8.0 mm. Univariate analysis demonstrated significant differences between the loss and nonloss patients in follow-up duration (65.9 +/- 20.4 months vs 45.9 +/- 26.4 months; P = .01), neck dilatation at the distal renal artery (4.6 +/- 4.5 mm vs 1.8 +/- 1.9 mm; P = .026), stent graft migration distance (17.7 +/- 12.0 mm vs 9.4 +/- 3.7 mm; P = .001), change in aortic neck length (-13.6 +/- 14.2 mm vs 9.6 +/- 8.4 mm; P < .0001), change in proximal fixation length (-14.0 +/- 7.6 mm vs 0.7 +/- 8.0 mm; P < .0001), change in AAA size (1.8 +/- 7.1 mm vs -3.6 +/- 9.7 mm; P = .033), and use of a stiff body stent graft (47.1% vs 19.4%; P = .043). However, only change in aortic neck length was statistically significant on multivariate analysis (odds ratio, 0.75; 95% confidence interval, 0.591-0.961; P = .022). There were no differences between the loss and nonloss patients in time to migration discovery, initial AAA size, initial aortic neck diameter or length, initial device oversizing, initial neck angle, neck angle increase, type II endoleak, or AAA rupture. Eight of the 17 loss patients have been treated with proximal aortic cuffs; the remainder have refused reintervention, died of unrelated causes, or elected to have open repair. Postoperative elongation of the infrarenal aortic neck may create the radiographic perception of migration without necessarily causing a loss of proximal stent graft fixation. Patients with a total loss of the proximal seal zone actually have infrarenal aortic neck shortening, with a degree of neck dilatation beyond initial device oversizing that may compromise proximal fixation length. Conversely, those with an intact proximal seal zone demonstrate aortic neck elongation equivalent to migration, with no loss of proximal fixation length; these patients have a benign natural history without intervention. Thus, aortic neck dilatation beyond oversizing, aortic neck shortening, and loss of proximal fixation length are more clinically relevant predictors of proximal stent graft failure than simple migration distance.

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.

Vascular surgical society of great britain and ireland: immunoglobulin A antibodies against chlamydia pneumoniae are associated with expansion of small abdominal aortic aneurysms and declining ankle blood pressure

BACKGROUND: The potential correlation between chronic infection with Chlamydia pneumoniae and the progression of small abdominal aortic aneurysms (AAAs) and lower limb atherosclerosis was studied. METHODS: Mass screening for AAA was carried out in outdoor clinics at all hospitals in the county. Some 139 men (aged 65-73 years) with a 3.0-4.9-cm AAA were followed prospectively for 1-3 (mean 2.7) years. Initially, an interview and examination was performed, and blood samples were taken. RESULTS: Some 62 per cent (53-71 per cent) had an immunoglobulin (Ig) A level of 40 or more, or an IgG level of 64 or above. Some 83 per cent (74-93 per cent) had an IgA level of 20 or more, or an IgG level of 32 or more. Men with an IgA level of 20 or more had 51 per cent greater AAA expansion and men with an IgA level of 40 or above had 24 per cent more expansion. An IgA level of 20 or more, or IgA of 40 or greater, were significant independent predictors of AAA expansion adjusted for age, smoking, initial AAA size, steroid treatment, diastolic blood pressure, pulmonary function and other plasma factors. The ankle blood pressure index (ABI) of the IgA-seropositive men decreased 11 per cent, while the ABI decreased by 5 per cent among IgA-seronegative men (P < 0.05). The significant difference persisted after adjusting for age, smoking, initial systolic ankle blood pressure, initial brachial systolic or diastolic blood pressure, but disappeared after adjusting for low-density lipoprotein (LDL) levels. CONCLUSION: A high proportion of men with a small AAA have signs of chronic C. pneumoniae infection. The progression of AAAs and lower limb atherosclerosis seems to be correlated to chronic infection with C. pneumoniae.

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.

Systemic levels of plasmin–antiplasmin complexes are correlated with the expansion rate of small abdominal aortic aneurysms

Abstract Background The cystatine proteolytic system, the serine proteolytic system and the metallodependent proteolytic system have all been reported to be involved in the matrix degradation of the aortic wall, causing abdominal aortic aneurysm (AAA). Plasmin is a common activator of all three systems and could theoretically be involved in the pathogenesis of AAA by activating all three systems. However, plasmin is immediately inactivated by antiplasmin, forming plasmin–antiplasmin (PAP) complexes when it reaches the circulation. This study was designed to assess whether the systemic levels of PAP complex in conservatively treated patients with AAA could be related to the natural history of AAA. Methods In 1994, 112 of 141 men with AAA (greater than 3 cm) diagnosed by population screening were interviewed, examined, and had blood samples taken and prepared for serum and ethylenediamine tetra-acetic acid plasma by a standard method. The serum and plasma were frozen at − 21°C until analysis. Of the 112 patients, 99 were followed with annual control scans and blood pressure measurements for 1–5 (mean 2·5) years, and were referred for operation if the AAA exceeded 5 cm in diameter. Of the 99 patients, a random sample of 70 had their level of PAP complexes determined (Dade Behring, Rødovre, Denmark). Furthermore, the level of serum elastin peptides (SEPs) was determined by enzyme-linked immunosorbent assay. Spearman's rank sum correlation test, multivariate linear regression analysis and receiver–operator characteristic (ROC) curve analysis were used for statistical analysis (SPSS 10.0; SPSS, Chicago, Illinois, USA). Results The level of PAP complex was positively correlated with annual expansion rate (r = 0·29, P = 0·01), but not with the initial AAA size (r = 0·17, P = 0·16) or SEP (r = 0·04, P = 0·77). The significant association to expansion persisted after adjustment for initial AAA size, SEP and smoking. Furthermore, the level of PAP complex was significantly predictive for AAAs expanding to operation recommendable size (area under ROC curve 65 per cent), with an optimal sensitivity and specificity of 65 and 67 per cent respectively. SEP level was also significantly predictive for AAAs expanding to operation recommendable size (area under ROC curve 56 per cent), with an optimal sensitivity and specificity of 56 and 57 per cent. Conclusion The progression of AAA seems to be caused by a general activation of the proteolytic systems involving plasmin and not by genetic or environmental factors causing increased activation of specific proteases or decreased activity of their specific inhibitors. Furthermore, the level of PAP complex in patients with an aneurysm seems to have a better and independently predictive value of the natural history of AAA, compared with the best serological predictor known to date, the serum level of elastin peptides.

Indications of infection with Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysm

Abstract Background This was a study of the possible association between the progression of abdominal aortic aneurysm (AAA) and indicators of infection with Chlamydia pneumoniae. Methods Blood samples were taken from patients with AAA (3 cm diameter or greater detected by an aneurysm screening programme) who had been followed prospectively for up to 11·5 (mean 4·1) years. A sex- and age-matched control group was also recruited. Immunoglobulin (Ig) G and IgA antibodies against C. pneumoniae were measured by a microimmunofixation test. Analysis of variance, multiple linear regression and logistic regression were used for statistical analysis. Ninety men and ten women with a small AAA and 20 age-matched male controls were investigated. Outcome measures studied were AAA expansion, and IgA and IgG titres of antibodies against C. pneumoniae. Results Forty-four (95 per cent confidence interval (c.i.) 31–55) per cent of the men with an AAA had IgA greater than 64 or IgA above 28 compared with 10 per cent of the women with an AAA (odds ratio (OR) 7·2 (95 per cent c.i. 1·0–160·8)) and 25 per cent of the controls (OR 2·24 (95 per cent c.i. 0·67–7·93)). IgA greater than 128 was significantly associated with greater expansion (5·3 versus 2·6 mm per year), even after adjustment for initial AAA size and age. A significant dose–response reaction was found between IgA titre and mean annual expansion (R = 0·45 (95 per cent c.i. 0·24–0·62)). The significant positive correlation remained after adjusting for initial AAA size and age. Finally, IgG greater than 128 was present significantly more often in patients with expansion above 1 cm annually (OR 12·6 (95 per cent c.i. 1·4–293)). Conclusion A high proportion of men with AAA have signs of infection by C. pneumoniae. The progression of AAAs correlated with the presence of indicators of C. pneumonia infection, and a dose–response reaction between IgA titre and expansion was observed.

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.

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.

Plasma levels of plasmin-antiplasmin-complexes are predictive for small abdominal aortic aneurysms expanding to operation-recommendable sizes

Objective: Three proteolytic systems seem involved in the aneurysmal degradation of the aortic wall. Plasmin is a common activator of the systems and could thus be predictive for the progression of abdominal aortic aneurysms (AAAs). Methods and Materials: In 1994, 112 of 141 male patients with AAA diagnosed through population screening (defined as 3 cm or more) were interviewed and examined and had blood samples taken. One hundred twelve cases were scanned annually for 1 to 5 years (mean, 2.5 years) and referred for surgery if the AAA exceeded 5 cm in diameter. A random sample of 70 of the 112 cases had P-plasmin-antiplasmin-complexes (PAPs), P-plasminogen, and S-elastin-peptides (SEPs). Results: PAP was positively correlated with annual expansion rate (r = 0.39, 0.16-0.56), persisting after adjustment for initial AAA size, SEP, age, and smoking. However, PAP levels did not correlate with the initial AAA size or SEP. Furthermore, PAP levels were significantly predictive for cases expanding to operation-recommendable AAA sizes. Combined with the initial AAA size, both optimal sensitivity and specificity were 82%, increasing to 95% and 96%, respectively, excluding those lost to follow-up and accepting 2 mm of interobserver variation. Conclusion: The progression of AAA is correlated with the PAP level, which seems to have a predictive value similar to the best serologic predictor known, serum-elastin-peptides. (J Vasc Surg 2001;34:611-5.)

Indicators of infection with Chlamydia pneumoniae are associated with expansion of abdominal aortic aneurysms

Purpose:Chlamydia Pneumoniae has been shown to be associated with atherosclerosis, myocardial infarction, and abdominal aortic aneurysms (AAAs). The possible association between AAA expansion and C pneumoniae infection was therefore assessed. Methods: Blood samples were taken from patients with an AAA that was considered for surgical repair after having been diagnosed by means of the Chichester aneurysm screening program (UK) as having an initially infrarenal aortic diameter of 3.0 to 5.9 cm. The patients were examined prospectively for as long as 11.5 years (mean, 4.1 years) with ultrasound scanning. Of 110 patients considered for surgery, 90 men and 10 women had blood samples taken. Their IgG and IgA antibodies against C pneumoniae were measured by means of a microimmunofluorescence test. Unpaired t tests, multiple linear regression analyses, and logistic regression analyses were used for statistical analysis. Results: A total of 44% (95% CI, 31%-55%) of the men with an AAA had an IgA titer of 64 or more, an IgG titer of 128 or more, or both, compared with 10% of the women with an AAA (OR = 7.2; 95% CI, 1.05-160.8). A titer of IgG of 128 or more was significantly associated with higher expansion (5.3 vs 2.6 mm per year), even after adjustment for initial AAA size and age. A significant positive correlation between both IgA and IgG titers and mean annual expansion was observed (r = 0.28; 95% CI, 0.05-0.49; and r = 0.45; 95% CI, 0.24-0.62, respectively), persisting after adjusting for initial AAA size and age. An IgG titer of 128 or more was present significantly more often in cases with an expansion greater than 1 cm annually (adjusted OR = 12.6; 95% CI, 1.37-293). Conclusion: A high proportion of men with an AAA has signs of infection with C pneumoniae. The progression of their AAAs was positively correlated with the presence of indicators of C pneumoniae infection. (J Vasc Surg 2001;34:212-5.)

Five-year results of elastin and collagen markers as predictive tools in the management of small abdominal aortic aneurysms.

small abdominal aortic aneurysms (AAAs) do rupture and only half of AAAs above 5 cm would have ruptured unoperated. Furthermore, conservative treatment of AAAs may cause psychological side effects and impaired quality of life. To optimise the indication and time for operation for AAAs, we analysed whether serum elastin peptides (EP), procollagen-IIIN-terminal propeptide (PIIINP), and the initial AAA size could predict operation for AAAs in initially conservatively treated AAA. in 1994, 4404 65-73 year old males were invited to hospital-based screening for AAAs by ultrasonography. Seventy-six percent attended. One hundred and forty-one (4.2%) had AAAs (def: +30 mm). Nineteen were offered operation (AAA +50 mm), and 112 were followed with annual control scans for 1-5 years (mean 2.5 years). Of these, 99 had their EP (ng/ml) and PIIINP (ng/ml) determined using ELISA and RIA techniques. Two observers and one scanner were used. the mean expansion rate was 2.7 mm/year. The initial AAA size (r =0.46; 0.26-0.61), EP ( r =0.31; 0.11-0.49), and NPIIIP ( r =0.24; 0.02-0.44) was independently significant associated to expansion rate in a multiple linear regression analysis including the three mentioned variables. The multivariate formula could by ROC curve analysis predict cases reaching 5 cm in diameter within 5 years with a sensitivity and specificity of 91% and 87%, respectively, increasing to 91% and 94%, respectively, by accepting a 2 mm variation in those measurements. Twenty-three were lost to follow up, 21 of these due to death or severe illness. Of these, seven would have been predicted to reach an AAA size recommendable for surgery. If all 23 were included in the analysis, the sensitivity and specificity would have been 87% and 85%, respectively. a predictive model using EP, PIIINP, and initial AAA size seems capable of predicting nine out of 10 AAAs that will be operated on within 5 years. However, a larger sample size is needed for clinical recommendations.

Smoking, but not lipids, lipoprotein(a) and antibodies against oxidised LDL, is correlated to the expansion of abdominal aortic aneurysms.

to study the role of smoking, lipids, lipoprotein (a), and autoantibodies against oxidised low density lipoprotein (Ab-oxLDL) in the expansion of small abdominal aortic aneurysms (AAA). To study the role of Ab-oxLDL and lp(a) in the progression of lower limb atherosclerosis. one hundred and thirty-eight male patients with AAA were interviewed, examined, and their serum lipids and S-Ab-oxLDL determined. Of these, 117 were followed annually with ultrasound and underwent control scans and blood pressure measurements for a mean of 2.5 (range 1-5) years. initial AAA size, smoking and level of triglycerides were positively correlated to increased aneurysmal expansion, while beta-blocker medication was associated with decreased expansion. Besides initial AAA size, only smoking had persisting significance after adjustment of the other significant variables. Initial ankle brachial pressure index (ABI) and Lp(A) but not ab-oxLDL were significantly correlated to ABI change. smoking cessation may inhibit aneurysmal expansion. Lipids seem to play a minor role in the progression of AAA.

Variables that affect the expansion rate and outcome of small abdominal aortic aneurysms

Seventy-three patients with small (<6 cm in diameter) abdominal aortic aneurysms (AAAs) were selected for nonoperative management and followed up with sequential ultrasound size measurements. Fifty-four men and 19 women, 51 to 89 years of age (mean 70 years), had an initial mean AAA size of 4.1 cm (anteroposterior) × 4.3 cm (lateral) diameter, with a calculated elliptic cross-sectional area of 14.3 cm2. After a mean of 37 months of follow-up, AAA area increased at a mean rate of 20% per year (3 cm2 yr; 0.4 to 0.5 cm/yr diameter). Expansion rate was not affected by initial aneurysm size. During follow-up, only 3 patients (4%) required urgent operation (1 died), 26 patients (36%) died of non-AAA causes, and 26 patients (36%) underwent elective AAA repair because of progressive size increase (1 died). Elective operations were performed at the rate of 10% per year, when mean AAA size had increased to 22 cm2 (5.1 cm in diameter). Multiple regression analysis of clinical parameters available at presentation indicated that subsequent elective AAA repair was predicted by younger age at diagnosis and larger initial aneurysm size. As anticipated, patients who underwent surgery had more rapid aneurysm expansion (5.3 cm2/yr) compared with patients who did not undergo surgery (1.6 cm2/yr; p < 0.05). This difference was caused by more rapid expansion during later follow-up intervals among patients selected for operation and was not predicted by the change in aneurysm size observed during initial ultrasonographic follow-up. Final aneurysm size was predicted by initial size, duration of follow-up, and both systolic and diastolic pressure. Larger initial size, longer follow-up, and widened pulse pressure predicted larger aneurysm size. Individual AAA expansion rates, however, were variable over time and could not be predicted by any parameters tested. Patients with small AAAs may be safely followed up if their pulse pressure is controlled and elective aneurysm repair is performed when aneurysm diameter reaches 5 to 6 cm based on sequential ultrasound size measurements.