The use of statins and fate of small abdominal aortic aneurysms

The aim of this study was to evaluate the value of statins in reducing abdominal aortic aneurysm (AAA) growth rate and improving freedom from aneurysm repair or rupture. One hundred and twenty-one patients with AAA undergoing ultrasonographic surveillance for at least one year were included in this retrospective study. Patients treated with statins had a decreased linear aneurysm growth rate than those not receiving statins (1.9+/-1.8 mm/year vs. 2.6+/-2.4 mm/year, P=0.27), but this difference did not reach statistical significance. Statin users had a better survival freedom from aneurysm repair or rupture (at 5 years: 72.3% vs. 52.5%, P=0.048). The impact of treatment with statins was even more evident in patients with a baseline aneurysm diameter<40 mm (at 5 years: 84.0% vs. 58.8%, P=0.022). When adjusted for age, coronary artery disease and baseline aneurysm diameter, treatment with statins had significantly better survival freedom from aneurysm repair or rupture (P=0.012, RR 0.34, 95% CI 0.14-0.78). The use of statins seems to slightly decrease the AAA growth rate and to significantly improve freedom from aneurysm repair and rupture.     

Growth rate and associated factors in small abdominal aortic aneurysms.

OBJECTIVE: To study the growth rate and factors influencing progression of small infrarenal abdominal aortic aneurysms (AAA). DESIGN: Observational, longitudinal, prospective study. PATIENTS AND METHODS: We followed patients with AAA <5 cm in diameter in two groups. Group I (AAA 3-3.9 cm, n = 246) underwent annual ultrasound scans. Group II (AAA 4-4.9 cm, n = 106) underwent 6-monthly CT scans. RESULTS: We included 352 patients (333 men and 19 women) followed for a mean of 55.2+/-37.4 months (6.3-199.8). The mean growth rate was significantly greater in group II (4.72+/-5.93 vs. 2.07+/-3.23 mm/year; p<0.0001). Group II had a greater percentage of patients with rapid aneurysm expansion (>4 mm/year) (36.8 vs. 13.8%; p<0.0001). The classical cardiovascular risk factors did not influence the AAA growth rate in group I. Chronic limb ischemia was associated with slower expansion (< or = 4 mm/year) (OR 0.47; CI 95% 0.22-0.99; p = 0.045). Diabetic patients in group II had a significantly smaller mean AAA growth rate than non-diabetics (1.69+/-3.51 vs. 5.22+/-6.11 mm/year; p = 0.032). CONCLUSIONS: The expansion rate of small AAA increases with the AAA size. AAA with a diameter of 3-3.9 cm expand slowly, and they are very unlikely to require surgical repair in 5 years. Many 4-4.9 cm AAA can be expected to reach a surgical size in the first 2 years of follow-up. Chronic limb ischemia and diabetes are associated with reduced aneurysm growth rates.     

Influence of sex on expansion rate of abdominal aortic aneurysms

BACKGROUND: The UK Small Aneurysm Trial suggested that female sex is an independent risk factor for rupture of abdominal aortic aneurysm (AAA). This study assessed the effect of sex on the growth rate of AAA. METHODS: Between January 1985 and August 2005 all patients who were referred to the Royal Infirmary of Edinburgh with an AAA who were not considered for early aneurysm repair were assessed by serial abdominal ultrasonography. Maximum anteroposterior and transverse diameters of the AAAs were measured. RESULTS: A total of 1255 patients (824 men and 431 women) were followed up for a median of 30 (range 6-185) months. A median of six examinations (range 2-37) was performed for each patient. Median diameter on initial examination was 41 (range 25-83) mm. Median growth rate overall was 2.79 (range - 4.80-37.02) mm per year. Median growth rate of AAA was significantly greater in women than men (3.67 (range - 1.2-37.02) versus 2.03 (range - 4.80-21.00) mm per year; P < 0.01). Weighted linear regression analysis revealed that large initial anteroposterior AAA diameter and female sex were significant predictors of faster aneurysm growth rate (P < 0.001 and P = 0.006 respectively). CONCLUSION: The growth rate of AAA was significantly greater in women than in men. This may have implications for the frequency of follow-up and timing of repair of AAA in women.     

Hyperhomocysteinaemia is associated with the rate of abdominal aortic aneurysm expansion.

OBJECTIVES: Previous literature has suggested an association between AAA and the presence of elevated plasma homocysteine levels (HCY). Homocysteine can stimulate elastolysis in the arterial media via activation of elastase and matrix metalloproteinases. No evidence in the literature exists correlating aneurysm expansion and HCY. The study objective is to identify whether the rate of AAA expansion is related to HCY. METHODS: 108 patients undergoing surveillance for AAA were identified at our vascular surgical unit. AAA size and growth rate were assessed by serial ultrasonographic measurements. Fasting total HCY levels were measured using fluorescence polarisation immunoassays. Demographic details and atherosclerotic risk factors were noted all AAA patients. A multivariate analysis was performed for growth rate vs. HCY, hypertension and hypercholesterolaemia. The correlation between AAA growth rate, AAA size and HCY levels were calculated. RESULTS: 60% of patients with AAA had some degree of hyperhomocysteinaemia (> 15 micromol/l). Multivariate analysis showed HCY to be the only significant factor affecting AAA growth rate. A positive correlation was demonstrated between HCY levels and AAA growth rate using a linear regression model (R=0.28, p=0.003). Median growth rate among patients with hyperHCY was double that of patients with normal HCY (0.5 mm/month vs. 0.25 mm/month, p=0.003). A growth rate of > 10 mm/year was seen in 25% of hyper HCY patients and in only 2% of patients with normal HCY. In addition patients with hyper HCY and larger AAAs (> 4 cm) had a growth rate twice as fast as patients with hyper HCY and AAAs < 4 cm. CONCLUSIONS: A correlation between HCY and growth rate exists, although this is weak due to the multifactorial aetiology of AAAs. HyperHCY patients have faster expansion rates than patients with normal HCY, with significant numbers demonstrating rapid expansion (> 10 mm/year) and therefore an increased risk of rupture.     

Surveillance of small aortic aneurysms does not alter anatomic suitability for endovascular repair

OBJECTIVE: Small abdominal aortic aneurysms (AAAs; 4-5.4 cm) are more likely to be suitable for endovascular aneurysm repair (EVAR) than large aortic aneurysms (>5.5 cm). The purpose of this study was to determine whether small AAA growth is associated with the development of morphologic characteristics that decrease eligibility for EVAR. METHODS: We studied 54 patients who underwent 2 or more computed tomography scans with 3-dimensional reconstruction during surveillance of small AAAs. Morphologic aortic aneurysm features and changes were measured according to Society for Vascular Surgery reporting standards. Suitability for EVAR was determined by neck anatomy (diameter, length, and angulations), iliac artery morphology, and total aortic aneurysm angulation and tortuosity. RESULTS: The median age of the study cohort was 73 years (interquartile range [IQR], 65-77 years). The median follow-up period was 24 months (IQR, 15-36 months). The median small AAA diameter increased from 44.5 mm (IQR, 41-48 mm) to 48.9 mm (IQR, 45.7-52.0 mm). The median aortic neck diameter increased from 23.0 to 24.0 mm (P = .002), whereas median neck length decreased from 26.5 to 20.0 mm (P = .001). Aortic aneurysm median tortuosity index increased from 1.09 to 1.11 (P = .05). No significant changes in iliac artery morphology occurred. Overall, the anatomic suitability for endovascular repair did not significantly change during the study period (74% vs 69%; McNemar test; P = .25). CONCLUSIONS: Changes in aortic morphology are frequently associated with small AAA growth at mid-term follow-up, but such changes are minor and do not affect overall anatomic suitability for EVAR. These data reveal that continued surveillance of small AAAs does not threaten the window of opportunity for EVAR.     

Abdominal aortic aneurysms following orthotopic heart transplantation

The purpose of these authors' study was to analyze their center's experience with orthotopic heart transplantation (OHT) and abdominal aortic aneurysms (AAA) with particular attention to corticosteroid dosing, hemodynamic parameters, and aneurysm growth rate. A retrospective review of all patients (453) who underwent OHT at their university-affiliated medical center over an 18-year period (1981-1999) was undertaken. Nine (2%) patients who developed AAAs were identified and aneurysm growth was correlated with corticosteroid immunosuppression and hemodynamic parameters. The mean age of OHT patients was 44.5 +/-15 years and the majority were males (371 males, 82%). Median follow-up was 5.7 years. Ischemic cardiomyopathy (IC) was the most common indication for transplantation (45.5% of patients). All AAA patients were male (p=0.157), with a mean age of 58.4 +/-4.8 years (p=0.001), and had undergone OHT for IC (p=0.001). Mean arterial blood pressure and ejection fraction in the AAA patients had increased from pretransplant values of 107 mm Hg and 14.3 +/-5.7% to 142 mm Hg (p=0.017) and 54.1 +/-14.1% (p<0.001), respectively, before aneurysm repair. Mean aneurysm diameter at the time of repair was 6.0 +/-0.8 cm, and the average growth rate was 1.2 +/-0.4 cm/year in the 4 patients in whom it could be measured. Aneurysm repair was performed urgently in 2 patients and electively in 7 patients with 1 early postoperative death (11%). The extent of corticosteroid immunosuppression, corticosteroid pulses, and total corticosteroid dosing did not correlate with the rate of aneurysm growth. Improved hemodynamics and progressive posttransplant hypertension may contribute to aneurysm formation and growth in this group of patients.     

Analysis of expansion patterns in 4-4.9 cm abdominal aortic aneurysms

Our objective was to analyze the growth pattern of 4-4.9 cm infrarenal abdominal aortic aneurysms (AAAs). We used an observational, longitudinal, prospective study design. We followed 4-4.9 cm AAAs with 6-monthly abdominal computed tomographic (CT) scans (January 1988-August 2004). AAA growth was defined as an increase in aortic diameter > or =2 mm in each surveillance period. We established the aortic expansion pattern in AAA with three or more CT scans as continuous, discontinuous. The latter includes at least one period of nongrowth (<2 mm/6 months). We studied the influence of cardiovascular risk factors (CVRFs), comorbidity, and AAA anatomical characteristics using the chi-squared test, t-test, life tables, and Kaplan-Meier for statistical analysis. We included 195 patients: 183 (93.8%) men, age 71 +/- 8.3 years (50-90). The follow-up period was 50 +/- 36.4 months (6.5-193.7). The growth pattern (n =131) was continuous in 15 (11.5%) and discontinuous in 116 (88.5%) AAA. The mean expansion rate was higher in AAAs with continuous expansion (7.92 +/- 3.74 vs. 2.74 +/- 2.94 mm/year, p < 0.0001). No CVRFs or comorbidity influenced the expansion pattern (p > 0.05). The eccentric thrombus was associated with a greater incidence of continuous growth (p = 0.05), with no influence of aortic calcification (p > 0.1). The expansion of 4-4.9 cm AAA is mostly irregular and unpredictable. We have not found any modifiable risk factors which influence their growth pattern. The eccentric distribution of the thrombus is associated with continuous expansion.     

Genotype-phenotype relationships in an investigation of the role of proteases in abdominal aortic aneurysm expansion

BACKGROUND: The aim of the study was to investigate the effect of functional polymorphisms in promoters of matrix metalloproteinase (MMP) 2, MMP-3, MMP-9, MMP-12 and plasminogen activator inhibitor (PAI) 1 genes on the growth rate of small abdominal aortic aneurysms (AAA). METHODS: Some 455 individuals with a small AAA (4.0-5.5 cm) were monitored for aneurysm growth by ultrasonography (mean follow-up 2.6 years). They also provided a DNA sample for analysis of the -1306 C > T, -1171 5A > 6A, -1562 C > T, -82 A > G and -675 4G > 5G alleles of MMP-2, MMP-3, MMP-9, MMP-12 and PAI-1, respectively. Mean linear AAA growth rates were calculated by flexible modelling; the sample size was sufficient to detect variants that influenced the growth rate by 25 per cent. RESULTS: For MMP-2, MMP-9 and MMP-12 genotypes, growth rates were similar to the mean linear growth rate of 3.08 mm per year. For MMP-3, growth rates were 3.05 (for 5A5A), 3.19 (for 5A6A) and 2.90 (for 6A6A) mm per year. For PAI-1, patients with 4G4G, 4G5G and 5G5G genotypes had growth rates of 3.18, 2.92 and 3.47 mm per year, respectively, for aneurysms with a baseline diameter of 45.1, 44.6 and 46.2 mm. The increased growth rate for patients with PAI-1 5G5G genotype was not statistically significant (P = 0.061), although these patients had the lowest plasma PAI-1 concentrations (P = 0.018). CONCLUSION: There was no evidence that any specific MMP polymorphism had a clinically significant effect on AAA expansion. The plasminogen system may have a small but clinically significant role in AAA development. Much larger studies would be needed to evaluate genes of smaller effect.     

Optimal interval screening and surveillance of abdominal aortic aneurysms.

OBJECTIVES: to determine safe and optimal intervals of rescreening and surveillance for AAA. METHODS: hospital-based mass screening of 6339 65-73-year-old men from 1994-98. 76.4% attended. One hundred and ninety-one (4%) had AAA53 cm. Twenty-four (0.5%) were initially >5 cm and referred for surgery, while the rest were offered annual control scans to check for expansion. Later, all 348 (7.5%) men who 3 to 5 years ago had an ectatic aorta (infrarenal aortic diameter of 25-29 mm or distal/renal aortic diameter ratio >1.2) were offered rescreening. Of these, 62 (18%) died before rescanning, while 248 of the survivors attended rescreening (87%). Furthermore, a random sample of 380 of those with non-ectatic aortas were offered rescreening. Of these, 49 (13%) died before rescreening (p=0.06), while 275 (83%) of the survivors attended re-screening. RESULTS: none of the controls had developed AAA. Of those who initially had an 25-29 mm aorta, 29% had developed AAA (size range 30-48 mm) with expansion rates varying from 1.0 to 4.7 mm/year. Only 3.5% with a ratio >1.2 developed AAA (size range: 30-34 mm) with expansion rates from 1.3 to 2.4 mm/year. During the fourth year of surveillance some AAA initially sized below 3.5 cm expanded to above 5 cm, while some sized 3.5-3.9 cm did so during the second year, >4 cm did so during the first year of surveillance. CONCLUSION: rescreening for AAA can be restricted to initially ectatic aortas sized 25-29 mm at 5-year intervals. Surveillance of small AAA can be restricted to 1-4 year intervals.     

Growth predictors and prognosis of small abdominal aortic aneurysms

OBJECTIVE: Evidence regarding the influence of cardiovascular risk factors, comorbidities, and patient characteristics on the growth of small abdominal aortic aneurysms (AAA) is limited. We assessed, in an observational cohort study, rupture rates, risks of mortality, and the effects of cardiovascular risk factors and patient demographics on growth rates of small AAAs. METHODS: Between September 1996 and January 2005, 5057 patients with manifest arterial vascular disease or cardiovascular risk factors were included in the Second Manifestation of ARTerial disease (SMART) study. Measurements of the abdominal aortic diameter were performed in all patients. All patients with an initial AAA diameter between 30 and 55 mm were selected for this study. All AAA measurements during follow-up until August 2007 were collected. Multivariate regression analysis was performed to calculate the effects of demographic patient characteristics, initial AAA diameter, and cardiovascular risk factors on AAA growth. RESULTS: Included were 230 patients, with a mean age of 66 years and 90% were male. Seven AAA ruptures (six fatal) occurred in 755 patient years of follow-up (rupture rate 0.9% per patient-year). In 147 patients, AAA measurements were performed for a period of more than 6 months. The median follow-up time was 3.3 years (mean 4.0, range 0.5 to 11.1 years, standard deviation (SD) 2.5). Mean AAA diameter was 38.8 mm (SD 6.8) and mean expansion rate 2.5 mm/y. Patients using lipid-lowering drugs had a 1.2 mm/y (95% confidence interval [CI] -2.34 to -0.060 mm/y) lower AAA growth rate compared to nonusers of these drugs. Initial AAA diameter was associated with a 0.09 mm/y (95% CI 0.01 to 0.18 mm/y) higher growth rate per millimetre increase of the diameter. No other factors, including blood lipid values, were independently associated with AAA growth. CONCLUSIONS: Lipid-lowering drug treatment and initial AAA diameter appear to be independently associated with lower AAA growth rates. The risk of rupture of these small abdominal aortic aneurysms was low, which pleads for watchful waiting.     

Endovascular repair or surveillance of patients with small AAA.

OBJECTIVE: To compare the outcome of patients with small abdominal aortic aneurysms (AAA) treated in a prospective trial of endovascular aneurysm repair (EVAR) to patients randomized to the surveillance arm of the UK Small Aneurysm Trial. METHOD: All patients with small AAA (< or = 5.5 cm diameter) treated with a stent graft (EVARsmall) in the multicenter AneuRx clinical trial from 1997 to 1999 were reviewed with follow up through 2003. A subgroup of patients (EVARmatch) who met the age (60-76 years) and aneurysm size (4.0-5.5 cm diameter) inclusion criteria of the UK Small Aneurysm Trial were compared to the published results of the surveillance patient cohort (UKsurveil) of the UK Small Aneurysm Trial (NEJM 346:1445, 2002). Endpoints of comparison were aneurysm rupture, fatal aneurysm rupture, operative mortality, aneurysm related death and overall mortality. The total patient years of follow-up for EVAR patients was 1369 years and for UK patients was 3048 years. Statistical comparisons of EVARmatch and UKsurveil patients were made for rates per 100 patient years of follow up (/100 years) to adjust for differences in follow-up time. RESULTS: The EVARsmall group of 478 patients comprised 40% of the total number of patients treated during the course of the AneuRx clinical trial. The EVARmatch group of 312 patients excluded 151 patients for age < 60 or > 76 years and 15 patients for AAA diameter < 4 cm. With the exception of age, there were no significant differences between EVARsmall and EVARmatch in pre-operative factors or post-operative outcomes. In comparison to the UKsurveil group of 527 patients, the EVARmatch group was slightly older (70 +/- 4 vs. 69 +/- 4 years, p = 0.009), had larger aneurysms (5.0 +/- 0.3 vs. 4.6 +/- 0.4 cm, p < 0.001), fewer women (7 vs. 18%, p < 0.001), and had a higher prevalence of diabetes and hypertension and a lower prevalence of smoking at baseline. Ruptures occurred in 1.6% of EVARmatch patients and 5.1% of UKsurveil patients; this difference was not significant when adjusted for the difference in length of follow up. Fatal aneurysm rupture rate, adjusted for follow up time, was four times higher in UKsurveil (0.8/100 patient years) than in EVARmatch (0.2/100 patient years, p < 0.001); this difference remained significant when adjusted for difference in gender mix. Elective operative mortality rate was significantly lower in EVARmatch (1.9%) than in UKsurveil (5.9%, p < 0.01). Aneurysm-related death rate was two times higher in UKsurveil (1.6/100 patient years) than in EVARmatch (0.8/100 patient years, p = 0.03). All-cause mortality rate was significantly higher in UKsurveil (8.3/100 patient years) than in EVARmatch (6.4/100 patient years, p = 0.02). CONCLUSIONS: It appears that endovascular repair of small abdominal aortic aneurysms (4.0-5.5 cm) significantly reduces the risk of fatal aneurysm rupture and aneurysm-related death and improves overall patient survival compared to an ultrasound surveillance strategy with selective open surgical repair.     

Does the presence of an iliac aneurysm affect outcome of endoluminal AAA repair? An analysis of 336 cases.

OBJECTIVE: To determine whether the presence of an iliac aneurysm compromises outcome of endovascular exclusion of AAA and to ascertain the fate of the iliac aneurysmal sac. PATIENTS AND METHODS: Between April 1997 and March 2001, data on 336 consecutive patients undergoing endovascular repair for AAA were entered in a prospective database. Suitability for endovascular repair was assessed by preoperative contrast-enhanced computed tomography. A maximum common iliac artery (CIA) diameter > or = 20 mm was defined as iliac aneurysm. Patients with and without iliac aneurysms were compared to early (immediate conversion or perioperative death) and late failure (increase in aneurysm diameter or persisting graft-related endoleak, or late AAA rupture or conversion). RESULTS: Fifty-nine patients (18%) had iliac aneurysms, 19 were bilateral, for a total of 78 aneurysmal iliac arteries (median diameter 23 mm; range 20-50 mm). A distal seal was achieved by landing in 33 external iliac arteries, in 20 ectatic CIAs, and in 25 normal CIAs. Operating time differed significantly between patients with and without CIA aneurysms (153 +/- 71 vs 123 +/- 55 min, p = 0.0001), whereas no statistically significant differences were found with respect to early and late failure (2% vs 3%, p = 0.5 and 14% vs 8%, p = 0.11, respectively). There were no cases of buttock or colon necrosis. At a median follow-up of 14 months (range 0-46; i.q.r. 7-27 months) common iliac diameter decreased > or = 2 mm in 49 cases, remained stable in 25, and increased > or = 2 mm in 3. CONCLUSION: The presence of iliac aneurysm rendered endoluminal AAA repair more complex but did not affect feasibility and long-term outcome of the procedure. In our experience internal iliac exclusion was never associated with significant morbidity. These data may be useful when considering endovascular repair in high-risk patients with challenging anatomy.     

Predicting risk of rupture and rupture‐preventing reinterventions following endovascular abdominal aortic aneurysm repair

Background

Clinical and imaging surveillance practices following endovascular aneurysm repair (EVAR) for intact abdominal aortic aneurysm (AAA) vary considerably and compliance with recommended lifelong surveillance is poor. The aim of this study was to develop a dynamic prognostic model to enable stratification of patients at risk of future secondary aortic rupture or the need for intervention to prevent rupture (rupture‐preventing reintervention) to enable the development of personalized surveillance intervals.

Methods

Baseline data and repeat measurements of postoperative aneurysm sac diameter from the EVAR‐1 and EVAR‐2 trials were used to develop the model, with external validation in a cohort from a single‐centre vascular database. Longitudinal mixed‐effects models were fitted to trajectories of sac diameter, and model‐predicted sac diameter and rate of growth were used in prognostic Cox proportional hazards models.

Results

Some 785 patients from the EVAR trials were included, of whom 155 (19·7 per cent) experienced at least one rupture or required a rupture‐preventing reintervention during follow‐up. An increased risk was associated with preoperative AAA size, rate of sac growth and the number of previously detected complications. A prognostic model using predicted sac growth alone had good discrimination at 2 years (C‐index 0·68), 3 years (C‐index 0·72) and 5 years (C‐index 0·75) after operation and had excellent external validation (C‐index 0·76–0·79). More than 5 years after operation, growth rates above 1 mm/year had a sensitivity of over 80 per cent and specificity over 50 per cent in identifying events occurring within 2 years.

Conclusion

Secondary sac growth is an important predictor of rupture or rupture‐preventing reintervention to enable the development of personalized surveillance intervals. A dynamic prognostic model has the potential to tailor surveillance by identifying a large proportion of patients who may require less intensive follow‐up.     

Does the angiotensin-converting enzyme (ACE) gene polymorphism affect rate of abdominal aortic aneurysm expansion?

OBJECTIVES: the tissue renin-angiotensin system (RAS), which plays an important role in vascular structure and function, is regulated in part by an insertion-deletion polymorphism of the angiotensin converting enzyme (ACE) gene. We hypothesised that ACE genotype might affect rate of AAA expansion via modulating long-term structural changes associated with RAS activation. METHODS: fifty-eight patients (50 M, mean age 70 years, mean initial aneurysm size 4.3 cm) with current or previous AAA and serial (>3) annual ultrasound measurements of antero-posterior AAA size provided a sample of leucocyte DNA for ACE genotyping. AAA expansion rate (cm per year) for individual subjects was calculated by linear regression. RESULTS: median AAA expansion rate was 0.28 cm/year (range 0-1.8 cm/year), and the genotype distribution included DD (n=14), DI (n=29) and II (n=15). Corresponding median AAA expansion rates for each of the three genetic subgroups were 0.22, 0.32 and 0.30 cm/year, respectively (p=0.6, nonparametric). CONCLUSIONS: the wide inter-individual variability in AAA expansion rate is likely to reflect complex genetic and environmental interactions, but the lack of any relationship with ACE genotype suggests that differences in vascular ACE activity in aortic tissue are not major determinants of the variability in rate of AAA dilatation.     

A myth exposed: fast growth in diameter does not justify precocious abdominal aortic aneurysm repair.

OBJECTIVES: fast growth of abdominal aortic aneurysm (AAA) diameter is claimed to be an indication for repair. We investigated the validity of this claim. METHODS: between January 1988 and October 2000, 277 patients have had duplex sonography at six-monthly intervals in our aneurysm surveillance programme. During this period fast AAA growth was not an indication for operation in our unit. RESULTS: we identified 63 patients whose aneurysms had grown 0.5 cm or more in 6 months. Thirty-one of the 63 patients had aneurysms measuring 5.5 cm or greater in anterior-posterior diameter after the fast growth and all have been operated on unless deemed not fit due to anaesthetic risk. The remaining 32 patients continued in surveillance for a total of 50 patient years and none had rupture of their aneurysm. The calculated 95% confidence interval for the risk of rupture was 0-6 per 100 patient years. Six patients, who would have been operated on if fast growth had been an indication, have been spared surgery of whom 3 died and 3 became unfit. Nine patients remained in surveillance at the end of the study. CONCLUSION: our data support the view that rapid increase in AAA diameter is not an indication for elective AAA repair.     

Discontinuous, staccato growth of abdominal aortic aneurysms

BACKGROUND: To evaluate whether abdominal aortic aneurysm (AAA) growth in individual patients can be characterized as continuous or discontinuous (staccato). STUDY DESIGN: From 1996 to 2002, 609 patients presented with unruptured AAAs. Of these, 278 underwent prompt repair and 331 were observed. In this study, we included 52 patients (16% of the latter group) who had at least four CT scans and were observed for 18 months or longer without any intervention. AAA growth was defined as any increase in diameter of >/= 3 mm over any observation period(s). AAA nongrowth was defined as absence of growth for at least 6 months. Staccato growth was defined as at least one period of nongrowth combined with at least one period of growth. RESULTS: The 52 patients had a mean age of 75 +/- 8 (SD) years. The mean observation period was 42 +/- 20 months and the mean AAA diameter growth rate was 3.6 +/- 2.4 mm/y. Only 12 of these 52 patients (23%) demonstrated continuous growth. Staccato growth occurred in 34 patients (65%). Six patients (12%) showed no growth at all over 18 to 57 months (mean 30 months). No correlation was observed between initial diameter of AAAs and a patient's individual growth rate during the whole observation period (R = 0.04, p = 0.46). CONCLUSIONS: Individual AAA behavior is usually characterized by periods of nongrowth alternating with periods of growth, ie, staccato growth. Some aneurysms may have long periods of nongrowth. Accordingly, management decisions cannot be based on the presumption that observed growth rates of AAAs can be extrapolated to predict future growth rates.     

Aortic necks of ruptured abdominal aneurysms dilate more than asymptomatic aneurysms after endovascular repair

BACKGROUND: Endovascular repair of abdominal aortic aneurysm (AAA) is increasingly used. We evaluated if a difference exists in the rate of change of the aortic neck diameter between non-ruptured and ruptured AAAs after endovascular aneurysm repair (EVAR). METHODS: Details of patients undergoing elective (group I) and emergency (group II) EVAR using Talent stents between October 1999 and September 2005 were reviewed. Top neck diameters were prospectively recorded on the hospital database from computed tomography scans preoperatively and at 1, 3, 12, and 24 months postoperatively. The aortic neck diameter rate of change was calculated for each group. RESULTS: Endovascular repair was performed on 110 elective and 41 emergency patients, of which 100 (80 male) elective and 29 (26 male) emergency patients were included in this analysis. Mean age was similar in each group. Stents were oversized by 20.9% +/- 13.6% in group I and by 24.7% +/- 16.3% in group II (P = .37). The preoperative mean proximal aortic neck was larger in group II (25.0 +/- 3.3 mm vs 23.5 +/- 2.8 mm; P = .029). The growth rate of the top neck diameter was significantly greater at 12 months (1.48 +/- 2.4 mm/year vs 3.89 +/- 6.24 mm/year; P = .04) and 24 months (.99 +/- 1.1 mm/year vs 2.61 +/- 3.3 mm/year; P = .04) in group II than in group I. A decreasing sac size was found in 68.2% of patients whose neck dilated. The complication rate was similar in each group. CONCLUSION: Aneurysm necks in patients with ruptured aneurysms are larger and dilate at a greater rate than those with nonruptured aneurysms. The accelerated rate of expansion in some patients must be borne in mind during follow-up and in secondary endovascular interventions and conversion to open surgery.     

Rate of change in abdominal aortic aneurysm diameter after endovascular repair

OBJECTIVE: Untreated abdominal aortic aneurysms (AAAs) enlarge at a mean rate of 3.9 mm/y with great individual variability. We sought to determine the effect of endovascular repair on the rate of change in aneurysm size. METHODS: There were 110 patients who underwent endovascular AAA repair at Stanford University Medical Center and who were followed up for 1 to 30 months (mean, 10 months) with serial contrast-infused helical computed tomography (CT). Maximal aneurysm diameter was determined using two independent methods: (1) measured manually, from cross-sectional computed tomography (XSCT) angiograms and (2) calculated from quantitative three-dimensional computed tomography (3DCT) data as orthonormal diameter. RESULTS: Maximal cross-sectional aneurysm diameter measured by hand (XSCT) and calculated as orthonormal values (3DCT) correlated closely (r = 0.915; P <.001). The XSCT-measured diameter was larger by 2.3 +/- 3. 75 mm (P <.001), and the 95% CI for SE of the bias was 1.85 to 2.75 mm. Preoperative aneurysm diameter (XSCT 59.1 +/- 8.4 mm; 3DCT 58.1 +/- 9.3 mm) did not differ significantly from the initial postoperative diameter. Considering all patients, XSCT diameter decreased at a rate of 0.34 +/- 0.69 mm/mo, and 3DCT diameter decreased at a rate of 0.28 +/- 0.79 mm/mo. Aneurysms in patients without endoleaks had a higher rate of decrease, an XSCT diameter by 0.50 +/- 0.74 mm/mo, and 3DCT diameter by 0.46 +/- 0.84 mm/mo. In these patients, mean absolute decrease in diameter at 6 months was 3. 4 +/- 4.5 mm (XSCT) and 3.3 +/- 5.9 mm (3DCT) and at 12 months, 5.9 +/- 5.7 mm (XSCT) and 5.4 +/- 5.7 mm (3DCT). Aneurysms in patients with persistent endoleaks did not change in mean XSCT diameter, and 3DCT diameter increased by 0.12 +/- 0.52 mm/mo (not significant). Aneurysm diameter remained within 4 mm of original size in 68% (3DCT) to 71% (XSCT) of patients. In one patient, aneurysm diameter increased (XSCT and 3DCT) more than 5 mm. Four patients who had a new onset endoleak had a much higher expansion rate than those with a chronic endoleak (P <.05). CONCLUSIONS: The rate of decrease in aneurysm size (annualized 3.4-4.1 mm/y) after endovascular repair of AAA approximates the reported expansion rate in untreated aneurysms. However, individual aneurysm behavior is unpredictable, and the presence of an endoleak is unreliable in predicting changes in diameter. New onset endoleaks are associated with an enlargement rate greater than that of untreated aneurysms.     

Hospital costs and benefits of screening for abdominal aortic aneurysms. Results from a randomised population screening trial.

OBJECTIVES: to analyse the hospital costs and benefits of screening older males for abdominal aortic aneurysm (AAA). MATERIALS and METHODS: in 1994 a hospital-based screening trial of 12 658 65-73-year-old males was started. AAA >5 cm were referred for surgery. The remaining AAA were offered annual scans. Those with aortic ectasia were rescreened at 5 yearly intervals. AAA-operations and hospital AAA-related deaths were researched. The costs of screening, surveillance, and treatment were also registered. RESULTS: the attendance rate was 76%; of whom 191 (4.0%) had AAA. Mean observation time was 5.13 years. Sixty in the screened and 41 in the control group were operated (p=0.06), of which 7 and 27 respectively were operated as an emergency (p<0.001), and 6 and 19 respectively died due to AAA (p=0.009). The costs per scan were 83.50 DKK, 81 400 DKK per emergency operation (71 485 DKK after screening), and 117 000 DKK per emergency operation. The cost per prevented hospital death was 67 855 DKK, equivalent to approximately life year saved approx. 7540 DKK (GBP1=12 DKK). CONCLUSION: screening appears to reduce hospital AAA mortality and to be cost-effective.     

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

BACKGROUND: 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). METHODS: 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. RESULTS: 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). CONCLUSION: 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.