Forecasting aortic aneurysm rupture: A systematic review of seasonal and atmospheric associations.

BACKGROUND: Abdominal aortic aneurysms (AAAs) represent a significant burden of disease worldwide, and their rupture, without treatment, has an invariably high mortality rate. Whereas some risk factors for ruptured AAAs (rAAAs) are well established, such as hypertension, smoking, and female sex, the impact of seasonal and meteorologic variables is less clear. We systematically reviewed the literature to determine whether these variables are associated with rAAA. METHODS: Review methods were according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We calculated pooled proportions and incidence rate ratios (IRRs) for the different months and seasons. Funnel plots were constructed to assess for publication bias. Given the poor methodologic quality of included studies, a sensitivity analysis was performed on better-quality studies, which scored 6 and above of 9 in the author-modified Newcastle-Ottawa Scale. RESULTS: The pooled proportion of rAAA was highest in the autumn season (incidence rate, 26.6%; 95% confidence interval [CI], 25.6%-27.7%; I2 = 15.4%), followed by winter (incidence rate, 26.2%; 95% CI, 24.1%-28.2%; I2 = 72.4%), and lowest in summer (incidence rate, 21.1%; 95% CI, 19.3%-23.0%; I2 = 70.4%). The IRRs of rAAA were -6.9% (95% CI, -9.8% to -3.9%), -19.5% (95% CI, -22% to -16.8%), +10.5% (95% CI, 7.2%-13.9%), and +18.1% (95% CI, 15%-22%) in spring, summer, autumn, and winter compared with the remaining seasons, respectively (all P < .0001), thus affirming existence of seasonal variation. The pooled proportion of rAAA was highest in December (incidence rate, 8.9%; 95% CI, 7.1%-10.9%; I2 = 54.5%) but lowest in July (incidence rate, 5.7%; 95% CI, 4.2%-7.3%; I2 = 54.5%). The IRR was significantly the highest in January (IRR, 1.14; 95% CI, 1.01-1.29; P = .031) but lowest in July (IRR, 0.75; 95% CI, 0.65-0.87; P < .0001). There is also some evidence for a possible association with atmospheric pressure. Associations with temperature and daylight hours, however, are at best speculative. CONCLUSIONS: Autumn and winter are significantly associated with a higher incidence of rAAAs, and autumn is associated with the highest rupture incidence of all the seasons. However, the inability to appropriately control for other confounding factors known to increase the risk of AAA rupture precludes any additional recommendations to alter current provision of vascular services on the basis of these data.

Forty hours with a traumatic carotid transection: A diagnostic caveat and review of the contemporary management of penetrating neck trauma.

Although penetrating neck trauma (PNT) is uncommon, it is associated with the significant morbidity and mortality. The management of PNT has changed significantly over the past 50 years. A radiological assessment now is a vital part of the management with a traditional surgical exploration. A 22 years old male was assaulted by a screwdriver and sustained multiple penetrating neck injuries. A contrast CT scan revealed a focal pseudoaneurysm in the left common carotid artery bulb. There was no active bleeding or any other vascular injuries and the patient remained haemodynamically stable. In view of these findings, he was initially managed conservatively without an open surgical exploration. However, the patient was noted to have an acute drop in his hemoglobin count overnight post injury and the catheter directed angiography showed active bleeding from the pseudoaneurysm. Surgical exploration 40 hours following the initial injury revealed a penetrating injury through both arterial walls of the left carotid bulb which was repaired with a great saphenous vein patch. A percutaneous drain was inserted in the carotid triangle and a course of intravenous antibiotics for five days was commenced. The patient recovered well with no complications and remained asymptomatic at five months followup.

Capillary ultrastructure and mitochondrial volume density in skeletal muscle in relation to reduced exercise capacity of patients with intermittent claudication.

Intermittent claudication (IC) is the most commonly reported symptom of peripheral arterial disease (PAD). Impaired limb blood flow is a major casual factor of lower exercise tolerance in PAD but cannot entirely explain it. We hypothesized that IC is associated with structural changes of the capillary-mitochondria interface that could contribute to the reduction of exercise tolerance in IC patients. Capillary and mitochondrial morphometry were performed after light and transmission electron microscopy using vastus lateralis muscle biopsies of 14 IC patients and 10 age-matched controls, and peak power output (PPO) was determined for all participants using an incremental single-leg knee-extension protocol. Capillary density was lower (411 ± 90 mm(-2) vs. 506 ± 95 mm(-2); P ≤ 0.05) in the biopsies of the IC patients than in those of the controls. The basement membrane (BM) around capillaries was thicker (543 ± 82 nm vs. 423 ± 97 nm; P ≤ 0.01) and the volume density of mitochondria was lower (3.51 ± 0.56% vs. 4.60 ± 0.74%; P ≤ 0.01) in the IC patients than the controls. In the IC patients, a higher proportion of capillaries appeared with collapsed slit-like lumen and/or swollen endothelium. PPO was lower (18.5 ± 9.9 W vs. 33.5 ± 9.4 W; P ≤ 0.01) in the IC patients than the controls. We suggest that several structural alterations in skeletal muscle, either collectively or separately, contribute to the reduction of exercise tolerance in IC patients.

Frailty and Geriatric Syndromes in Vascular Surgical Ward Patients.

BACKGROUND: Preoperative frailty is an important predictor of poor outcomes but the relationship between frailty and geriatric syndromes is less clear. The aims of this study were to describe the prevalence of frailty and incidence of geriatric syndromes in a cohort of older vascular surgical ward patients, and investigate the association of frailty and other key risk factors with the occurrence of one or more geriatric syndromes (delirium, functional decline, falls, and/or pressure ulcers) and two hospital outcomes (acute length of stay and discharge destination). METHODS: This prospective cohort study was conducted in a vascular surgical ward in a tertiary teaching hospital in Brisbane, Australia. Consecutive patients aged ≥65 years, admitted for ≥72 hr, were eligible for inclusion. Frailty was defined as one or more of functional dependency, cognitive impairment, or nutritional impairment at admission. Delirium was identified using the Confusion Assessment Method and a validated chart extraction tool. Functional decline from admission to discharge was identified from daily nursing documentation of activities of daily living. Falls were identified according to documentation in the medical record cross-checked with the incident reporting system. Pressure ulcers, acute length of stay, and discharge destination were identified by documentation in the medical record. Risk factors associated with geriatric syndromes, acute length of stay, and discharge destination were assessed using multivariable logistic regression models. RESULTS: Of 110 participants, 43 (39%) patients were frail and geriatric syndromes occurred in 40 (36%). Functional decline occurred in 25% of participants, followed by delirium (20%), pressure ulcers (12%), and falls (4%). In multivariable logistic analysis, frailty [odds ratio (OR) 6.7, 95% confidence interval (CI) 2.0-22.1, P = 0.002], nonelective admission (OR 7.2, 95% CI 2.2-25.3, P = 0.002), higher physiological severity (OR 5.5, 95% CI 1.1-26.8, P = 0.03), and operative severity (OR 4.6, 95% CI 1.2-17.7, P = 0.03) increased the likelihood of any geriatric syndrome. Frailty was an important predictor of longer length of stay (OR 2.6, 95% CI 1.0-6.8, P = 0.06) and discharge destination (OR 4.2, 95% CI 1.2-13.8, P = 0.02). Nonelective admission significantly increased the likelihood of discharge to a higher level of care (OR 5.3, 95% CI 1.3-21.6, P = 0.02). CONCLUSIONS: Frailty and geriatric syndromes were common in elderly vascular surgical ward patients. Frail patients and nonelective admissions were more likely to develop geriatric syndromes, have a longer length of stay, and be discharged to a higher level of care.

Long-term outcomes and factors influencing late survival following elective abdominal aortic aneurysm repair: A 24-year experience.

BACKGROUND: Abdominal aortic aneurysms can be either treated by an open abdominal aortic aneurysm repair or an endovascular repair. Comparing clinical predictors of outcomes and those which influence survival rates in the long term is important in determining the choice of treatment offered and the decision-making process with patients. AIMS: To determine the influence of pre-existing clinical predictors and perioperative determinants on late survival of elective open abdominal aortic aneurysm repair and endovascular repair at a tertiary hospital. METHODS: Consecutive patients undergoing elective abdominal aortic aneurysm repair from 1990 to 2013 were included. Data were collected from a prospectively acquired database and death data were gathered from the Queensland state death registry. Pre-existing risks and perioperative factors were assessed independently. Kaplan-Meier and Cox regression modeling were performed. RESULTS: During the study period, 1340 abdominal aortic aneurysms were repaired electively, of which 982 were open abdominal aortic aneurysm repair. The average age was 72.4 years old and 81.7% were males. The cumulative percentage survival rates for open abdominal aortic aneurysms repair at 5, 10, 15 and 20 years were 79, 49, 31 and 22, respectively. The corresponding 5-, 10- and 15-year survival rates for endovascular repair were not significantly different at 75, 49 and 33%, respectively (P = 0.75). Predictors of reduced survival were advanced age, American Society of Anaesthesiology scores, chronic obstructive pulmonary disease, renal impairment, bifurcated grafts, peripheral vascular disease and congestive heart failure. CONCLUSIONS: Open repair offers a good long-term treatment option for patients with an abdominal aortic aneurysm and in our experience there is no significant difference in late survival between open abdominal aortic aneurysms repair and endovascular repair. Consideration of the factors identified in this study that predict reduced long-term survival for open abdominal aortic aneurysms repair and endovascular repair should be considered when deciding repair of abdominal aortic aneurysm.

Thrombus volume is similar in patients with ruptured and intact abdominal aortic aneurysms.

OBJECTIVE: Most abdominal aortic aneurysms (AAAs) contain intraluminal thrombus (ILT), which has been demonstrated to contain proteolytic enzymes and proinflammatory cytokines implicated in AAA progression and rupture. In animal models, anticoagulants have been shown to limit AAA progression. Whether ILT plays a role in AAA rupture is unknown. The aim of this study was to compare the volume of ILT in patients with ruptured and intact AAAs. METHODS: We matched by maximum axial diameter alone, on a 1:2 basis, 28 patients with ruptured AAAs and 56 patients with intact AAAs. Total infrarenal aortic volume and ILT volume were measured from computed tomography angiograms using a previously validated and reproducible semiautomated workstation protocol. Clinical risk factors were also recorded. The Mann-Whitney U test was used to compare ILT volumes between patients with ruptured and intact AAAs. RESULTS: Median (interquartile range [IQR]) maximum AAA diameter (84.0 [77.5-93.9] mm vs 82.6 [77.1-93.3] mm; P = .769) and median (IQR) total AAA volume (372.8 [277.4-486.1] cm(3) vs 358.4 [289.1-563.4] cm(3); P = .977) were similar in patients with ruptured and intact AAAs. Median (IQR) AAA ILT volume was similar in patients with ruptured (152.7 [84.8-252.4] cm(3)) and intact (180.1 [89.9-254.8] cm(3); P = .414) AAAs. CONCLUSIONS: This study suggests that ILT volume is not different in ruptured and intact AAAs.

A deletion in chromosome 6q is associated with human abdominal aortic aneurysm.

Current efforts to identify the genetic contribution to abdominal aortic aneurysm (AAA) have mainly focused on the assessment of germ-line variants such as single-nucleotide polymorphisms. The aim of the present study was to assess the presence of acquired chromosomal aberrations in human AAA. Microarray data of ten biopsies obtained from the site of main AAA dilatation (AAA body) and three control biopsies obtained from the macroscopically non-dilated neck of the AAA (AAA neck) were initially compared with identified chromosomal aneuploidies using the Chromosomal Aberration Region Miner (ChARM) software. A commonly deleted segment of chromosome bands 6 (q22.1-23.2) was predicted within AAA biopsies. This finding was confirmed by quantitative real-time PCR (qPCR)-based DNA copy number assessments of an independent set of six AAA body and neck biopsies which identified a fold copy number change (∆KCt) of -1±0.35, suggesting the loss of one copy of the long interspersed nucleotide element type 1 (LINE-1) mapped to chromosome 6 (q22.1-23.2). The median relative genomic content of LINE-1 DNA was also reduced in AAA body compared with AAA neck biopsies (1.540 compared with 3.159; P=0.031). A gene important for vascular homoeostasis mapped to 6q23.1, connective tissue growth factor (CTGF), was assessed and found to be significantly down-regulated within AAA bodies compared with AAA necks (0.261 compared with 0.627; P=0.031), as determined by reverse transcription qPCR using total RNA as a template. Histology demonstrated marked staining for macrophages within AAA body biopsies. We found in vitro that the median relative genomic content of LINE-1 DNA in aortic vascular smooth muscle cells (AoSMCs) exposed to pro-inflammatory medium was ~1.5 times greater than that measured in control AoSMCs exposed to non-conditioned medium (3.044 compared with 2.040; P=0.015). Our findings suggest that acquired chromosomal aberrations associated with retrotransposon propagation may predispose to sporadic AAA.

microRNA profiling in patients with abdominal aortic aneurysms: the significance of miR-155.

AAA (abdominal aortic aneurysm) is a potentially life-threatening late-onset degenerative condition. miRNAs (microRNAs), the small non-coding RNA molecules that regulate gene expression, have been shown previously to be associated with a broad range of human pathologies, including cardiovascular diseases. The aim of the present study was to identify AAA-associated miRNAs potentially contributing to AAA pathology. We analysed the expression of 124 miRNAs within AAA biopsies and serum of ten patients undergoing AAA repair, and serum from ten age- and sex-matched subjects without AAA, using the FlexmiR™ MicroRNA Assay. RNA extracted from the site of main AAA dilatation (AAA body) was compared with that extracted from the macroscopically non-dilated neck of the AAA (AAA neck). Similarly, RNA extracted from the serum of AAA patients (AAA serum) was compared with that extracted from age- and sex-matched controls (control serum). qPCR (quantitative real-time PCR), Western blot analysis and histology were performed using an independent set of six paired AAA body and neck biopsies to examine the validity of findings. Seven miRNAs were up-regulated [>2-fold difference, FDR (false discovery rate) <0.5] within AAA biopsies, of which miR-155 was the most differentially expressed (11.32-fold, FDR=0.414). This finding was confirmed by qPCR with the median relative expression of miR-155 being 3.26 and 0.63 within AAA body and AAA neck biopsies respectively (P=0.031). Circulating miR-155 was also increased in AAA patients compared with controls, with a 2.67-fold up-regulation at borderline significance (FDR=0.554). Two immunologically important miR-155 target genes, CTLA4 (cytotoxic T-lymphocyte-associated protein) and SMAD2, were assessed and found to be significantly down-regulated within AAA bodies compared with AAA necks (P=0.032 and P=0.026) as determined by qPCR and Western blotting respectively. Histology demonstrated dense accumulation of T-lymphocytes within the adventitial and outer medial layers of AAA body, but not neck tissue. The results of the present study suggest that miR-155 is overexpressed in AAA with potential implications in the pathogenesis of the condition.

Urocortin 2 is associated with abdominal aortic aneurysm and mediates anti-proliferative effects on vascular smooth muscle cells via corticotrophin releasing factor receptor 2.

AAA (abdominal aortic aneurysm) is an important cause of sudden death in older adults, but there is no current effective drug therapy for this disease. The UCNs (urocortins1-3) and their receptors: CRFR (corticotrophin-releasing factor receptor)-1 and -2 have been implicated in various CVDs (cardiovascular diseases). We assessed the relative expression of UCN1-3 in AAA by qRT-PCR (quantitative reverse transcription-PCR) and ELISA, and examined in vitro how UCN2 affects human aortic VSMC (vascular smooth muscle cell) Akt phosphorylation, pro-inflammatory cytokine IL (interleukin)-6 secretion, proliferation, cell cycle and apoptosis. UCN2 and CRFR2 expression were significantly up-regulated in biopsies from the AAA body. AAA body biopsies released high amounts of UCN2 in vitro. Median plasma UCN2 concentrations were 2.20 ng/ml (interquartile range 1.14-4.55 ng/ml, n=67) in AAA patients and 1.11 ng/ml (interquartile range 0.76-2.55 ng/ml, n=67) in patients with non-aneurysmal PAD (peripheral artery disease) (P=0.001). Patients with UCN2 in the highest quartile had a 4.12-fold (95% confidence interval, 1.37-12.40) greater prevalence of AAA independent of other risk factors, P=0.012. In vitro, UCN2 significantly inhibited VSMC Akt phosphorylation and proliferation in a dose-dependent manner. UCN2 induced VSMC G1 cell-cycle arrest and increased IL-6 secretion over 24 h. The CRFR2 antagonist astressin-2B significantly abrogated the effects of UCN2 on VSMCs. In conclusion, UCN2 is significantly associated with AAA and inhibits VSMC proliferation by inducing a G1 cell cycle arrest suggesting a plausible regulatory role in AAA pathogenesis.

Abdominal aortic aneurysm calcification and thrombus volume are not associated with outcome following endovascular abdominal aortic aneurysm repair.

OBJECTIVES: Aortic calcification and thrombus have been postulated to worsen outcome following endovascular abdominal aortic aneurysm repair (EVAR). The purpose of this study was to assess the association of abdominal aortic aneurysm (AAA) calcification and thrombus volume with outcome following EVAR using a reproducible, quantifiable computed tomography (CT) assessment protocol. METHODS: Patients with elective EVAR performed between January 2002 and 2012 at the Townsville Hospital, Mater Private Hospital (Townsville) and Royal Brisbane and Women's Hospital (RBWH) were included if preoperative CTAs were available for analysis. AAA calcification and thrombus volume were measured using a semiautomated workstation protocol. Outcomes were assessed in terms of clinical failure, endoleak (type I, type II) and reintervention. Univariate and multivariate analyses were performed. Median follow-up was 1.7 years and the interquartile range 1.0-3.8 years. RESULTS: One hundred thirty-four patients undergoing elective EVAR were included in the study. Rates of primary clinical success and freedom from reintervention were 82.8% and 88.9% at the 24-month follow-up. AAA calcification and thrombus volume were not associated with clinical failure, type I endoleak, type II endoleak or reintervention. CONCLUSIONS: AAA calcification and thrombus volume were not associated with poorer outcome after EVAR in this study. KEY POINTS: • The association of calcification and thrombus volumes with EVAR outcome is unclear • Quantifiable methods for assessing calcification and thrombus were not used previously • This study used reproducible methods for assessing AAA calcification and thrombus volumes.

Visceral adiposity is not associated with abdominal aortic aneurysm presence and growth.

Previous studies in rodent models and patients suggest that visceral adipose could play a direct role in the development and progression of abdominal aortic aneurysm (AAA). This study aimed to assess the association of visceral adiposity with AAA presence and growth. This study was a case-control investigation of patients that did (n=196) and did not (n=181) have an AAA who presented to The Townsville Hospital vascular clinic between 2003 and 2012. Cases were patients with AAA (infra-renal aortic diameter >30 mm) and controls were patients with intermittent claudication but no AAA (infra-renal aortic diameter <30 mm). All patients underwent computed tomography angiography (CTA). The visceral to total abdominal adipose volume ratio was estimated from CTAs by assessing total and visceral adipose deposits using an imaging software program. Measurements were assessed for reproducibility by repeat assessments on 15 patients. AAA risk factors were recorded at entry. Forty-five cases underwent two CTAs more than 6 months apart to assess AAA expansion. The association of visceral adiposity with AAA presence and growth was examined using logistic regression. Visceral adipose assessment by CTA was highly reproducible (mean coefficient of variation 1.0%). AAA was positively associated with older age and negatively associated with diabetes. The visceral to total abdominal adipose volume ratio was not significantly associated with AAA after adjustment for other risk factors. Patients with a visceral to total abdominal adipose volume ratio in quartile four had a 1.63-fold increased risk of AAA but with wide confidence intervals (95% CI 0.71-3.70; p=0.248). Visceral adiposity was not associated with AAA growth. In conclusion, this study suggests that visceral adiposity is not specifically associated with AAA presence or growth although larger studies are required to confirm these findings.

Fenofibrate increases high-density lipoprotein and sphingosine 1 phosphate concentrations limiting abdominal aortic aneurysm progression in a mouse model.

There are currently no acceptable treatments to limit progression of abdominal aortic aneurysm (AAA). Increased serum concentrations of high-density lipoprotein (HDL) are associated with reduced risk of developing an AAA. The present study aimed to assess the effects of fenofibrate on aortic dilatation in a mouse model of AAA. Male low-density lipoprotein receptor-deficient (Ldlr(-/-)) mice were maintained on a high-fat diet for 3 weeks followed by 6 weeks of oral administration of vehicle or fenofibrate. From 14 to 18 weeks of age, all mice were infused with angiotensin II (AngII). At 18 weeks of age, blood and aortas were collected for assessment of serum lipoproteins, aortic pathology, aortic Akt1 and endothelial nitric oxide synthase (eNOS) activities, immune cell infiltration, eNOS and inducible NOS (iNOS) expression, sphingosine 1 phosphate (S1P) receptor status, and apoptosis. Mice receiving fenofibrate had reduced suprarenal aortic diameter, reduced aortic arch Sudan IV staining, higher serum HDL levels, increased serum S1P concentrations, and increased aortic Akt1 and eNOS activities compared with control mice. Macrophages, T lymphocytes, and apoptotic cells were less evident and eNOS, iNOS, and S1P receptors 1 and 3 were up-regulated in aortas from mice receiving fenofibrate. The present findings suggest that fenofibrate antagonizes AngII-induced AAA and atherosclerosis by up-regulating serum HDL and S1P levels, with associated activation of NO-producing enzymes and reduction of aortic inflammation.

Barriers to screening and diagnosis of peripheral artery disease by general practitioners.

Peripheral artery disease (PAD) is a strong predictor of cardiovascular morbidity and mortality yet it is under-recognised and undertreated. General practitioners (GPs) are best positioned to detect patients with PAD. This article investigates awareness of PAD by GPs; the prevalence of screening for PAD and tools used for screening and diagnosis, in particular the ankle-brachial index (ABI); and the barriers to PAD screening and measurement of the ABI in the general practice setting. A cross-sectional survey of primary care practitioners was conducted between September 2011 and March 2012. A mail-out survey was distributed to 1120 GPs practising in Queensland, Australia: 287 (26%) responded; 61% of GPs reported screening for PAD; 58% of GPs reported 'never' measuring the ABI; and 70% reported using arterial duplex ultrasound as their first-line diagnostic tool. Equipment availability, time constraints and lack of training and skills were identified as the most significant barriers to screening and ABI testing. In conclusion, there are deficits in the utilisation of guideline recommendations relating to PAD screening and diagnosis by Australian GPs. Our data suggest that earlier detection of PAD may be achieved through GP education combined with increased access to ABI equipment or the availability of a more time-efficient test.

Effect of ramipril on walking times and quality of life among patients with peripheral artery disease and intermittent claudication: a randomized controlled trial.

IMPORTANCE: Approximately one-third of patients with peripheral artery disease experience intermittent claudication, with consequent loss of quality of life. OBJECTIVE: To determine the efficacy of ramipril for improving walking ability, patient-perceived walking performance, and quality of life in patients with claudication. DESIGN, SETTING, AND PATIENTS: Randomized, double-blind, placebo-controlled trial conducted among 212 patients with peripheral artery disease (mean age, 65.5 [SD, 6.2] years), initiated in May 2008 and completed in August 2011 and conducted at 3 hospitals in Australia. INTERVENTION: Patients were randomized to receive 10 mg/d of ramipril (n = 106) or matching placebo (n = 106) for 24 weeks. MAIN OUTCOME MEASURES: Maximum and pain-free walking times were recorded during a standard treadmill test. The Walking Impairment Questionnaire (WIQ) and Short-Form 36 Health Survey (SF-36) were used to assess walking ability and quality of life, respectively. RESULTS: At 6 months, relative to placebo, ramipril was associated with a 75-second (95% CI, 60-89 seconds) increase in mean pain-free walking time (P < .001) and a 255-second (95% CI, 215-295 seconds) increase in maximum walking time (P < .001). Relative to placebo, ramipril improved the WIQ median distance score by 13.8 (Hodges-Lehmann 95% CI, 12.2-15.5), speed score by 13.3 (95% CI, 11.9-15.2), and stair climbing score by 25.2 (95% CI, 25.1-29.4) (P < .001 for all). The overall SF-36 median Physical Component Summary score improved by 8.2 (Hodges-Lehmann 95% CI, 3.6-11.4; P = .02) in the ramipril group relative to placebo. Ramipril did not affect the overall SF-36 median Mental Component Summary score. CONCLUSIONS AND RELEVANCE: Among patients with intermittent claudication, 24-week treatment with ramipril resulted in significant increases in pain-free and maximum treadmill walking times compared with placebo. This was associated with a significant increase in the physical functioning component of the SF-36 score. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00681226.

Peripheral arterial disease - screening in general practice.

BACKGROUND: As a manifestation of systemic atherosclerosis, peripheral arterial disease (PAD) signifies an increased risk of cardiovascular events. Peripheral arterial disease has received less attention than other atherosclerotic diseases, leading to under-diagnosis and under-treatment. Peripheral arterial disease affects approximately 10-15% of the general population, and approximately 50% of PAD patients are asymptomatic. OBJECTIVE: This article aims to review the literature on the rationale for screening for lower extremity PAD in the general practice setting, and to identify the barriers to screening for PAD experienced by general practitioners, with a focus on the Australian context. DISCUSSION: Screening for asymptomatic PAD among high risk groups has been recommended by major PAD authorities to increase early diagnosis. Screening for PAD using the ankle-brachial index can detect asymptomatic patients. Research into the effect of cardiovascular risk reduction therapies for asymptomatic patients is lacking, and available evidence is inconclusive. The prevalence of screening and barriers to screening experienced by Australian GPs has not yet been studied. Available data on the benefits of PAD screening is inconclusive, and further research is required to determine a survival benefit with treatment of asymptomatic PAD.

Peripheral arterial disease - diagnosis and management in general practice.

BACKGROUND: Peripheral arterial disease (PAD) is a manifestation of systemic atherosclerosis. It affects 10-15% of the general population, and is often asymptomatic; leading to under-diagnosis and under-treatment. Atherosclerotic risk factors are often not intensively managed in PAD patients. OBJECTIVE: To summarise the information around the diagnosis and management of PAD in the general practice setting. DISCUSSION: Careful history, clinical examination, and measurement of ankle-brachial index remain the initial means of diagnosing PAD. More detailed anatomic information from duplex imaging, computed tomography angiography and magnetic resonance angiography, is usually unnecessary unless endovascular or surgical intervention is being considered, or if abdominal aortic aneurysm or popliteal aneurysm need to be excluded. Management is focused on lifestyle modification, including smoking cessation and exercise; medical management of atherosclerotic risk factors, including antiplatelet agents, statins, antihypertensive therapy; and agents to improve walking distance, such as cilostazol and ramipril. Endovascular or surgical interventions are usually considered for lifestyle limiting intermittent claudication not responding to conservative therapies, and for critical limb ischaemia.

Predictors of outcome after elective endovascular abdominal aortic aneurysm repair and external validation of a risk prediction model.

INTRODUCTION: Endovascular abdominal aortic aneurysm (AAA) repair (EVAR) has been associated with lower operative mortality and morbidity than open surgery but comparable long-term mortality and higher delayed complication and reintervention rates. Attention has therefore been directed to identifying preoperative and operative variables that influence outcomes after EVAR. Risk-prediction models, such as the EVAR Risk Assessment (ERA) model, have also been developed to help surgeons plan EVAR procedures. The aims of this study were (1) to describe outcomes of elective EVAR at the Royal Brisbane and Women's Hospital (RBWH), (2) to identify preoperative and operative variables predictive of outcomes after EVAR, and (3) to externally validate the ERA model. METHODS: All elective EVAR procedures at the RBWH before July 1, 2009, were reviewed. Descriptive analyses were performed to determine the outcomes. Univariate and multivariate analyses were performed to identify preoperative and operative variables predictive of outcomes after EVAR. Binomial logistic regression analyses were used to externally validate the ERA model. RESULTS: Before July 1, 2009, 197 patients (172 men), who were a mean age of 72.8 years, underwent elective EVAR at the RBWH. Operative mortality was 1.0%. Survival was 81.1% at 3 years and 63.2% at 5 years. Multivariate analysis showed predictors of survival were age (P = .0126), American Society of Anesthesiologists (ASA) score (P = .0180), and chronic obstructive pulmonary disease (P = .0348) at 3 years and age (P = .0103), ASA score (P = .0006), renal failure (P = .0048), and serum creatinine (P = .0022) at 5 years. Aortic branch vessel score was predictive of initial (30-day) type II endoleak (P = .0015). AAA tortuosity was predictive of midterm type I endoleak (P = .0251). Female sex was associated with lower rates of initial clinical success (P = .0406). The ERA model fitted RBWH data well for early death (C statistic = .906), 3-year survival (C statistic = .735), 5-year survival (C statistic = .800), and initial type I endoleak (C statistic = .850). CONCLUSIONS: The outcomes of elective EVAR at the RBWH are broadly consistent with those of a nationwide Australian audit and recent randomized trials. Age and ASA score are independent predictors of midterm survival after elective EVAR. The ERA model predicts mortality-related outcomes and initial type I endoleak well for RBWH elective EVAR patients.

A meta-analysis of the outcome of endovascular and noninvasive therapies in the treatment of intermittent claudication.

PURPOSE: Intermittent claudication is a common symptom of peripheral arterial disease. Currently, there is a lack of consensus on the most effective therapies for this problem. We conducted a meta-analysis of randomized trials assessing the efficacy of endovascular therapy (EVT) compared with noninvasive therapies for the treatment of intermittent claudication. METHODS: Randomized trials comparing the efficacy of EVT and noninvasive therapies, such as medical therapy (MT) and supervised exercise (SVE) in patients with intermittent claudication were identified by a systematic search. Data were pooled, and combined overall effect sizes (standardized differences of mean values) were calculated for a random effect model in terms of ankle-brachial index (ABI) and treadmill walking for initial claudication distance (ICD) and maximum walking distance (MWD). Nine eligible trials (873 participants) were included: two compared EVT and MT alone, four compared EVT and SVE, and three trials compared EVT plus SVE vs SVE alone. RESULTS: Heterogeneity between studies was marked. Quantitative data analysis suggested that EVT improved outcomes over MT alone at early follow-up evaluations. Outcomes of EVT plus SVE were better than those of SVE alone in terms of both ABI and treadmill walking at immediate, early, and intermediate follow-up. No substantial differences in outcomes of EVT alone compared with SVE alone were found. CONCLUSION: In patients with intermittent claudication, current evidence supports improved ABI and treadmill walking when EVT is added to MT or SVE during early and intermediate follow-up. There is no evidence that EVT alone provides improved outcome over SVE alone. There is low confidence in these findings for a number of reasons, including the small number of trials, the small size of these studies, the heterogeneity in study design, and the limited use of quality of life tools in assessing outcomes. More consistent data from larger, more homogenous studies, including longer follow-up, are required.

Association of statin prescription with small abdominal aortic aneurysm progression.

BACKGROUND: Statins have been suggested to reduce expansion of abdominal aortic aneurysms (AAAs) independent of lipid-lowering effects. METHODS: We assessed the association of statin treatment and serum low-density lipoprotein (LDL) concentrations with small AAA expansion. Six hundred fifty-two patients undergoing surveillance of small AAAs were entered into the study from 5 vascular centers. In a subset, fasting lipids (n = 451) and other biomarkers (n = 216) were measured. The AAA diameter was followed by ultrasound surveillance for a median of 5 years. RESULTS: Three hundred forty-nine (54%) of the patients were prescribed statins. Adjusting for other risk factors, statin prescription was not associated with AAA growth (odds ratio [OR] 1.23, 95% CI 0.86-1.76). Above-median AAA growth was positively associated with initial diameter (OR 1.78 per 4.35-mm-larger initial aortic diameter, 95% CI 1.49-2.14) and negatively associated with diabetes (OR 0.37, 95% CI 0.22-0.62). Above-median serum LDL concentration was not associated with AAA growth. Patients receiving statins had lower serum C-reactive protein concentrations but similar matrix metalloproteinase-9 and interleukin-6 concentrations to those not prescribed these medications. CONCLUSIONS: We found no association between statin prescription or LDL concentration with AAA expansion. The results do not support the findings of smaller studies and suggest that statins may have no benefit in reducing AAA progression.

Important observations made managing carotid body tumors during a 25-year experience.

OBJECTIVES: Our objective was to assess the short- and long-term outcome for patients after carotid body tumor (CBT) resection and discuss the potential pitfalls of the treatment. METHODS: An analysis was undertaken of all patients who underwent CBT resection at Royal Brisbane and Women's Hospital and Greenslopes Private Hospital between 1982 and 2007. Primary tumor characteristics, surgical technique, and outcomes were recorded and analyzed. RESULTS: A total of 49 consecutive CBT resections (2 recurrent tumors) were carried out in 39 patients (26 women [56%]) who were a mean age of 49 years (range, 17-75 years). A nontender neck mass was the presenting complaint in 85%, followed by screening in familial or contralateral tumors in 26%. Familial cases occurred in 11 patients (28%). There were no operative deaths. Complications occurred in 13 of the 49 operations (27%), predominantly temporary nerve palsies and were more likely to occur in tumors of large volume or in cases of removal of coexisting vagal tumors. Malignant disease was present in seven cases (15%). All patients have been followed-up postoperatively for a mean of 11 years (range, 2-26 years). Metachronous paragangliomas have been discovered in six patients, all with familial disease. CONCLUSIONS: Early resection of carotid body tumors should be undertaken while still small to minimize the risk of neural injury, which increases with tumor size. In cases of bilateral CBT, we recommend that the smaller tumor be resected first, before the staged resection of the larger contralateral tumor. In familial or bilateral tumor cases, other synchronous and metachronous paragangliomas should be excluded. Mandatory lifelong follow-up is essential.