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Background: There is a well-established link between exposure to hot and cold temperatures and an increased risk of cardiovascular hospitalization or death. There is also contrasting evidence of a seasonal increase in aortic ruptures related to atmospheric pressure, but an association with environmental temperature has never been formally modelled., Methods: Using a prospective database, we identified 295 patients who were operated in a single centre for ruptured abdominal aortic aneurysm in south-east Queensland between 1990 and 2010. We matched patients to their nearest weather station to estimate their exposure to temperature and air pressure in the days leading up to their rupture. We used the case-crossover method to estimate the risks of temperature, which we allowed to be non-linear (increased risks at high and low temperatures) and delayed by up to 25 days., Results: There was an immediate increase in risk after exposure to cold, and a delayed risk after exposure to heat. An increased risk after exposure to high pressures disappeared after adjusting for temperature. At a mean temperature of 19°C (66°F), the odds ratio for rupture was 1.73 (95% confidence interval: 1.09, 2.76) compared with the reference temperature of 24°C., Conclusion: This is the first study to demonstrate an association between temperature and risk of aortic aneurysm rupture in the Southern Hemisphere. The physiological changes caused by thermoregulation may be a trigger for those people with a fragile aneurysm., (© 2013 Royal Australasian College of Surgeons.)

Objective: Mutations in FBN1 and TGFBR2 genes are the main causative mutations identified in Marfan syndrome (MFS). The major vascular complication of MFS is aneurysm formation. Abdominal aortic aneurysm (AAA) is an acquired disease of later life of unknown etiology. The aim of this study was to examine if genetic aberrations in MFS-related genes FBN1 and TGFBR2 are present in patients with AAA., Methods: We assessed the presence of copy number variation (CNV) in FBN1 and TGFBR2 genes in AAA biopsies from twelve patients. We also analyzed the expression of these genes in AAA biopsies compared to control biopsies from six organ donors. In addition we assessed the expression of two members of the Notch signaling pathway NOTCH3 and HEY2 as well as aortic smooth muscle cell (AoSMC) differentiation marker TAGLN in AAA and control biopsies., Results: Loss of one copy (deletion) of the FBN1 exon 66 sequence and TGFBR2 exon 8 was identified in 7 (58%) and 11 (92%) of the 12 AAA biopsies. No copy number amplifications (duplications) were detected. Patients carrying TGFBR2 exon 8 deletion showed marked downregulation of this gene in AAA biopsies compared to control biopsies (0.699 vs. 1.765, p = 0.038). Notch signaling components NOTCH3 and HEY2 were markedly downregulated in AAA, while expression of the AoSMC differentiation marker TAGLN did not differ between AAA and control biopsies (0.468 vs. 0.486, p = 0.546)., Conclusion: This study suggests an acquired impairment in TGF-β signaling that along with downregulation of the Notch signaling pathway may contribute to the pathogenesis of AAA., (Copyright © 2012 Elsevier Ireland Ltd. All rights reserved.)

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., (Copyright © 2011 Society for Vascular Surgery. All rights reserved.)

Objective: Abdominal aortic aneurysm (AAA) is a late onset degenerative condition with an inherited component thought to be due to multiple risk alleles. A locus on chromosomes 19q13 has been previously associated with AAA. The gene encoding kallikrein 1 (KLK1) is located on chromosome 19q13 and the single nucleotide polymorphism (SNP) rs5516 has been previously shown to lead to structural changes in the KLK1 transcription regulatory region. The aim of this study was to investigate whether rs5516 was associated with AAA and aortic diameter., Methods: We performed a case-control study on two independent subject groups from Western Australia (n=1304) and Queensland (n=325) of which 609 and 225 had an AAA, respectively. In addition, we analysed RNA extracted from abdominal aortic biopsies from 12 patients undergoing AAA surgery and 6 organ donors., Results: After adjusting for other risk factors the G allele of the rs5516 polymorphism was associated with large but not small AAA using a dominant model in the Western Australian men and a recessive model in Queensland subjects. In subjects with large AAA the G allele was associated with aortic diameter. The short splice variant of KLK1 was upregulated within AAA compared to control biopsies., Conclusion: This study suggests that a genetic polymorphism in KLK1 may contribute to the risk of developing later stage AAA., (Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.)

Objective: The aim of this study was to review the results of carotid endarterectomy (CEA) at the Royal Brisbane and Women's Hospital (RBWH) to provide a benchmark for comparison with carotid stenting and to document changes in imaging and procedural techniques over time., Methods: Analysis of RBWH CEA database from 1992 to 2007., Results: 1313 consecutive patients (average age 69.2 years, 9% 80 years or older, 69% males) underwent carotid endarterectomy at the RBWH between 1992 and May 2007. Indication for surgery was symptomatic disease in 67%. Preoperative investigations included a duplex scan in 97%, an angiogram in 24% and a CT brain in 33%. Angiogram related neurological events occurred in 3.5% of patients (1.6% stroke, 1.9% TIA). There were 7 deaths (0.5%) and 28 strokes (2.1%) for a combined stroke and death rate of 2.4%. The rate of transient ischemic attacks was 1.1%. Gender patch use and trainees operating with the surgeon unscrubbed predicted a higher combined stroke and death rate. Trends over time included: reduction in preoperative angiography from 66% to <5% and increased rate of patching from 39% to approximately 100%., Conclusions: Performance of CEA at the RBWH is in keeping with published literature standards. There has been an evolution to surgery performed on the basis of duplex ultrasound alone and an almost universal use of patching.

Chronic gill-associated virus (GAV) infection is endemic in Penaeus monodon broodstock captured from north-east Queensland in Australia and in farmed shrimp produced from these. We investigated the role of vertical transmission in perpetuating the high prevalence of these chronic GAV infections. Reverse transcription (RT)-nested PCR detected GAV in spermatophores and mature ovarian tissue from broodstock and in fertilized eggs and nauplii spawned from wild-fertilized females. In laboratory-reared P. monodon (> 12 mo old) that had a high mortality rate, RT-nested PCR detected GAV in male spermatophores at levels significantly higher than that detected in the lymphoid organ. By transmission electron microscopy (TEM), GAV virions were detected in spermatophore seminal fluid, but not sperm cells. Histological evidence of hypertrophied cell foci (spheroids) and TEM observation of GAV nucleocapsids and virions in spheroid cells was also found in 100% of lymphoid organs of approximately 1.2 g juvenile P. monodon reared in the laboratory from postlarvae collected from commercial hatcheries. Sequence analysis of PCR amplicons from parental P. monodon and fertilized eggs of artificially inseminated broodstock indicated that GAV associated with eggs can originate from both the male and female parents. Although the female GAV genotype was predominant in eggs, there was some dependence on infection levels in the male and female shrimp as indicated by RT-PCR. RT-nested PCR data on GAV levels in eggs, nauplii, protozoea and PL5 progeny of the artificial matings suggests that vertically transmitted virus is most probably associated with the egg surface.

Four species of penaeid prawn cultured in Australia (Penaeus monodon, Penaeus esculentus, Marsupenaeus japonicus and Fenneropenaeus merguiensis) were injected with a virulent preparation of gill-associated virus (GAV). P. monodon (average weight = 8.9, 13.9 and 19.2 g), P. esculentus (average weight = 19.5 g), F. merguiensis (average weight = 10.5 g), and small (average weight = 5.8 g) M. japonicus displayed overt signs of disease and mortalities which reached 82 to 100% within 23 d post-injection. Cumulative mortalities in P. esculentus and F. merguiensis were significantly lower than for P. monodon of the same size class. Medium (average weight = 13.0 g) M. japonicus also developed overt signs of disease but cumulative mortalities were not significantly higher than uninfected controls. Large (average weight = 20.3 g) M. japoncius did not display symptoms of disease and there were no significant mortalities up to 23 d post-injection.

A highly sensitive test based on reverse transcription followed by nested polymerase chain reaction (RT-nPCR) was developed to detect the Australian yellow-head-like viruses, gill-associated virus (GAV) and lymphoid organ virus (LOV) of Penaeus monodon. The RT-nPCR detected viral RNA in as little as 10 fg lymphoid organ total RNA isolated from GAV-infected P. monodon. Amplification of serial dilutions of a GAV cDNA clone showed that the nested PCR was sufficiently sensitive to detect a single genome equivalent using a DNA template. The specificity and sensitivity of the RT-nPCR was also demonstrated using experimentally infected P. (Marsupenaeus) japonicus, where GAV sequences could be amplified from lymphoid organ and haemocyte RNA as early as 6 h post infection (p.i.), and from gills by 24 h p.i. In contrast, transmission electron microscopy (TEM) identified nucleocapsids and virions in lymphoid organ cells and haemocytes from Days 3 and 6 p.i., respectively, while there was no evidence of infection in gill cells at any time. The practical application of the RT-nPCR was demonstrated by screening healthy wild-caught P. monodon broodstock. The high prevalence (>98%) of broodstock that were positive by RT-nPCR suggests that LOV is endemic in northern Queensland. In addition, results with lymphoid organ, gill and haemocyte RNA suggest that small gill biopsies may be best suited to the non-sacrificial testing of valuable broodstock. The speed and sensitivity of the RT-nPCR make it a useful adjunct to TEM for diagnosing LOV/GAV infection of P. monodon, with the additional benefit that screening of gill biopsies may facilitate selection of LOV-free broodstock.