Kathryn J. Griffin

Pulse wave velocity and the non-invasive methods used to assess it: Complior, SphygmoCor, Arteriograph and Vicorder.

Pulse wave velocity (PWV) is a known indicator of arterial stiffness and cardiovascular risk. We critically evaluated the evidence supporting the four main non-invasive devices available to assess it: Complior, SphygmoCor, Arteriograph and Vicorder. PubMed and Medline databases (1960–2011) were searched to identify studies reporting carotid–femoral PWV in humans using one or more of the four devices. Of the 183 articles retrieved, 43 met inclusion criteria. The Arteriograph device demonstrated least variance but had poor agreement with the other devices. Undisputable reference values for PWV need to be established and internationally agreed, and a standardized method for superficial distance measurement generated to reduce variability. Further studies comparing all four devices with invasive assessment are necessary.

Statins: the holy grail of Abdominal Aortic Aneurysm (AAA) growth attenuation? A systematic review of the literature.

BACKGROUND In the era of Abdominal Aortic Aneurysm (AAA) screening, pharmacotherapies to attenuate AAA growth are sought. HMG Co-A reductase inhibitors (statins) have pleiotropic actions independent of their lipid lowering effects and have been suggested as potential treatment for small AAAs. We systematically review the clinical evidence for this effect. METHODS Medline, EMBASE and the Cochrane Central Register of Controlled Trials (1950-2011) were searched for studies reporting data on the role of statin therapy on AAA growth rate. No language restrictions were placed on the search. References of retrieved articles and pertinent journals were hand searched. Included studies were reviewed by 2 independent observers. The search retrieved 164 papers, 100 were irrelevant based on their title, 47 were reviews and 1 was a letter. 8 studies were excluded based on review of their abstract leaving 8 for inclusion in the study. RESULTS Eight observational clinical studies with a total of 4,466 patients were reviewed. Four studies demonstrated reduced AAA expansion in statin users while 4 studies failed to demonstrate this effect. The method of determining AAA growth rates varied significantly between the studies and the ability of many studies to control for misclassification bias was poor. CONCLUSIONS The claim that statins attenuate AAA growth remains questionable. Further prospective studies with stringent identification and verification of statin usage and a standardised method of estimating AAA growth rates are required. Statin type and dose also merit consideration.

Cardiovascular risk in patients with small and medium abdominal aortic aneurysms, and no history of cardiovascular disease.

Cardiovascular disease (CVD) is the main cause of death in people with abdominal aortic aneurysm (AAA). There is little evidence that screening for AAA reduces all‐cause or cardiovascular mortality. The aim of the study was to assess whether subjects with a small or medium AAA (3·0–5·4 cm), without previous history of clinical CVD, had raised levels of CVD biomarkers or increased total mortality.

Assessment of a multifactorial risk index for predicting postoperative pneumonia after open abdominal aortic aneurysm repair.

Pneumonia is a common postoperative complication, with a mortality of up to 40%. The Post-operative Pneumonia Risk Index (PPRI) was derived from a large cohort of general surgical patients but has not been validated in patients undergoing open abdominal aortic aneurysm (AAA) repair. The PPRI was applied to patients undergoing elective open AAA repair in a tertiary referral vascular unit. Pneumonia occurred in 20% of patients. Receiver operating characteristic curve analysis identified 36 as the optimum PPRI cutoff value. At this cutoff, the likelihood ratio for pneumonia was 1.35 (95% confidence interval 1.08–1.62). However, in a multivariate analysis, only weight loss in excess of 10% over the preceding 6 months was an independent predictor of postoperative pneumonia. Although the PPRI is of some value in identifying high-risk patients undergoing AAA repair, weight loss alone may be predictive, allowing targeted preventive measures in aneurysm patients at increased risk.

Cysts and Swellings: A Systematic Review of the Association Between Polycystic Kidney Disease and Abdominal Aortic Aneurysm

BACKGROUND Whether abdominal aortic aneurysm (AAA) forms part of the extrarenal manifestations of autosomal-dominant polycystic kidney disease (ADPKD) is unclear. We set out to review the evidence for an association. MATERIALS AND METHODS PubMed, Medline, Embase, and Web of Science databases 1960-2011 were searched [abdominal aortic aneurysm OR AAA OR triple A] AND [polycystic kidney disease OR PKD OR ADPKD OR Renal Cysts]. No limitations were placed on article type or language. Reference lists were recursively searched as were pertinent journal contents. RESULTS Eighteen papers were included. Since the first documented case of ADPKD and AAA in 1980, there have been 23 case reports. The voluminous kidneys make AAA diagnosis challenging and surgical exposure difficult. Two studies have assessed aortic diameter in patients with ADPKD and controls, one finding increased aortic diameter in ADPKD (2.7 cm vs. 2.3 cm, P < 0.02) and the other finding no difference. A further study identified a higher incidence of renal cysts in patients with AAA compared to controls (54% vs. 30%, P = 0.0006). CONCLUSION There is not enough clinical evidence to determine if ADPKD and AAA share a common pathology. Larger multicenter trials are required to determine if a link exists.

Calcium channel blockers enhance sac shrinkage after endovascular aneurysm repair

OBJECTIVE Sac shrinkage is a surrogate marker of success after endovascular aneurysm repair (EVAR). We set out to determine if any common cardioprotective medications had a beneficial effect on sac shrinkage. METHODS This retrospective observational study took place at Leeds Vascular Institute, a tertiary vascular unit in the Northern United Kingdom. The cohort comprised 149 patients undergoing EVAR between January 1, 2005, and December 31, 2008. Medication use was recorded at intervention (verified at study completion in 33 patients), and patients were monitored for 2 years. The main outcome measures were the effect of medication on sac shrinkage as determined by percentage change in maximal idealized cross-sectional area of the aneurysm at 1 month, 6 months, 1 year, and 2 years by linear regression model, in addition to 2-year endoleak and death rates determined by a binary logistic regression model. RESULTS After exclusions, 112 patients, who were a median age of 78 years (interquartile range, 78-83 years), remained for analysis. The median Glasgow Aneurysm Score was 85 (interquartile range, 79-92). At 2 years, mortality was 13.4%, endoleak developed in 37.5%, and significant endoleak developed in 14.3%. Patients taking a calcium channel blocker had enhanced sac shrinkage, compared with those not taking a calcium channel blocker, by 6.6% at 6 months (-3.0% to 16.3%, P = .09), 12.3% at 1 year (2.9% to 21.7%, P = .008), and 13.1% at 2 years (0.005% to 26.2%, P = .007) independent of other medication use, graft type, endoleak development, or death. CONCLUSIONS Enhanced sac shrinkage occurred after EVAR in patients taking calcium channel blockers. This warrants further study in other centers and at the molecular level.

Bare below the elbows

We read with interest the work of Burger et al and commend the authors for attempting to address the ‘paucity of evidence’ supporting the current UK Department of Health guidelines on uniforms and work wear, colloquially known as the ‘bare below the elbows’ policy. Nevertheless, we feel several points require consideration by the authors before meaningful, robust conclusions can be made in this important subject area. Firstly, the authors focus on the absence of clothing around the wrists facilitating more effective hand hygiene. However, the more important reason for the policy may in fact be the risk of transmission of pathogens from clothing and jewellery to patients and hence the guidance that these ‘should not unintentionally come into contact with patients’1 during routine clinical care. This is supported by research from many authors,2–5 including Treakle et al (reporting a high rate of bacterial contamination on the white coats of physicians) and Trick et al (reporting that ring wearing increases the frequency of hand contamination), and highlights the need to define clearly the terms ‘bare below the elbows’ (BBE) and ‘not bare’ (NB); Burger et al imply that there were individuals in both of their study groups wearing rings and watches and this may have introduced considerable confounding to the results. Secondly, we would question both the intervention under study (hand washing) and the sampling and culture methods used to detect colony counts in the participants. There is now an abundance of literature that supports the efficacy of hand rubbing with alcohol versus the use of antiseptic soap6 and hand washing between each patient (unless the hands are visibly soiled) is inefficient, unnecessary and may lead to skin conditions that can reduce both compliance and effectiveness of hand decontamination.7 We would advocate that the application of alcoholic hand rub, now considered the norm in most institutions, would be a more appropriate intervention in this instance. Previous studies have found the prevalence of healthcare worker MRSA colonisation to be up to 10% and that of the general population to be ∼1%; the low yields (0 out of 1,112 plates) in this study may indicate an insensitive sampling method rather than low prevalence. The wide range in colony counts observed (0–1,000) supports the hypothesis that the sampling and culture method is too inaccurate for the study to be interpretable and this may also explain the paradoxical increase in colony counts following hand washing that was seen in some participants. Finally, we would hypothesise that significant bias is present within the study, both due to the considerable publicity surrounding healthcare infections and the ‘zero tolerance’ approach to those not following local guidelines. These factors would incentivise any participant in the study (and particularly those not adhering to BBE policy) to ‘perform well’ during a hand washing exercise. The potentially uneven distribution of specialties in the BBE and NB groups (not reported by Burger et al) would again risk the introduction of bias. Differences in attire (surgical scrubs vs traditional work wear) and in type of patient interaction exist between specialties and indeed within clinical grades and these factors need careful consideration when designing a study of this type as well as when interpreting study findings. We recognise the many difficulties inherent in undertaking a study in this complex field and while we do not wish to be overly critical of this work we feel that the considerations above are both valid and important. In order to reach firm conclusions about the effectiveness of the BBE policy, it is therefore essential that any clinical results are interpreted in the context of the current literature and that bias and confounding are minimised during study design.

Aspirin therapy is associated with less compact fibrin networks and enhanced fibrinolysis in patients with abdominal aortic aneurysm.

Thrombotic changes in fibrin networks contribute to increased cardiovascular risk in patients with abdominal aortic aneurysm (AAA). Given that aspirin modulates the fibrin network, we aimed to determine if aspirin therapy is associated with changes in ex‐vivo fibrin clot characteristics in AAA patients and also conducted an exploratory analysis of 5‐year mortality in these individuals.

Carotid-femoral pulse wave velocity is negatively correlated with aortic diameter

Cardiovascular events pose significant morbidity and mortality burden to abdominal aortic aneurysm (AAA) patients. Arterial stiffness as measured by pulse wave velocity (PWV) is an independent predictor of cardiovascular risk. We investigated the relationship between aortic diameter and PWV. Consecutive patients with AAA were invited to participate. Patients completed a health questionnaire, received aortic ultrasound and carotid-femoral PWV (cfPWV) recordings with a Vicorder. Thirty patients were used for reproducibility assessment. A linear regression model was used to identify significant predictors of cfPWV. Observer variation was assessed using Bland and Altman analysis and the intraclass correlation coefficient. Three hundred and nine patients were included—148 with AAA and 161 controls. The mean difference for repeated cfPWV between observers was 0.11 ms−1. cfPWV was positively correlated with age (r=0.24, P<0.001) and systolic blood pressure (r=0.29, P<0.001) and negatively correlated with aortic diameter (r=−0.15, P=0.008). There was no difference in cfPWV between AAA and control groups (9.75±2.3 ms−1 vs. 9.55±2.3 ms−1, P=0.43). Aortic diameter (P=0.003) and systolic blood pressure (P<0.001) were significant predictors of cfPWV independent of age, aspirin usage and a history of myocardial infarction. Patients with large AAA (>5 cm) had decreased cfPWV compared with patients with small AAA (P=0.02) or normal diameter aorta (P=0.02). Vicorder measurements of cfPWV are repeatable. cfPWV is negatively associated with infra-renal aortic diameter and reduced in large AAA. cfPWV is likely invalid for accurate arterial stiffness assessment in patients with AAA owing to the apparent confounding effect of aortic size.

Pericytes in diabetes-associated vascular disease

Pericytes are mural cells that support and stabilise the microvasculature, and are present in all vascular beds. Pericyte-endothelial cell crosstalk is essential in both remodelling and quiescent vasculature, and this complex interaction is often disrupted in disease states. Pericyte loss is believed to be an early hallmark of diabetes-associated microvascular disease, including retinopathy and nephropathy. Here we review the current literature defining pericyte biology in the context of diabetes-associated vascular disease, with a particular focus on whether pericytes contribute actively to disease progression. We also speculate regarding the role of pericytes in the recovery from macrovascular complications, such as critical limb ischaemia. It becomes clear that dysfunctional pericytes are likely to actively induce disease progression by causing vasoconstriction and basement membrane thickening, resulting in tissue ischaemia. Moreover, their altered interactions with endothelial cells are likely to cause abnormal and inadequate neovascularisation in diverse vascular beds. Further research is needed to identify mechanisms by which pericyte function is altered by diabetes, with a view to developing therapeutic approaches that normalise vascular function and remodelling.