Introduction: An important challenge physicians face when treating acute heart failure (AHF) patients in the emergency department (ED) is deciding whether to admit or discharge, with or without early follow-up. The overall goal of our project was to improve care for AHF patients seen in the ED while avoiding unnecessary hospital admissions. The specific goal was to introduce hospital rapid referral clinics to ensure AHF patients were seen within 7 days of ED discharge. Methods: This prospective before-after study was conducted at two campuses of a large tertiary care hospital, including the EDs and specialty outpatient clinics. We enrolled AHF patients ≥50 years who presented to the ED with shortness of breath (<7 days). The 12-month before (control) period was separated from the 12-month after (intervention) period by a 3-month implementation period. Implementation included creation of rapid access AHF clinics staffed by cardiology and internal medicine, and development of referral procedures. There was extensive in-servicing of all ED staff. The primary outcome measure was hospital admission at the index visit or within 30 days. Secondary outcomes included mortality and actual access to rapid follow-up. We used segmented autoregression analysis of the monthly proportions to determine whether there was a change in admissions coinciding with the introduction of the intervention and estimated a sample size of 700 patients. Results: The patients in the before period (N = 355) and the after period (N = 374) were similar for age (77.8 vs. 78.1 years), arrival by ambulance (48.7% vs 51.1%), comorbidities, current medications, and need for non-invasive ventilation (10.4% vs. 6.7%). Comparing the before to the after periods, we observed a decrease in hospital admissions on index visit (from 57.7% to 42.0%; P <0.01), as well as all admissions within 30 days (from 65.1% to 53.5% (P < 0.01). The autoregression analysis, however, demonstrated a pre-existing trend to fewer admissions and could not attribute this to the intervention (P = 0.91). Attendance at a specialty clinic, amongst those discharged increased from 17.8% to 42.1% (P < 0.01) and the median days to clinic decreased from 13 to 6 days (P < 0.01). 30-day mortality did not change (4.5% vs. 4.0%; P = 0.76). Conclusion: Implementation of rapid-access dedicated AHF clinics led to considerably increased access to specialist care, much reduced follow-up times, and possible reduction in hospital admissions. Widespread use of this approach can improve AHF care in Canada.

Introduction: Guidelines recommend serial conventional cardiac troponin (cTn) measurements 6-9 hours apart for non-ST-elevation myocardial infarction (NSTEMI) diagnosis. We sought to develop a pathway based on absolute/relative changes between two serial conventional cardiac troponin I (cTnI) values 3-hours apart for 15-day MACE identification. Methods: This was a prospective cohort study conducted in the two large ED's at the Ottawa Hospital. Adults with NSTEMI symptoms were enrolled over 32 months. Patients with STEMI, hospitalized for unstable angina, or with only one cTnI were excluded. We collected baseline characteristics, Siemens Vista cTnI at 0 and 3-hours after ED presentation, disposition, and ED length of stay (LOS). Adjudicated primary outcome was 15-day MACE (AMI, revascularization, or death due to cardiac ischemia/unknown cause). We analysed cTnI values by 99th percentile cut-off multiples (45, 100 and 250ng/L). Results: 1,683 patients (mean age 64.7 years; 55.3% female; median ED LOS 7 hours; 88 patients with 15-day MACE) were included. 1,346 (80.0%) patients with both cTnI ≤45ng/L; and 58 (3.4%) of the 213 patients with one value≥100ng/L but both <250ng/L or ≤20% change did not suffer MACE. Among 124 patients (7.4%) with one value >45ng/L but both <100ng/L based on 3 or 6-hour cTnI, one patient with Δ<10ng/L and 6 of 19 patients with Δ≥20ng/L were diagnosed with NSTEMI (patients with Δ10-19ng/L between first and second cTnI had third one at 6-hours). Based on the results, we developed the Ottawa Troponin Pathway (OTP) with a 98.9% sensitivity (95%CI 96.7-100%) and 94.6% specificity (95%CI 93.4-95.7%). Conclusion: The OTP, using two conventional cTnI measurements performed 3-hours apart, should lead to better identification of NSTEMI particularly those with values >99th percentile cut-off, standardize management and reduce the ED LOS.

Arterial wall thickening, stimulated by low-grade systemic inflammation, underlies many cardiovascular events. As diet is a significant moderator of systemic inflammation, the dietary inflammatory index (DIITM) has recently been devised to assess the overall inflammatory potential of an individual’s diet. The primary objective of this study was to assess the association of the DII with common carotid artery–intima-media thickness (CCA–IMT) and carotid plaques. To substantiate the clinical importance of these findings we assessed the relationship of DII score with atherosclerotic vascular disease (ASVD)-related mortality, ischaemic cerebrovascular disease (CVA)-related mortality and ischaemic heart disease (IHD)-related mortality more. The study was conducted in Western Australian women aged over 70 years (n 1304). Dietary data derived from a validated FFQ (completed at baseline) were used to calculate a DII score for each individual. In multivariable-adjusted models, DII scores were associated with sub-clinical atherosclerosis: a 1 sd (2·13 units) higher DII score was associated with a 0·013-mm higher mean CCA–IMT (P=0·016) and a 0·016-mm higher maximum CCA–IMT (P=0·008), measured at 36 months. No relationship was seen between DII score and carotid plaque severity. There were 269 deaths during follow-up. High DII scores were positively associated with ASVD-related death (per sd, hazard ratio (HR): 1·36; 95 % CI 1·15, 1·60), CVA-related death (per sd, HR: 1·30; 95 % CI 1·00, 1·69) and IHD-related death (per sd, HR: 1·40; 95 % CI 1·13, 1·75). These results support the hypothesis that a pro-inflammatory diet increases systemic inflammation leading to development and progression of atherosclerosis and eventual ASVD-related death.

Childhood overweight and obesity are worldwide public health problems and risk factors for chronic diseases. The presence of SNP in several genes has been associated with the presence of obesity. A total of 580 children (8–13 years old) from Queretaro, Mexico, participated in this cross-sectional study, which evaluated the associations of rs9939609 (fat mass obesity-associated (FTO)), rs17782313 (melanocortin 4 receptor (MC4R)) and rs6548238 (transmembrane protein 18 (TMEM18)) SNP with obesity and metabolic risk factors. Overweight and obesity prevalence was 19·8 and 19·1 %, respectively. FTO, MC4R and TMEM18 risk allele frequency was 17, 9·8 and 89·5 %, respectively. A significant association between FTO homozygous and MC4R heterozygous risk alleles and obesity was found (OR 3·9; 95 % CI 1·46, 10·22, and OR 2·1; 95 % CI 1·22, 3·71; respectively). The FTO heterozygous subjects showed higher systolic and diastolic blood pressures, compared with the homozygous for the ancestral allele subjects. These results remain significant after considering adiposity as a covariate. The FTO and MC4R genotypes were not significantly associated with total cholesterol, HDL-cholesterol and insulin concentration. No association was found between TMEM18 risk allele and obesity and/or metabolic alterations. Our results show that, in addition to a higher BMI, there is also an association of the risk genotype with blood pressure in the presence of the FTO risk genotype. The possible presence of a risk genotype in obese children must be considered to offer a more comprehensive therapeutic approach in order to delay and/or prevent the development of chronic diseases.

From a ferrite/martensite cold-rolled microstructure, the interaction between ferrite recrystallization and austenite formation is investigated. It is observed that a slow heating rate promotes the ferrite recrystallization and a homogeneous microstructure, whereas a fast heating rate delays the recrystallization and leads to heterogeneously distributed austenite islands.

Extended abstract of a paper presented at Microscopy and Microanalysis 2013 in Indianapolis, Indiana, USA, August 4 – August 8, 2013.

Extended abstract of a paper presented at Microscopy and Microanalysis 2013 in Indianapolis, Indiana, USA, August 4 – August 8, 2013.

A fully instrumented microscale shock tube, believed to be the smallest to date, has been fabricated and tested. This facility is used to study the transmission of a shock wave, produced in a large (37 mm) shock tube, into a 34  $\mathrm{\mu} \mathrm{m} $ hydraulic diameter and 2 mm long microchannel. Pressure microsensors of a novel design, with gigahertz bandwidth, are used to obtain pressure–time histories of the microchannel shock wave at five axial stations. In all cases the transmitted shock wave is found to be weaker than the incident shock wave, and is observed to decay both in pressure and velocity as it propagates down the microchannel. These results are compared with various analytical and numerical models, and the best agreement is obtained with a Navier–Stokes computational fluid dynamics computation, which assumes a no-slip isothermal wall boundary condition; good agreement is also obtained with a simple shock tube laminar boundary layer model. It is also found that the flow developing within the microchannel is highly dependent on conditions at the microchannel entrance, which control the mass flux entering into the device. Regardless of the micrometre dimensions of the present facility, shock wave propagation in a microchannel of that scale exhibits a behaviour similar to that observed in large-scale facilities operated at low pressures, and the shock attenuation can be explained in terms of accepted laminar boundary models.

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012.

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012.

Extended abstract of a paper presented at Microscopy and Microanalysis 2012 in Phoenix, Arizona, USA, July 29 – August 2, 2012.

Extended abstract of a paper presented at Microscopy and Microanalysis 2011 in Nashville, Tennessee, USA, August 7–August 11, 2011.

Extended abstract of a paper presented at Microscopy and Microanalysis 2011 in Nashville, Tennessee, USA, August 7–August 11, 2011.

In this work two aspects of momentum-dependent electron energy loss spectrometry are studied, both in the core-loss and in the low-loss region. In the case of core losses, we focus on the demonstration and the interpretation of an unexpected non-Lorentzian behavior in the angular part of the double-differential scattering cross-section. The silicon L3 edge is taken as an example. Using calculations we show that the non-Lorentzian behavior is due to a change in the wavefunction overlap between the initial and the final states. In the case of low losses, we first analyze the momentum-dependent loss functions of coinage metals Cu, Ag, and Au. We then demonstrate how advanced electronic structure calculations can be used to build simple models for the dielectric function that can then serve as a basis for the calculation of more complicated sample geometries.