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Background: Previous research has raised substantial concerns regarding the validity of the International Statistical Classification of Diseases and Related Health Problems (ICD) codes (ICD-10 I05–I09) for rheumatic heart disease (RHD) due to likely misclassification of non-rheumatic valvular disease (non-rheumatic VHD) as RHD. There is currently no validated, quantitative approach for reliable case ascertainment of RHD in administrative hospital data. Methods: A comprehensive dataset of validated Australian RHD cases was compiled and linked to inpatient hospital records with an RHD ICD code (2000– 2018, n=7555). A prediction model was developed based on a generalized linear mixed model structure considering an extensive range of demographic and clinical variables. It was validated internally using randomly selected cross-validation samples and externally. Conditional optimal probability cutpoints were calculated, maximising discrimination separately for high-risk versus low-risk populations. Results: The proposed model reduced the false-positive rate (FPR) from acute rheumatic fever (ARF) cases misclassified as RHD from 0.59 to 0.27; similarly for non-rheumatic VHD from 0.77 to 0.22. Overall, the model achieved strong discriminant capacity (AUC: 0.93) and maintained a similar robust performance during external validation (AUC: 0.88). It can also be used when only basic demographic and diagnosis data are available. Conclusion: This paper is the first to show that not only misclassification of non-rheumatic VHD but also of ARF as RHD yields substantial FPRs. Both sources of bias can be successfully addressed with the proposed model which provides an effective solution for reliable RHD case ascertainment from hospital data for epidemiological disease monitoring and policy evaluation. [ABSTRACT FROM AUTHOR]

Background: Accurate coded diagnostic data are important for epidemiological research of stroke., Objective: To develop, implement and evaluate an online education program for improving clinical coding of stroke., Method: The Australia and New Zealand Stroke Coding Working Group co-developed an education program comprising eight modules: rationale for coding of stroke; understanding stroke; management of stroke; national coding standards; coding trees; good clinical documentation; coding practices; and scenarios. Clinical coders and health information managers participated in the 90-minute education program. Pre- and post-education surveys were administered to assess knowledge of stroke and coding, and to obtain feedback. Descriptive analyses were used for quantitative data, inductive thematic analysis for open-text responses, with all results triangulated., Results: Of 615 participants, 404 (66%) completed both pre- and post-education assessments. Respondents had improved knowledge for 9/12 questions ( p  < 0.05), including knowledge of applicable coding standards, coding of intracerebral haemorrhage and the actions to take when coding stroke (all p  < 0.001). Majority of respondents agreed that information was pitched at an appropriate level; education materials were well organised; presenters had adequate knowledge; and that they would recommend the session to colleagues. In qualitative evaluations, the education program was beneficial for newly trained clinical coders, or as a knowledge refresher, and respondents valued clinical information from a stroke neurologist., Conclusion: Our education program was associated with increased knowledge for clinical coding of stroke. To continue to address the quality of coded stroke data through improved stroke documentation, the next stage will be to adapt the educational program for clinicians., Competing Interests: Declaration of conflicting interestsThe author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Background and Aim: Quantifying stroke incidence and mortality is crucial for disease surveillance and health system planning. Administrative data offer a cost-effective alternative to "gold standard" population-based studies. However, the optimal methodology for establishing stroke deaths from administrative data remains unclear. We aimed to determine the optimal method for identifying stroke-related deaths in administrative datasets as the fatal component of stroke incidence, comparing counts derived using underlying and all causes of death (CoD)., Method: Using whole-population multijurisdictional person-level linked data from hospital and death datasets from South Australia, the Northern Territory, and Western Australia, we identified first-ever stroke events between 2012 and 2015, using underlying CoD and all CoD to identify fatal stroke counts. We determined the 28-day case fatality for both counts and compared results with gold standard Australian population-based stroke incidence studies., Results: The total number of incident stroke events was 16,150 using underlying CoD and 18,074 using all CoD. Case fatality was 24.7% and 32.7% using underlying and all CoD, respectively. Case fatality using underlying CoD was similar to that observed in four Australian "gold standard" population-based studies (20%-24%)., Conclusions: Underlying CoD generates fatal incident stroke estimates more consistent with population-based studies than estimates based on stroke deaths identified from all-cause fields in death registers., Competing Interests: Conflicts of Interests There are no conflicts of interest to disclose., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Introduction: Survivors of stroke are at risk of experiencing subsequent major adverse cardiovascular events (MACE). We aimed to determine the incidence of, and risk factors for, MACE after first-ever ischemic stroke, by age group (18-64 years vs. ≥65 years)., Methods: Observational cohort study using patient-level data from the Australian Stroke Clinical Registry (2009-2013), linked with hospital administrative data. We included adults with first-ever ischemic stroke who had no previous acute cardiovascular admissions and followed these patients for 2 years post-discharge, or until the first post-stroke MACE event. A Fine-Gray sub-distribution hazard model, accounting for the competing risk of non-cardiovascular death, was used to determine factors for incident post-stroke MACE., Results: Among 5,994 patients with a first-ever ischemic stroke (median age 73 years, 45% female), 17% were admitted for MACE within 2 years (129 events per 1,000 person-years). The median time to first post-stroke MACE was 117 days (89 days if aged &lt;65 years vs. 126 days if aged ≥65 years; p = 0.025). Among patients aged 18-64 years, receiving intravenous thrombolysis (sub-distribution hazard ratio [SHR] 0.51 [95% CI, 0.28-0.92]) or being discharged to inpatient rehabilitation (SHR 0.65 [95% CI, 0.46-0.92]) were associated with a reduced incidence of post-stroke MACE. In those aged ≥65 years, being unable to walk on admission (SHR 1.33 [95% CI 1.15-1.54]), and history of smoking (SHR 1.40 [95% CI 1.14-1.71]) or atrial fibrillation (SHR 1.31 [95% CI 1.14-1.51]) were associated with an increased incidence of post-stroke MACE. Acute management in a large hospital (&gt;300 beds) for the initial stroke event was associated with reduced incidence of post-stroke MACE, irrespective of age group., Conclusions: MACE is common within 2 years of stroke, with most events occurring within the first year. We have identified important factors to consider when designing interventions to prevent MACE after stroke, particularly among those aged &lt;65 years., (© 2023 The Author(s). Published by S. Karger AG, Basel.)

During 2013-2017, the mortality rate ratio for rheumatic heart disease among Indigenous versus non-Indigenous persons in Australia was 15.9, reflecting health inequity. Using excess mortality methods, we found that deaths associated with rheumatic heart disease among Indigenous Australians were probably substantially undercounted, affecting accuracy of calculations based solely on Australian Bureau of Statistics data.

Background: Sudden cardiac arrest (SCA) in young people aged 1 to 50 years often occurs with no presenting symptoms or risk factors prompting screening for cardiovascular disease prior to their cardiac arrest. Approximately 3,000 young Australians suffer from sudden cardiac death (SCD) each year, making this a major public health issue. However, there is significant variation in the way incidence is estimated resulting in discrepancy across reporting which impacts our ability to understand and prevent these devastating events. We describe the New South Wales (NSW) Sudden Cardiac Arrest Registry: a retrospective, data linkage study which will identify all SCAs in the young in NSW from 2009 through to June 2022., Objective: To determine the incidence, demographic characteristics and causes of SCA in young people. We will develop an NSW-based registry that will contribute to a greater understanding of SCA including risk factors and outcomes., Methods: The cohort will include all people who experience a SCA in the NSW community aged between 1 to 50 years. Cases will be identified using the following three datasets: the Out of Hospital Cardiac Arrest Register housed at NSW Ambulance, the NSW Emergency Department Data Collection, and the National Coronial Information System. Data from eight datasets will be collected, anonymised and linked for the entire cohort. Analysis will be undertaken and reported using descriptive statistics., Conclusions: The NSW SCA registry will be an important resource for the improved understanding of SCA and inform the widespread impacts it has on individuals, their families and society., (Copyright © 2023 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Objective: Rheumatic heart disease (RHD) comprises heart-valve damage caused by acute rheumatic fever (ARF). The Australian Government Rheumatic Fever Strategy funds RHD Control Programs to support detection and management of ARF and RHD. We assessed epidemiological changes during the years of RHD Control Program operation., Methods: Linked RHD register, hospital and death data from four Australian jurisdictions were used to measure ARF/RHD outcomes between 2010 and 2017, including: 2-year progression to severe RHD/death; ARF recurrence; secondary prophylaxis delivery and earlier disease detection., Results: Delivery of secondary prophylaxis improved from 53% median proportion of days covered (95%CI: 46-61%, 2010) to 70% (95%CI: 71-68%, 2017). Secondary prophylaxis adherence protected against progression to severe RHD/death (hazard ratio 0.2, 95% CI 0.1-0.8). Other measures of program effectiveness (ARF recurrences, progression to severe RHD/death) remained stable. ARF case numbers and concurrent ARF/RHD diagnoses increased., Conclusions: RHD Control Programs have contributed to major success in the management of ARF/RHD through increased delivery of secondary prevention yet ARF case numbers, not impacted by secondary prophylaxis and sensitive to increased awareness/surveillance, increased., Implications for Public Health: RHD Control Programs have a major role in delivering cost-effective RHD prevention. Sustained investment is needed but with greatly strengthened primordial and primary prevention., Competing Interests: Conflicts of interest The authors have no conflicts of interest to declare., (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Most estimates of stroke incidence among Aboriginal and Torres Strait Islander (hereinafter Aboriginal) Australians are confined to single regions and include small sample sizes. We aimed to measure and compare stroke incidence in Aboriginal and non-Aboriginal residents across central and western Australia., Methods: Whole-population multijurisdictional person-linked data from hospital and death datasets were used to identify stroke admissions and stroke-related deaths (2001-2015) in Western Australia, South Australia, and the Northern Territory. Fatal (including out-of-hospital deaths) and nonfatal incident (first-ever) strokes in patients aged 20-84 years were identified during the 4-year study period (2012-2015), using a 10-year lookback period to exclude people with prior stroke. Incidence rates per 100 000 population/year were estimated for Aboriginal and non-Aboriginal populations, age-standardized to the World Health Organization World Standard population., Results: In a population of 3 223 711 people (3.7% Aboriginal), 11 740 incident (first-ever) strokes (20.6% regional/remote location of residence; 15.6% fatal) were identified from 2012 to 2015, 675 (5.7%) in Aboriginal people (73.6% regional/remote; 17.0% fatal). Median age of Aboriginal cases (54.5 years; 50.1% female) was 16 years younger than non-Aboriginal cases (70.3 years; 44.1% female; P <0.001), with significantly greater prevalence of comorbidities. Age-standardized stroke incidence in Aboriginal people (192/100 000 [95% CI, 177-208]) was 2.9-fold greater than in non-Aboriginal people (66/100 000 [95% CI, 65-68]) aged 20-84 years; fatal incidence was 4.2-fold greater (38/100 000 [95% CI, 31-46] versus 9/100 000 [95% CI, 9-10]). Disparities were particularly apparent at younger ages (20-54 years), where age-standardized stroke incidence was 4.3-fold greater in Aboriginal people (90/100 000 [95% CI, 81-100]) than non-Aboriginal people (21/100 000 [95% CI, 20-22])., Conclusions: Stroke occurred more commonly, and at younger ages, in Aboriginal than non-Aboriginal populations. Greater prevalence of baseline comorbidities was present in the younger Aboriginal population. Improved primary prevention is required. To optimize stroke prevention, interventions should include culturally appropriate community-based health promotion and integrated support for nonmetropolitan health services., Competing Interests: Disclosures The authors acknowledge scholarship (Dr Balabanski; 1169269), fellowship (Dr Thrift; 1042600), and Synergy Grant (Dr Kleinig/Dr Thrift/Dr Katzenellenbogen/Dr Nedkoff; 1182071) support from the National Health and Medical Research Council and Heart Foundation (Dr Katzenellenbogen/Dr Nedkoff). Dr Thrift was employed by Monash University and chaired the National Stroke Foundation’s research advisory committee. Dr Brown reports compensation from Amgen.

Objectives: To generate contemporary age-specific mortality rates for Indigenous and non-Indigenous Australians aged <65 years who died from rheumatic heart disease (RHD) between 2013 and 2017, and to ascertain the underlying causes of death (COD) of a prevalent RHD cohort aged <65 years who died during the same period., Methods: For this retrospective, cross-sectional epidemiological study, Australian RHD deaths for 2013-2017 were investigated by first, mortality rates generated using Australian Bureau of Statistics death registrations where RHD was a coded COD, and second COD analyses of death records for a prevalent RHD cohort identified from RHD register and hospitalisations. All analyses were undertaken by Indigenous status and age group (0-24, 25-44, 45-64 years)., Results: Age-specific RHD mortality rates per 100 000 were 0.32, 2.63 and 7.41 among Indigenous 0-24, 25-44 and 45-64 year olds, respectively, and the age-standardised mortality ratio (Indigenous vs non-Indigenous 0-64 year olds) was 14.0. Within the prevalent cohort who died (n=726), RHD was the underlying COD in 15.0% of all deaths, increasing to 24.6% when RHD was included as associated COD. However, other cardiovascular and non-cardiovascular conditions were the underlying COD in 34% and 43% respectively., Conclusion: Premature mortality in people with RHD aged <65 years has approximately halved in Australia since 1997-2005, most notably among younger Indigenous people. Mortality rates based solely on underlying COD potentially underestimates true RHD mortality burden. Further strategies are required to reduce the high Indigenous to non-Indigenous mortality rate disparity, in addition to optimising major comorbidities that contribute to non-RHD mortality., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2023. No commercial re-use. See rights and permissions. Published by BMJ.)

Objective Burden of disease studies measure the impact of disease at the population level;however, methods and data sources for estimates of prevalence vary. Using a selection of cardiovascular diseases, we aimed to describe the implications of using different disease models and linked administrative data on prevalence estimation within three Australian burden of disease studies. Methods Three different methods (A = 2011 Australian Burden of Disease Study; B = 2015 Australian Burden of Disease Study; C = 2015 Western Australian Burden of Disease Study), which used linked data, were used to compare prevalence estimates of stroke, aortic aneurysm, rheumatic valvular heart disease (VHD) and non-rheumatic VHD. We applied these methods to 2015 Western Australian data, and calculated crude overall and age-specific prevalence for each condition. Results Overall, Method C produced estimates of cardiovascular prevalence that were lower than the other methods, excluding non-rheumatic VHD. Prevalence of acute and chronic stroke was up to one-third higher in Method A and B compared to Method C. Aortic aneurysms had the largest change in prevalence, with Method A producing an eight-fold higher estimate compared to Method C, but Method B was 10-20% lower. Estimates of VHD varied dramatically, with an up to six-fold change in prevalence in Method C due to substantial changes to disease models and the use of linked data. Conclusions Prevalence estimates require the best available data sources, updated disease models and constant review to inform government policy and health reform. Availability of nation-wide linked data will markedly improve future burden estimates.

Background: International Classification of Disease (ICD) codes are central for identifying myocardial infarction (MI) in administrative hospitalisation data, however validation of MI subtype codes is limited. We measured the sensitivity and specificity of ICD-10-AM (Australian Modification) codes for ST-elevation MI (STEMI) and non-STEMI (NSTEMI)., Methods: A sample of MI admissions was obtained from a dataset containing all MI hospitalisations in Western Australia (WA) for 2003, 2008 and 2013. Clinical data were collected from hospital medical records (n=799 patients). Cases were classified by ICD-10-AM codes for STEMI, NSTEMI and unspecified MI, and compared to clinical classification from review of available electrocardiographs (ECGs) and cardiac biomarkers (n=660). Sensitivity and specificity for ICD-10-AM coding versus clinical classification was measured, stratified by calendar year of discharge., Results: The majority of classifiable cases had MI recorded in the principal diagnosis field (STEMI n=293, 84.2%; NSTEMI n=202, 74.3%; unspecified MI n=20, 50.0%). Overall sensitivity of the ICD-10-AM STEMI code was 86.3% (95% CI 81.7-90.0%) and was higher when restricted to MI as a principal versus secondary diagnosis (88.8% vs 66.7%). Comparable values for NSTEMI were 66.7% (95% CI 61.5-71.6%), and 68.8% vs 61.4% respectively. Between 2003 and 2013, sensitivity for both MI subtypes increased: 80.2-89.5% for STEMI, and 51.2-73.8% for NSTEMI. Specificity was high for NSTEMI throughout (88.2% 95% CI 84.1-91.6%), although improving over time for STEMI (68.1-76.4%)., Conclusions: The sensitivity and specificity of ICD-10-AM codes for MI subtypes in hospitalisation data are generally high, particularly for principal diagnosis cases. However, the temporal improvement in sensitivity in coding of MI subtypes, particularly NSTEMI, may necessitate modification to trend studies using administrative hospitalisation data., (Copyright © 2021 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). All rights reserved.)

Background: Myocardial infarction mortality has declined since the 1970s, but contemporary drivers of this trend remain unexplained. The aim of this study was to compare the contribution of trends in event rates and case fatality to declines in myocardial infarction mortality in four high-income jurisdictions from 2002-15., Methods: Linked hospitalisation and mortality data were obtained from New South Wales (NSW), Australia; Ontario, Canada; New Zealand; and England, UK. People aged between 30 years and 105 years were included in the study. Age-adjusted trends in myocardial infarction event rates and case fatality were estimated from Poisson and binomial regression models, and their relative contribution to trends in myocardial infarction mortality calculated., Findings: 1 947 895 myocardial infarction events from a population of 80·4 million people were identified in people aged 30 years or older. There were significant declines in myocardial infarction mortality, event rates, and case fatality in all jurisdictions. Age-standardised myocardial infarction event rates were highest in New Zealand (men 893/100 000 person-years in 2002, 536/100 000 person-years in 2015; women 482/100 000 person-years in 2002, 271/100 000 person-years in 2015) and lowest in England (men 513/100 000 person-years in 2002, 382/100 000 person-years in 2015; women 238/100 000 person-years in 2002, 173/100 000 person-years in 2015). Annual age-adjusted reductions in event rates ranged from -2·6% (95% CI -3·0 to -2·3) in men in England to -4·3% (-4·4 to -4·1) in women in Ontario. Age-standardised case fatality was highest in England in 2002 (48%), but declined at a greater rate than in the other jurisdictions (men -4·1%/year, 95% CI -4·2 to -4·0%; women -4·4%/year, -4·5 to -4·3%). Declines in myocardial infarction mortality rates ranged from -6·1%/year to -7·6%/year. Event rate declines were the greater contributor to myocardial infarction mortality reductions in Ontario (69·4% for men and women), New Zealand (men 68·4%; women 67·5%), and NSW women (60·1%), whereas reductions in case fatality were the greater contributor in England (60% in men and women) and for NSW men (54%). There were greater contributions from case fatality than event rate reductions in people younger than 55 years in all jurisdictions, with contributions to mortality declines varying by country in those aged 55-74 years. Event rate declines had a greater impact than changes in case fatality in those aged 75 years and older., Interpretation: While the mortality burden of myocardial infarction has continued to fall across these four populations, the relative contribution of trends in myocardial infarction event rates and case fatality to declining mortality varied between jurisdictions, including by age and sex. Understanding the causes of this variation will enable optimisation of prevention and treatment efforts., Funding: National Health and Medical Research Council, Australia; Australian Research Council; Health Research Council of New Zealand; Canadian Institutes of Health Research, Canada; National Institute for Health Research, UK., Competing Interests: Declaration of interests We declare no competing interests., (Copyright © 2022 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY-NC-ND 4.0 license. Published by Elsevier Ltd.. All rights reserved.)

Cardiovascular diseases (CVD) are leading causes of death and morbidity in Australia and worldwide. Despite improvements in treatment, there remain large gaps in our understanding to prevent, treat and manage CVD events and associated morbidities. This article lays out a vision for enhancing CVD research in Australia through the development of a Big Data system, bringing together the multitude of rich administrative and health datasets available. The article describes the different types of Big Data available for CVD research in Australia and presents an overview of the potential benefits of a Big Data system for CVD research and some of the major challenges in establishing the system for Australia. The steps for progressing this vision are outlined., (Copyright © 2021 Australian and New Zealand Society of Cardiac and Thoracic Surgeons (ANZSCTS) and the Cardiac Society of Australia and New Zealand (CSANZ). Published by Elsevier B.V. All rights reserved.)

Objective: To determine the incidence, risk predictors and relative mortality risk of incident heart failure (HF) in patients following atrial fibrillation (AF) hospitalisation., Methods: The Western Australian Hospitalisation Morbidity Data Collection was used to identify patients aged 25-94 years with index (first-in-period) AF hospitalisation, but without a prior HF admission, between 2000 and 2013. We evaluated the risk of incident HF hospitalisation within 3 years after AF admission, and the impact of HF hospitalisation on all-cause mortality., Results: The cohort comprised 52 447 patients, 57.5% men, with a median age of 73.1 (IQR 63.2-80.8) years. At 3 years after AF discharge, the cumulative incidence of HF (n=6153) was 11.7% (95% CI 11.5% to 12.0%) and all-cause death (n=9702) was 18.5% (95% CI 18.2% to 18.8%). Independent predictors of incident HF included advancing age, any history of myocardial infarction (MI), peripheral vascular disease, valvular heart disease, chronic kidney disease, chronic obstructive pulmonary disease, hypertension, diabetes, obesity and excessive alcohol use (all p<0.001). Patients hospitalised for first-ever HF compared with those without HF hospitalisation had an adjusted HR of 3.3 (95% CI 3.1 to 3.4) for all-cause mortality (p<0.001). Independent predictors of HF were also shared with those for mortality, with the exception of hypertension., Conclusion: Hospitalisation for new HF is common in patients with AF and independently associated with a 3-fold hazard for death. The clinical predictors of incident HF emphasise the importance of integrated management of common comorbid conditions and lifestyle risk factors in patients with AF to reduce their morbidity and mortality., Competing Interests: Competing interests: None declared., (© Author(s) (or their employer(s)) 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

The Australasian guidelines recommend use of the CHA 2 DS 2 -VA schema to stratify ischaemic stroke risk in patients with non-valvular atrial fibrillation (N-VAF) and determine risk thresholds for recommending oral anticoagulant (OAC) therapy. However, the CHA 2 DS 2 -VA score has not been validated in a representative Australian population cohort with N-VAF, including in Aboriginal people who are known to have a higher age-adjusted stroke risk than other Australians. In a retrospective data-linkage study of 49 114 patients aged 24-84 years with N-VAF, 40.0% women and 2.5% Aboriginal, we found that patients with a CHA 2 DS 2 -VA score >2 had high annual stroke rates (>2%) that would justify OAC therapy. This occurred regardless of Aboriginal status. Non-Aboriginal patients with a CHA 2 DS 2 -VA score of 0 had a mean annual stroke rate of 0.4%, and hence were not likely to benefit from antithrombotic therapy. However, Aboriginal patients with a zero CHA 2 DS 2 -VA score had a significantly higher annual stroke rate of 0.9%, and could potentially obtain net clinical benefit from anticoagulation, primarily with the safer non-vitamin K antagonist OAC. We conclude that clinicians can confidently use the CHA 2 DS 2 -VA score to make decisions regarding anticoagulation in accordance with stroke risk in patients with N-VAF, except in Aboriginal people in whom the risk score was unable to identify those at truly low risk of stroke., (© 2021 Royal Australasian College of Physicians.)

While there is clear evidence that high levels of pollution are associated with increased all-cause mortality and cardiovascular mortality and morbidity, the biological mechanisms that would explain this association are less understood. We examined the association between long-term exposure to air pollutants and risk factors associated with cardiovascular disease. Air pollutant concentrations were estimated at place of residence for cohort members in the Western Australian Centre for Health and Ageing Health in Men Study. Blood samples and blood pressure measures were taken for a cohort of 4249 men aged 70 years and above between 2001 and 2004. We examined the association between 1-year average pollutant concentrations with blood pressure, cholesterol, triglycerides, C-reactive protein, and total homocysteine. Linear regression analyses were carried out, with adjustment for confounding, as well as an assessment of potential effect modification. The four pollutants examined were fine particulate matter, black carbon (BC), nitrogen dioxide, and nitrogen oxides. We found that a 2.25 μg/m3 higher exposure to fine particulate matter was associated with a 1.1 percent lower high-density cholesterol (95% confidence interval: -2.4 to 0.1) and 4.0 percent higher serum triglycerides (95% confidence interval: 1.5 to 6.6). Effect modification of these associations by diabetes history was apparent. We found no evidence of an association between any of the remaining risk factors or biomarkers with measures of outdoor air pollution. These findings indicate that long-term PM2.5 exposure is associated with elevated serum triglycerides and decreased HDL cholesterol. This requires further investigation to determine the reasons for this association., Competing Interests: The authors have declared that no competing interests exist.

Background In 2018, the World Health Organization prioritized control of acute rheumatic fever (ARF) and rheumatic heart disease (RHD), including disease surveillance. We developed strategies for estimating contemporary ARF/RHD incidence and prevalence in Australia (2015-2017) by age group, sex, and region for Indigenous and non-Indigenous Australians based on innovative, direct methods. Methods and Results This population-based study used linked administrative data from 5 Australian jurisdictions. A cohort of ARF (age <45 years) and RHD cases (<55 years) were sourced from jurisdictional ARF/RHD registers, surgical registries, and inpatient data. We developed robust methods for epidemiologic case ascertainment for ARF/RHD. We calculated age-specific and age-standardized incidence and prevalence. Age-standardized rate and prevalence ratios compared disease burden between demographic subgroups. Of 1425 ARF episodes, 72.1% were first-ever, 88.8% in Indigenous people and 78.6% were aged <25 years. The age-standardized ARF first-ever rates were 71.9 and 0.60/100 000 for Indigenous and non-Indigenous populations, respectively (age-standardized rate ratio=124.1; 95% CI, 105.2-146.3). The 2017 Global Burden of Disease RHD prevalent counts for Australia (<55 years) underestimate the burden (1518 versus 6156 Australia-wide extrapolated from our study). The Indigenous age-standardized RHD prevalence (666.3/100 000) was 61.4 times higher (95% CI, 59.3-63.5) than non-Indigenous (10.9/100 000). Female RHD prevalence was double that in males. Regions in northern Australia had the highest rates. Conclusions This study provides the most accurate estimates to date of Australian ARF and RHD rates. The high Indigenous burden necessitates urgent government action. Findings suggest RHD may be underestimated in many high-resource settings. The linked data methods outlined here have potential for global applicability.

Adherence to cardioprotective medications following myocardial infarction (MI) is commonly assessed using a binary threshold of 80%. We investigated the relationship between medication adherence as a continuous measure and outcomes in MI survivors using restricted cubic splines (RCS). We identified all patients aged ≥65 years hospitalised for MI from 2003-2008 who survived one-year post-discharge (n = 5938). Adherence to statins, beta-blockers, renin angiotensin system inhibitors (RASI) and clopidogrel was calculated using proportion of days covered to one-year post-discharge (landmark date). Outcomes were 1-year all-cause death and major adverse cardiac events (MACE) after the landmark date. Adherence-outcome associations were estimated from RCS Cox regression models. RCS analyses indicated decreasing risk for both outcomes above 60% adherence for statins, RASI and clopidogrel, with each 10% increase in adherence associated with a 13.9%, 12.1% and 18.0% decrease respectively in adjusted risk of all-cause death (all p < 0.02). Similar results were observed for MACE (all p < 0.03). Beta-blockers had no effect on outcomes at any level of adherence. In MI survivors, increasing adherence to statins, RASI, and clopidogrel, but not beta blockers, is associated with a decreasing risk of death/MACE with no adherence threshold beyond 60%. Medication adherence should be considered as a continuous measure in outcomes analyses.

Objective: To compare population-level trends in 30-day case fatality following incident myocardial infarction (MI) in people with diabetes and those without diabetes., Methods: We identified all hospitalised incident MIs in 35-84 year olds from the Western Australian Data Linkage System for 1998-2010, stratified by diabetes status. Crude and age- and sex-standardised 30-day case fatality were estimated, and age- and sex-adjusted trends were calculated from logistic regression. We calculated the trend in risk of 30-day death associated with diabetes from multivariable logistic regression, adjusting for demographics, comorbidities and MI type., Results: 26 610 hospitalised incident MI cases were identified, 24.8% of whom had diabetes. The prevalence of heart failure fell in people with diabetes, concurrent with increasing chronic kidney disease and prior coronary heart disease and increasing levels of evidence-based therapies. Case fatality in people with diabetes fell from 11.65%, in 1998-2001, to 3.96% by 2008-2010. Age- and sex-standardised case fatality declined at a greater rate in those with diabetes (-10.6%/year, 95% CI -12.8% to -8.2%) compared to non-diabetics (-6.9%/year, 95% CI -8.3% to -5.3%; interaction p=0.005). The adjusted risk of 30-day death after incident MI was 1.23 times higher in diabetics than non-diabetics in 1998-2001 (95% CI 1.01 to 1.50), but was lower by 2008-2010 (OR 0.64, 95% CI 0.46 to 0.88)., Conclusions: Greater improvements in 30-day case fatality following incident MI in people with diabetes during the 13-year study period has led to diabetes no longer being an independent predictor of early death following incident MI by 2008-2010., (Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://group.bmj.com/group/rights-licensing/permissions.)

Background: Higher mortality following myocardial infarction (MI) is reported in women compared with men with short-term follow-up. Our study aim was to compare long-term gender- and age-specific outcomes following incident MI., Methods: 30-day survivors of incident MI from 2003-2009 were identified from linked administrative data in Western Australia. Outcomes identified were recurrent MI, and cardiovascular and all-cause mortality. Follow-up data was available until 30(th) June 2011. Unadjusted risk out to eight-years was estimated from Kaplan-Meier survival curves, and multivariate Cox regression models were used to estimate relative risk in women compared with men by age group., Results: There were 12,420 30-day survivors of incident MI from 2003-2009 (males 71.2%). Women had higher levels of comorbidities across all age groups compared with men. Unadjusted event risks were higher in women than men overall, underpinned by higher risk of recurrent MI in 55-69 year-old women and of cardiovascular mortality across all age groups in women. Gender differences were generally attenuated after adjustment for demographic factors and comorbidities., Conclusions: This study highlights the elevated risk of cardiovascular events in women compared with men with long-term follow-up, and demonstrates the need for improved long-term secondary prevention in this patient group., (Crown Copyright © 2014. Published by Elsevier B.V. All rights reserved.)

Background: The risk of myocardial infarction (MI) is elevated in people with diabetes mellitus (DM) compared with non-DM counterparts. The aim of this study was to compare population trends in the incidence of hospitalized MI and coronary heart disease (CHD) in adults with and without DM., Methods and Results: All incident hospitalized MI and CHD events were identified from whole-population hospital data in Western Australia for 1998 to 2010. Annual age-standardized MI and CHD incidence rates were calculated for people with and without DM aged 35 to 84 years and age-adjusted trends estimated from Poisson regression. There were 26 610 incident MI and 56 142 incident CHD cases during the study period. MI incidence rates fell in men (-2.9%/y; 95% confidence interval [CI], -3.7 to -2.1) and women (-3.8%/y; 95% CI, -4.8 to -2.1) with DM, representing overall reductions of 35% and 43% respectively, with comparable reductions in incident CHD. Downward trends in MI incidence in those with DM were most apparent in 55- to 84-year olds. In adults without DM, there was no decline in MI incidence but a small significant decrease in incident CHD (men, -1.5%/y; 95% CI, -1.8 to -1.2 and women, -1.3%/y; 95% CI, -1.8 to -0.9). Incidence rate ratios for MI in men with versus without DM declined from 4.5 (95% CI, 4.2-4.8) to 3.1 (95% CI, 2.9-3.3) and from 6.0 (95% CI, 5.4-6.6) to 3.8 (95% CI, 3.5-4.1) in women between 1998 and 2010., Conclusions: There have been significant reductions in incidence rates of MI and CHD in adults with DM between 1998 and 2010; however, the excess risk of MI incidence remains 3 to 4× greater in people with DM., (© 2014 American Heart Association, Inc.)