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Aims To determine exposure to warfarin and the associated outcomes in a population of older patients with non-valvular atrial fibrillation (NVAF). Methods Cohort study of patients aged 65-89 years admitted to hospital July 2003-December 2008 with newly-diagnosed or pre-existing AF. Outcomes at three years among one-year survivors post-index admission (landmark date) were all-cause mortality, stroke/systemic thromboembolism (stroke/TE) and bleeding. Multivariate Cox models were used to identify factors associated with each outcome. Results AF was the principal diagnosis for 27.5% of 17,336 index AF admissions. Of 14,634 (84.4%) patients alive at one-year 1,384 (9.5%) died in the following year. Vascular disease (42%) was the most frequent cause of death.Warfarin use, prior to the index admission and/or the 1-year landmark, did not exceed 40%.Compared to non-exposure or discontinuation at the index admission, initiation or persistence with warfarin prior to the landmark date was associated with reduced risk for all-cause mortality, a statistically non-significant reduction in risk for stroke/TE, and an increased risk for bleeding. Higher CHA2DS2-VASc scores were associated with increased risk for each outcome. Conclusions In a population-based cohort of hospitalised NVAF patients, the initiation and persistent use of warfarin was associated with lower all-cause mortality risk to three years, although reduction in risk for stroke/TE did not reach statistical significance. The apparent under-use of warfarin in this older, high-risk cohort reinforces the opportunity for further reduction in stroke/TE with the uptake of non-vitamin K oral anti-coagulants (NOACs) among those not prescribed, or not persistent with, warfarin.

Background: Age-specific death from cardiovascular disease among Australian Aboriginals is estimated to be four to seven times that of general population, and the major cause of premature death. There is little reliable information on the incidence of coronary heart disease (CHD). This study compares CHD event rates in urban dwelling Aboriginal people and the general population. Methods: The Perth Aboriginal Atherosclerosis Risk Study (PAARS) cohort was assessed at baseline (1998/1999) and 913 participants followed-up to 2006. A comparison group of age-matched, sex-matched and postcode-matched non-Aboriginals (n¼3582) were selected from the Perth, Western Australia, Electoral Roll. Electronic record linkage captured prior CHD and first CHD events in both groups. The rates of first CHD events (hospital admission or CHD death) per 1000 person years (PY) and incidence rate ratios (IRR) were calculated. Results: The event rate for the PAARS population was 14.9 per 1000 PY (95% CI 12.3 to 18.2) versus 2.4 (1.9 to 3.1) for the general population. The IRR was 6.1 (4.5 to 8.4). For Aboriginal men the rate was 15.0 (11.2 to 20.0) versus 3.8 (2.5 to 5.0) per 1000 PY, with age-specific rates being two to five times that of non-Aboriginals. Incidence for Aboriginal women was 15.0(11.5 to 19.5) versus 1.4 (0.9 to 2.1) with age-specific rates being 8-25 times that of non-Aboriginals. Conclusions: Age and sex-specific CHD event rates in urban Aboriginals far exceeded that of a matched general population. Events occurred at a much younger age among the Aboriginal participants and were equally excessive among men and women. Refereed/Peer-reviewed

Objective: To assess the sensitivity of the recording of Aboriginality in the Western Australia Linked Data. Methods: This was a follow-up study using record linkage. Demographic data was obtained from 993 adult, urban-dwelling Aboriginal Australian participants in the Perth Aboriginal Atherosclerosis Risk study (PAARS). These were linked to the Western Australian Linked Data (State-wide hospital admissions and discharges, and deaths) to provide the number of admissions and Indigenous status coding from 1980 to 2006. Results: There were 14,413 admissions for PAARS participants in the study period. The sensitivity of coding of Indigenous status in hospital admissions data significantly improved over time, exceeding 0.9 in every year since 2002. Prior to 2002 sensitivity was around 0.8, but poorer for males, with some anomalous years. Conclusions: The coding of Indigenous status in the Western Australia Hospital Morbidity Database since 2002 has improved. The data from earlier decades must be approached with more caution. Implications: The improved accuracy of identification of Indigenous status in the Western Australia Hospital Morbidity Database allows comparative studies of adult Aboriginal and non-Aboriginal population health outcomes to be undertaken with confidence.

Objective: To determine the incidence of coronary heart disease (CHD) events in an urban Aboriginal population. Design, setting and participants: Cohort study of 906 Aboriginal people without CHD from 998 who had undergone risk‐factor assessment in the Perth Aboriginal Atherosclerosis Risk Study (PAARS) in 1998–1999. PAARS cohort data were electronically linked to a range of databases that included Western Australian hospital morbidity data and death registry data. We analysed data from January 1980 to December 2006 to identify previous admissions for CHD from 1980 to baseline (1998–1999) and new events from baseline to 2006. Main outcome measure: First CHD event (hospital admission or death). Results: There were 891 linked records for the 906 participants without previous CHD. The event rate was 12.6/1000 person‐years (95% CI, 10.2–15.6/1000 person‐years). Annual CHD event rates ranged from 8 to 18/1000 person‐years. After adjustment for age (sex was not associated with the risk factors assessed), factors associated with risk of a CHD event in the PAARS cohort were a history of diabetes, overweight or obesity (indicated by body mass index), smoking, and hypertension, but not waist circumference. People with these risk factors were 1.9–2.7 times more likely to experience a CHD event. Compared with previously published information from a remote Aboriginal community in the Northern Territory, the incidence of CHD events among urban‐dwelling Aboriginal people was not significantly different (P > 0.05 overall and for subgroups defined by age and sex). Conclusions: City‐dwelling Aboriginal Australians have an incidence of CHD events comparable to that of Aboriginal people living in remote northern Australia. Refereed/Peer-reviewed