Search

Aim To assess the relationships of diabetes and albuminuria with all-cause mortality and cardiovascular disease outcomes in a population without prior cardiovascular disease using data from the Darwin Region Urban Indigenous Diabetes (DRUID) study. Methods We conducted a prospective cohort study of 706 participants (aged 15-81 years, 68% women) without prior cardiovascular disease who underwent a 75-g oral glucose tolerance test. Deaths and fatal or non-fatal cardiovascular disease were determined over 7 years, and hazard ratios with 95% CIs and population attributable risks were estimated for baseline glycaemia and albuminuria. Results Compared with normoglycaemia and after adjustment for age, sex, hypertension, dyslipidaemia and smoking, known diabetes was associated with an adjusted hazard ratio of 4.8 (95% CI 1.5-14.7) for all-cause mortality and 5.6 (95% CI 2.1-15.2) for cardiovascular disease. Compared with normoalbuminuria, the respective adjusted risks for macroalbuminuria were 10.9 (95% CI 3.7-32.1) and 3.9 (95% CI 1.4-10.8). The Adjusted all-cause mortality and cardiovascular disease estimated population attributable risks for diabetes were 27% and 32%, and for albuminuria they were 32% and 21%, respectively. Conclusions In our study population, the burden of mortality and cardiovascular disease was largely driven by diabetes and albuminuria. This finding on the influence of diabetes and albuminuria is consistent with reports in other high-risk Indigenous populations and should be better reflected in risk scores and intervention programmes. [ABSTRACT FROM AUTHOR]

Objective To investigate whether cardiovascular risk factors can explain the higher carotid intima–media thickness (CIMT) in Indigenous compared with European Australians. Design Cross-sectional study in three subgroups. Patients Non-diabetic urban European ( n = 86), urban Indigenous ( n = 69), and remote Indigenous ( n = 60) Australians aged 25–64 years. Measurements CIMT, age, sex, anthropometry, blood pressure, smoking status, fasting glucose and insulin, haemoglobin (Hb)A1c, homocysteine, C-reactive protein (CRP), lipids, urinary albumin and creatinine. Results CIMT and levels of risk factors, except fasting glucose and total cholesterol, worsened across the three groups. Logn fasting insulin [β = 0·022, 95% confidence interval (CI) 0–0·0439], age (β = 0·006, 95% CI 0·004–0·007), gender (female β = –0·005 vs. male, 95% CI –0·084 to –0·026), mean arterial pressure (MAP) (β = 0·001, 95% CI 0·001–0·002) and ethnicity/location [urban Indigenous (β = 0·027, 95% CI –0·010 to 0·064 vs. European); remote Indigenous (β = 0·083, 95% CI 0·042–0·123 vs. European)] explained 41% of variance in CIMT. Significant interactions were seen for ethnicity/location with age ( P = 0·014) and MAP ( P = 0·018). Age was consistently associated with CIMT across the three populations, and was associated with larger increments in CIMT for the Indigenous subgroups (β = 0·007, 95% CI 0·005–0·009 urban; β = 0·007, 95% CI 0·004–0·010 remote) compared with Europeans (β = 0·003, 95% CI 0·002–0·006) in models including age, sex and MAP. MAP was only associated with CIMT in the remote Indigenous subgroup. Conclusion After adjusting for selected risk factors, CIMT in remote Indigenous participants was still higher than in Europeans. The slope of the association between age and CIMT steepened from urban Europeans to remote Indigenous. [ABSTRACT FROM AUTHOR]

Objective Indigenous Australians have rates of cardiovascular (CVD) mortality some seven to 10-fold higher than non-Indigenous Australians aged 25–64 years. We aimed to evaluate the impact of type 2 diabetes and components of the metabolic syndrome on carotid intima-media thickness (CIMT) as a marker of cardiovascular risk in Indigenous Australians living in remote and urban environments and in Australians of European ancestry. Design, patients and measurements CIMT was measured by high-resolution B-mode ultrasound imaging of the common carotid artery in 119 remote Indigenous, 144 urban Indigenous and 122 urban European Australians with and without diabetes. Results In nondiabetic participants, CIMT was lowest in Europeans (mean (SD) 0·64 mm (0·10)), higher in urban Indigenous Australians (0·67 mm (0·12)) and highest in remote Indigenous Australians (0·73 mm (0·15), P < 0·001). CIMT was higher with diabetes with the same pattern observed between populations: 0·73 mm, 0·79 mm and 0·82 mm, respectively ( P < 0·001). Traditional risk factors (age, male gender, blood pressure and HbA1c) explained 35–45% of the variance of CIMT within each population group. However, differences in CIMT between population groups were maintained after adjustment for these cardiovascular risks plus cholesterol and smoking ( P < 0·001). Factor analysis revealed that variables of the metabolic syndrome, together with smoking and elevated C-reactive protein (CRP) and urinary albumin-creatinine ratio (ACR), are likely to explain the higher CIMT in Indigenous Australians (and the urban-remote gradient). Unmeasured variables (genetic, psychosocial and socioeconomic) may also contribute to higher CIMT in these populations. Conclusion Glycaemic control and metabolic syndrome components contribute significantly to premature atherogenesis in Indigenous Australians and we recommend that therapy should be targeted accordingly. [ABSTRACT FROM AUTHOR]

Type 2 diabetes mellitus and other chronic cardio-metabolic conditions are significant contributors to the large disparities in life expectancy between Indigenous and non-Indigenous Australians. Type 2 diabetes is more prevalent from a young age among Indigenous Australians and is often preceded by a cluster of risk factors, including central obesity, dyslipidaemia, albuminuria and socio-economic disadvantage. Management of type 2 diabetes in Australian Indigenous peoples can be challenging in the setting of limited resources and socio-economic disadvantage. Key strategies to address these challenges include working in partnership with patients, communities and primary healthcare services ( PHC, Aboriginal community controlled and government services) and working in a multidisciplinary team. Population prevention measures are required within and beyond the health system, commencing as early as possible in the life course. [ABSTRACT FROM AUTHOR]