• Med. J. Aust. · May 2011

    Glycaemia and albuminuria as predictors of coronary heart disease in Aboriginal and Torres Strait Islander adults: a north Queensland cohort.

    • Robyn A McDermott, Brad McCulloch, and Ming Li.
    • Sansom Institute for Health Research, University of South Australia, Adelaide. Robyn.McdermottATunisa.edu.au
    • Med. J. Aust. 2011 May 16; 194 (10): 514518514-8.

    ObjectiveTo evaluate the contribution of non-traditional risk factors to coronary heart disease (CHD) incidence in Indigenous adults.Design, Setting And ParticipantsCohort study of 1706 Aboriginal and Torres Strait Islander adults from 26 remote communities in far north Queensland who were initially free of CHD, with a mean of 7.5 years of follow-up.Main Outcome MeasuresCHD-related deaths and hospitalisations obtained by record matching.ResultsCHD incidence was similar in men and women and in Aboriginals and Torres Strait Islanders; overall incidence was 12.1 (95% CI, 10.1-14.1) events per 1000 person-years. At baseline, prevalence of diabetes was 12.4% in Aboriginals and 22.3% in Torres Strait Islanders, prevalence of any albuminuria was similarly high (33.5%) in both groups, and participants with diabetes were 5.5 (95% CI, 4.2-7.3) times more likely to have albuminuria than those without diabetes. At follow-up, adjusted hazard ratios for CHD were 1.7 (95% CI, 1.01-2.8) for obesity based on waist circumference; 1.5 (95% CI, 1.01-2.3) for hypertension; 1.4 (95% CI, 0.9-2.2) for previous or current smoking; 1.9 (95% CI, 1.3-2.7) for elevated triglycerides; 1.3 (95% CI, 0.9-1.9) for low high-density lipoprotein cholesterol; 1.3 (95% CI, 0.8-2.2) for impaired fasting glucose; 2.4 (95% CI, 1.7-3.5) for diabetes; and 4.6 (95% CI, 2.9-7.1) for macroalbuminuria. Baseline albuminuria without diabetes increased risk by 50% (adjusted rate ratio, 1.5 [95% CI, 0.9-2.4]) but diabetes with macroalbuminuria amplified risk sixfold (adjusted rate ratio, 5.9 [95% CI, 3.4-10.1]).ConclusionHigh prevalence of glycaemia and albuminuria in this population, especially when combined, account for much of the excess CHD risk beyond the traditional Framingham risk factors. They can be measured simply, lend themselves to cardioprotective interventions, and should be used routinely to estimate risk and monitor effectiveness of treatment.

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