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Original research article
High-sensitivity cardiac troponin I and risk of cardiovascular disease in an Australian population-based cohort
  1. Kun Zhu1,2,
  2. Matthew Knuiman3,
  3. Mark Divitini3,
  4. Kevin Murray3,
  5. Ee Mun Lim4,
  6. Andrew St John5,
  7. John P Walsh1,2,
  8. Joseph Hung2
  1. 1 Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
  2. 2 School of Medicine and Pharmacology, University of Western Australia, Crawley, Western Australia, Australia
  3. 3 School of Population and Global Health, University of Western Australia, Crawley, Western Australia, Australia
  4. 4 Department of Clinical Biochemistry, PathWest Laboratory Medicine Western Australia, Queen Elizabeth II Medical Centre, Nedlands, Western Australia, Australia
  5. 5 ARC Consulting, Mount Lawley, Western Australia, Australia
  1. Correspondence to Dr Kun Zhu, Department of Endocrinology and Diabetes, Sir Charles Gardiner Hospital, Nedlands, WA 6009, Australia; kun.zhu{at}uwa.edu.au

Abstract

Objective High-sensitivity cardiac troponin I (hs-cTnI) is an emerging biomarker for cardiovascular risk. We examined hs-cTnI as a predictor of mortality and cardiovascular outcomes in an Australian population-based cohort and evaluated if a sex difference exists.

Methods Serum hs-cTnI was measured in the Busselton Health Study 1994/1995 Cohort (n=3939). Outcome measures were total and cardiovascular mortality, cardiovascular disease (CVD) and coronary heart disease (CHD) events, heart failure and stroke.

Results Hs-cTnI was detectable (>1.2 ng/L) in 66.1% of participants (males 81.8%, females 54.4%) at baseline. There were 886 deaths (including 361 from CVD) and 940 CVD events during 20-year follow-up. Adjusting for Framingham Risk Score variables, hs-cTnI was a significant predictor of total mortality (HR (95% CI): 1.16 (1.09 to 1.24)), CVD mortality (1.33 (1.23 to 1.44)), CVD events (1.18 (1.11 to 1.25)), CHD events (1.11 (1.03 to 1.20)), heart failure (1.44 (1.31 to 1.58)) and stroke (1.13 (1.03 to 1.24)) per doubling of hs-cTnI at baseline. HRs remained significant in CVD-free individuals at baseline (n=3215), except for CHD events. There were no significant interactions between sex and hs-cTnI as a predictor of outcomes. Compared with individuals with hs-cTnI ≤1.2 ng/L, men with hs-cTnI ≥6.0 ng/L and women with hs-cTnI ≥4.0 ng/L had an HR of 2.18 (1.42 to 3.37) and 1.84 (1.30 to 2.62), respectively, for any CVD event, which persisted in the CVD-free subgroup.

Conclusions Cardiac troponin I, measured with a high-sensitive assay, is an independent predictor of fatal and non-fatal CVD events and may help identify at-risk individuals in a general population.

  • epidemiology
  • coronary artery disease
  • heart failure
  • stroke
  • cardiac risk factors and prevention

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Footnotes

  • Contributors Conception: MK, ASJ, JW and JH; study design: KZ, MK, EML, ASJ, JW and JH; data acquisition: MK, EML, ASJ and JW; data analysis: MK, MD and KM; data interpretation: KZ, MK, JW and JH; manuscript drafting: KZ, MK, MD, KM, JW and JH; critical revision: all authors.

  • Funding The 1994/1995 Busselton survey was supported by a grant from the Health Promotion Foundation of Western Australia. Abbott Australasia Pty Ltd donated assay kits for the Abbott ARCHITECT STAT hsTnI immunoassay and funded the relevant staff to perform the specimen preparation and biochemical analysis. None of the funding agencies had any role in the conduct of the study; collection, management, analysis, or interpretation of the data; or preparation, review or approval of the manuscript.

  • Competing interests Dr St John reports personal fees from Abbott Diagnostics Australia, outside the submitted work.

  • Patient consent Obtained.

  • Ethics approval The survey received ethics approval from the University of Western Australia Human Research Ethics Committee (approval number 05/06/004/674).

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Data sharing statement Access to the baseline data on this cohort from the 1994/1995 Busselton health survey is by application to the Busselton Population Medical Research Institute (http://bpmri.org.au). Access to the linked hospital admission and death data for this cohort is by application to Data Linkage Western Australia (http://www.datalinkage-wa.org.au).

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