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Abdominal aortic calcification, cardiac troponin I and atherosclerotic vascular disease mortality in older women
  1. Ryan Teh1,2,
  2. Richard L Prince1,3,
  3. Marc Sim1,4,
  4. John T Schousboe5,
  5. Warren D Raymond1,4,
  6. Pawel Szulc6,
  7. Wai Lim1,7,
  8. Jonathan M Hodgson1,4,
  9. Kun Zhu1,3,
  10. Douglas P Kiel8,
  11. Carl Schultz1,9,
  12. Peter L Thompson1,10,11,
  13. Joshua R Lewis1,4,12
  1. 1 Medical School, The University of Western Australia, Perth, Western Australia, Australia
  2. 2 Fiona Stanley Hospital, Murdoch, Western Australia, Australia
  3. 3 Department of Endocrinology and Diabetes, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
  4. 4 Institute for Nutrition Research, School of Medical and Health Sciences, Edith Cowan University, Joondalup, Western Australia, Australia
  5. 5 Park Nicollet Osteoporosis Center and Health Partners Institute, Minneapolis, Division of Health Policy and Management, University of Minnesota, Minneapolis, Minnesota, USA
  6. 6 INSERM UMR1033, University of Lyon, Hôpital Edouard Herriot, Lyon, France
  7. 7 Department of Renal Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
  8. 8 Department of Medicine, Harvard Medical School, Boston, Massachusetts, USA
  9. 9 Department of Cardiology, Royal Perth Hospital Campus, School of Medicine and Pharmacology, University of Western Australia, Perth, Western Australia, Australia
  10. 10 Department of Cardiovascular Medicine, Sir Charles Gairdner Hospital, Perth, Western Australia, Australia
  11. 11 Harry Perkins Institute of Medical Research, Nedlands, Western Australia, Australia
  12. 12 Centre for Kidney Research, Sydney Medical School, School of Public Health, The University of Sydney, Sydney, New South Wales, Australia
  1. Correspondence to Dr Joshua R Lewis, The University of Western Australia, Perth, Western Australia 6027, Australia; joshua.lewis{at}


Objective Examine if two inexpensive measures of atherosclerotic vascular diseases (ASVD), abdominal aortic calcification (AAC) and high-sensitivity cardiac troponin I (hs-cTnI) provide complementary information for 10-year ASVD mortality and all-cause mortality risk in older women.

Methods 908 community-dwelling women without prevalent ASVD (≥75 years) were followed-up between 2003 and 2013. AAC and plasma hs-cTnI measures were obtained in 2003. AAC was assessed on lateral spine images using a semiquantitative method (AAC24). Linked health records were used for mortality outcomes.

Results Mean±SD age was 79.9±2.6 years. 276 (30.4%) women died during follow-up, including 138 (15.2%) ASVD-related deaths. AAC24 and hs-cTnI were independently associated with ASVD and all-cause mortality (p<0.001). The cohort was dichotomised into four groups: (1) low AAC24 (AAC24: 0 or 1) and <median hs-cTnI (n=163, referent), (2) moderate-extensive AAC24 (AAC24:>1) and <median hs-cTnI (n=280), (3) low AAC24 and ≥median hs-cTnI (n=148) and (4) moderate-extensive AAC24 and ≥median hs-cTnI (n=317). Compared with the referent group, a stepwise increase in relative hazard (HR (95% CI)) for ASVD mortality was seen at 2.39 (1.05 to 5.46), 3.18 (1.35 to 7.79) and 5.38 (2.44 to 11.85), respectively. A similar associations were observed for all-cause mortality, at 1.58 (0.99–2.52), 2.38 (1.46–3.89) and 3.02 (1.93–4.72), respectively (all p<0.05).

Conclusion Higher AAC and elevated hs-cTnI were associated with higher risk of ASVD mortality and all-cause mortality, independent of each other. Stratifying by moderate to extensive AAC and elevated hs-cTnI identified women at very high risk. Further studies investigating whether combining factors may improve risk prediction are needed.

Trial registration number ACTRN12617000640303.

  • biomarkers
  • diagnostic imaging
  • epidemiology

Data availability statement

Data are available on reasonable request. Data used for this paper are available on reasonable request from the corresponding author or through the study website

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Data availability statement

Data are available on reasonable request. Data used for this paper are available on reasonable request from the corresponding author or through the study website

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  • Contributors RT, MS, RLP and JRL conceived and designed the study; JTS, DPK, RLP and JRL collected the data; RT, MS and JRL analysed the data; RT prepared the manuscript with input from all authors, and is the guarantor for the study; RT and MS had the primary responsibility for the final content. WDR, PS, WHL, JMH, KZ, CS and and PLT provided intellectual input and edited the paper. All authors read and approved the final manuscript.

  • Funding This study was funded by National Health and Medical Research Council (254627, 303169 and 572604). The effort of DPK was supported by a grant from the National Institute of Arthritis, Musculoskeletal and Skin Diseases R01 AR 041398. The Salary of MS is supported by a Royal Perth Hospital Career Advancement Fellowship (RPH CAF 130/2020). The salary of JMH is supported by an NHMRC of Australia Senior Research Fellowship (ID: 1116973). The salary of JRL is supported by a National Heart Foundation of Australia Future Leader Fellowship (ID: 102817). None of these 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. None of the authors have relationships with industry.

  • Competing interests None declared.

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

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