Biomarkers in stable coronary heart disease, their modulation and cardiovascular risk: the LIPID biomarker study

Tonkin, Andrew M., Blankenberg, Stefan, Kirby, Adrienne, Zeller, Tanja, Colquhoun, David M., Funke-Kaiser, Anne, Hague, Wendy, Hunt, David, Keech, Anthony C., Nestel, Paul, Stewart, Ralph, Sullivan, David R., Thompson, Peter L., West, Malcolm, White, Harvey D., Simes, John and for the LIPID study investigators (2015) Biomarkers in stable coronary heart disease, their modulation and cardiovascular risk: the LIPID biomarker study. International Journal of Cardiology, 201 499-507. doi:10.1016/j.ijcard.2015.07.080

Author Tonkin, Andrew M.
Blankenberg, Stefan
Kirby, Adrienne
Zeller, Tanja
Colquhoun, David M.
Funke-Kaiser, Anne
Hague, Wendy
Hunt, David
Keech, Anthony C.
Nestel, Paul
Stewart, Ralph
Sullivan, David R.
Thompson, Peter L.
West, Malcolm
White, Harvey D.
Simes, John
for the LIPID study investigators
Title Biomarkers in stable coronary heart disease, their modulation and cardiovascular risk: the LIPID biomarker study
Journal name International Journal of Cardiology   Check publisher's open access policy
ISSN 1874-1754
Publication date 2015-10-10
Sub-type Article (original research)
DOI 10.1016/j.ijcard.2015.07.080
Open Access Status Not Open Access
Volume 201
Start page 499
End page 507
Total pages 9
Place of publication Shannon, Ireland
Publisher Elsevier
Collection year 2016
Formatted abstract

In patients with stable coronary heart disease (CHD), we aimed to assess 1. the prognostic power of biomarkers reflecting haemodynamics, micronecrosis, inflammation, coagulation, lipids, neurohumoral activity, and renal function; 2. whether changes in concentrations of these biomarkers over 12 months affected subsequent CHD risk; and 3. whether pravastatin modified the change in biomarker concentrations and this influenced the risk of future events.


In the LIPID study, 9014 patients were randomised to pravastatin 40 mg or placebo 3–36 months after an acute coronary syndrome. Eight biomarkers were measured at baseline (n = 7863) and 12 months later (n = 6434).


During a median of 6.0 (IQR 5.5–6.5) years follow-up, 1100 CHD-related deaths and nonfatal myocardial infarctions occurred, 694 after biomarker measurement at 12 months. Baseline BNP, CRP, cystatin C, D-dimer, midregional pro-adrenomedullin, and sensitive troponin I predicted recurrent CHD events. In a multivariable model, sensitive troponin I, BNP, and cystatin C had the strongest associations with outcome (P < 0.001 for trend). The strongest improvement in risk prediction was achieved by including sensitive troponin I (net reclassification improvement (NRI) 5.5%; P = 0.003), BNP (4.3%; P = 0.02), history of MI (NRI 7.0%; P < 0.001). In landmark analyses, among biomarkers, changes to 12 months in sensitive troponin I (HR 1.32 (1.03–1.70) for T3/T1), BNP (HR 1.37 (1.10–1.69) for Q4/Q1) and Lp-PLA2 (HR 1.52 (1.16–1.97)) improved CHD risk prediction.


Baseline levels and changes in sensitive troponin I, and BNP may have the potential to guide the intensity of secondary prevention therapy.
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Official 2016 Collection
School of Medicine Publications
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