Improving the primary prevention of cardiovascular events by using biomarkers to identify individuals with silent heart disease

M. Adnan. Nadir, Sushma Rekhraj, Li Wei, Tiong.K. Lim, John Davidson, Thomas. M. MacDonald, Chim C. Lang, Ellie Dow, Allan. D. Struthers (Lead / Corresponding author)

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    73 Citations (Scopus)


    The aim of this study was to examine whether biomarkers can identify silent cardiac target organ damage (cTOD) in a primary prevention population.

    One possible way to improve primary prevention of cardiovascular events is to identify those patients who already harbor silent cTOD (i.e., myocardial ischemia, left ventricular hypertrophy, systolic dysfunction, diastolic dysfunction, or left atrial enlargement). This might be possible by screening with a biomarker (e.g. high sensitivity cardiac troponin T [hs-cTnT] or B-type natriuretic peptide [BNP]).

    We prospectively recruited 300 asymptomatic individuals already receiving primary prevention therapy. Transthoracic echocardiography, stress echocardiography, and/or myocardial perfusion imaging were performed to identify silent cTOD.

    One hundred two (34%) patients had evidence of cTOD. Left ventricular hypertrophy was the most prevalent (29.7%) form of cTOD, followed by diastolic dysfunction (21.3%), left atrial enlargement (15.3%), systolic dysfunction (6.3%), and ischemia (6.3%). The area under the curve (AUC) for BNP to identify any form of silent cTOD was 0.78 overall and 0.82 in men. The equivalent figures for hs-cTnT were 0.70 and 0.75 in women. The AUC for BNP and hs-cTnT together was 0.81 and 0.82 in men. However, the discrimination power of other markers was poor, with AUCs of 0.61 for microalbuminuria, 0.49 for uric acid, and 0.58 for eGFR.

    In asymptomatic treated primary prevention patients, BNP screening is able to identify existing silent cTOD. The performance of hs-cTnT was not as good as that of BNP. B-type natriuretic peptide plus hs-cTnT together performed best. Prescreening with BNP +/- cTnT followed by targeted phenotyping is worth exploring further as a possible way to improve primary prevention. (J Am Coll Cardiol 2012;60:960-8) (C) 2012 by the American College of Cardiology Foundation

    Original languageEnglish
    Pages (from-to)960-968
    Number of pages9
    JournalJournal of the American College of Cardiology
    Issue number11
    Publication statusPublished - 11 Sept 2012


    • biomarkers
    • Cardiovascular risk
    • Primary prevention


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