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Elevated troponin in stable coronary artery disease: the sound of silence
  1. William Wijns1,
  2. Filippo Crea2
  1. 1Cardiovascular Center Aalst, Belgium
  2. 2Division of Cardiology, Università Cattolica del Sacro Cuore, Rome, Italy
  1. Correspondence to Dr William Wijns, Cardiovascular Center Aalst, OLV Hospital, 164 Moorselbaan, B 9300 Aalst, Belgium; william.wijns{at}

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The emergence of cardiac troponins as sensitive and specific biomarkers of myocardial damage has led to the redefinition of criteria that establish the diagnosis of myocardial infarction.1 With the availability of highly sensitive troponin T (hsTnT) assays,2 our understanding of minor myocardial damage in various cardiac conditions will be challenged again and existing paradigms may need to be revisited.

Korosoglou et al3 studied 124 patients with stable angina and correlated hsTnT levels with detailed analysis of coronary anatomy using coronary CT angiography (CTA) (see page 823). A 256-slice coronary CTA machine with submillimetre spatial resolution was used to measure coronary calcification, plaque localisation and stenosis severity, non-calcified plaque volume, plaque composition (soft or mixed, described as ‘non-calcified’ vs ‘calcified’) and vascular remodelling in areas of non-calcified plaque.

Much to our surprise at least, hsTnT values above the 99th centile were measured in nearly one out of three patients with coronary CTA-documented coronary artery disease, all in stable condition.

Biomarker elevation was not related to clinical presentation (type or …

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  • Funding The Meijer Lavino Foundation for Cardiac Research and the Academia Belgica, Rome.

  • Competing interests None.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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