Development of high-sensitivity assays for cardiac troponin I (hs-TnI) has enhanced the
ability to detect low circulating levels of cardiac troponins, which are often present in
individuals with common cardiac conditions and risk factors who have not manifested clinical
cardiovascular disease (CVD). Lowering the detection threshold of troponin assays has
expanded the potential use of cardiac troponins from a diagnostic tool in the setting of
acute coronary syndrome to a biomarker for risk stratification in individuals without known
CVD. Detectable levels of cardiac troponins have been associated with increased incidence of
coronary heart disease (CHD), heart failure (HF), and cardiovascular mortality in
community-based studies.
Traditional cardiovascular risk prediction does not identify everyone who will develop
cardiovascular disease with up to 50% of individuals having none or only one risk factor at
the time of diagnosis. Although traditional risk estimations perform moderately well, there
remain significant limitations in their use in the prevention of cardiovascular disease
especially at an individual level. At an individual level, the clinician not only needs to
correctly identify those at increased risk, but also weigh up the importance of each risk
factor and determine who needs medical therapy in addition to lifestyle advice Many risk
estimation systems in existence are based on a core set of cardiovascular risk factors and
based on participants either selected randomly from the general population or those attending
their general practitioner. All these risk scoring systems show a good level of
discrimination, for cardiovascular events, with the area under the receiving operator curve
ranging from 0.73 to 0.82. However, adopting these risk scoring systems to guide current
clinical practice has limitations. First, most of these scoring systems, except QRISK1 and
QRISK2 have been developed from old prospective cohorts with participants recruited in the
1980's and 1990's Second, applying risk estimation scores to regions with different rates of
baseline rates of cardiovascular disease will lead to either under- or over-estimation of
risk: a result of mis-calibration. Third, the value of incorporating new risk factors
including biomarkers such as high-sensitivity C reactive protein has been disappointing in
improving discrimination, with age and sex alone contributing to 0.70 of the area under the
receiver operating curve statistic. None of these risk estimation scores, to date,
incorporate a direct measure of cardiac injury such as cardiac troponin and its potential
role in guiding primary prevention in a contemporaneous population remains uncertain.
