Highly sensitive troponin assays — a two-edged sword?

To the Editor: Scott and colleagues address the vexed issue of using highly sensitive (hs) cardiac troponin (cTn) assays to detect myocardial infarction (MI) and likely increases in hospitalisations.1 Greater numbers of MIs detected by hs-cTn assays also confound population surveillance of MI trends and our understanding of disease prevention.

The initial introduction of cTn assays resulted in predictions of marked increases in MI rates, based on 23%–83% increases in convenience samples.2 However, such increases did not fully materialise in population data. MI diagnosis does not depend on elevated troponin levels alone — it is assessed with the rise and fall of troponin levels, and non-biomarker parameters that identify troponin elevations due to causes other than acute coronary syndromes (ACS), improving the specificity of MI diagnosis. In addition, administrative data reflect final diagnoses made by treating physicians, which potentially reduces the proportion of false-positive results in MI counts.

Routinely collected statewide hospital morbidity data are available in every Australian jurisdiction and include all hospital admissions for ACS and chest pain. They provide a platform for monitoring activities and, if linked to and adjusted for biomarkers,3,4 are invaluable for measuring the impact of MI prevention and treatment strategies. Although the national rate of decline of MI may have plateaued, reductions in the incidence of ACS and reductions in incidence and recurrence of coronary heart disease have continued in Western Australia5 despite the use of more sensitive cTn assays.

The advent of hs-cTn assays therefore confirms the need for vigilant monitoring of MI diagnosis at the clinical level, as advocated by Scott et al, but also at the population level, to determine whether emergency department trends will translate into increased MI rates. The implications for future service provision are significant.