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August 3, 2011

Sensitive Troponin I Assay in Patients With Suspected Acute Coronary Syndrome—Reply

Author Affiliations

Author Affiliations: Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, United Kingdom (Drs Mills and Newby) (nick.mills@ed.ac.uk); and Department of Clinical Biochemistry, Royal Infirmary of Edinburgh, Edinburgh (Dr Walker).

JAMA. 2011;306(5):488-489. doi:10.1001/jama.2011.1063

In Reply: Lowering the diagnostic threshold for MI is a highly contentious issue in clinical practice. Dr Clough and colleagues argue that by lowering the threshold, we may have overdiagnosed MI in patients with secondary causes of myocardial ischemia. In contrast, Dr Jaffe and colleagues recommend that we lower the diagnostic threshold further to the 99th percentile of a normal reference population in the interests of better patient care.

Clough et al suggest that the increase in use of recommended therapies following implementation of the more sensitive assay was modest and insufficient to account for improvements in clinical outcomes. They highlight that there was only a 2% absolute (20% relative) risk reduction in the CURE trial,1 and this contrasts with our observations of an 18% absolute (46% relative) risk reduction. However, the primary end point occurred in only 11% of patients in the CURE trial whereas the absolute event rate in our study was 39%, reflecting our real-world population of consecutive patients with suspected ACS rather than a highly selected, low-risk, randomized controlled trial population. Moreover, our study findings reflect the composite of all evidence-based therapies available to patients given the correct clinical diagnosis and not just dual antiplatelet therapy. An accurate diagnosis, specialist care, and follow-up are also key determinants of clinical outcome, and we therefore believe that a halving of clinical event rates is credible.