Sensitive Troponin I Assay in Patients With Suspected Acute Coronary Syndrome

Abstract

1 demonstrated a significant reduction in myocardial infarction (MI) and death in patients with suspected acute coronary syndrome (ACS) through use of a lower-threshold troponin assay.One surprising finding was a modest increase in use of recommended therapies in patients with plasma troponin concentrations of 0.05 to 0.19 ng/mL during the implementation phase, which would be expected to result in reduced events. In fact, revascularization rates were stable despite more than a doubling in coronary angiography. Aspirin, ␤-blocker, and angiotensin-converting enzyme inhibitor use did not differ between the phases. Although more statins were prescribed at discharge in the implementation phase, a similar difference was present on admission, suggesting possible baseline differences between these nonrandomized samples.The most striking difference was in clopidogrel use, 31% in the validation phase vs 61% in the implementation phase. If the outcome difference between the 2 groups was driven by clopidogrel, this would be a substantially greater benefit than demonstrated in prior studies. For example, the Clopidogrel in Unstable Angina to Prevent Recurrent Events (CURE) trial 2 showed a 2.1% absolute risk reduction in death from cardiovascular causes, nonfatal MI, or stroke over 12 months (9.3% in clopidogrel group vs 11.4% in placebo group) for patients with ACS without ST-segment elevation compared with an 18% difference in death or recurrent MI at 12 months (39% in validation cohort vs 21% in implementation cohort) in the report by Mills et al.1 Determination of the rates of clopidogrel use in patients who did or did not have an event would be interesting.In addition, other than the presence of cardiac risk factors and interventions, little is known about the population. Given the high overall mortality rates and low rates of revascularization despite angiography, many patients may have had noncardiac medical issues, and the results may be due to higher attention to underlying coronary artery disease in a population with comorbid illnesses. This is supported by the low rates of use of recommended therapies. For instance, only 47% of validation phase patients with peak troponin concentrations of 0.05 to 0.19 ng/mL were taking a ␤-blocker at discharge when 69% of these patients carried a diagnosis of ischemic heart disease prior to admission. It would be useful to know the number of patients who underwent stress testing, the percentage diagnosed with ischemic heart disease, other discharge diagnoses, and creatinine levels as alternate explanations for elevated troponin levels.