In Reply

We thank Dr. Christenson for his attention to our article entitled “Validation of the Vancouver Chest Pain Rule: A Prospective Cohort Study” recently published in Academic Emergency Medicine. Dr. Christenson pointed out to two differences in the methodology between the original1 and the validation2 studies. The diagnosis of acute coronary syndrome (ACS) in our study was established according to the criteria consistent with universal definition of myocardial infarction (MI) and the American College of Cardiology and American Heart Association criteria.3, 4 As we described in our article,2 creatine kinase myocardial band isoenzyme (CK-MB) was the most available cardiac biomarker during the first hours of presentation for patients with acute chest pain; however, our physicians order both troponin and CK-MB for all patients with suspected ACS routinely. In the original study by Christenson et al.,1 we observed more emphasis on applying CK-MB level to identify very-low-risk patients compared to troponin level. This issue is clearly recognizable in the decision-making algorithm they suggested, where CK-MB is the only discriminating factor for patients 40 years of age and older. We also agree with the comment that high levels of troponin may be caused by several and even noncardiac conditions; however, two of our patients with normal initial ECG and CK-MB and abnormally high initial troponin underwent angiography and were diagnosed with two-vessel coronary disease. The cutoff for an upper limit of normal of 3.77 ng/mL for females and 6.73 ng/mL for males is according to Roche CARDIAC CK-MB technical specification, and also at the 99th percentile of our reference population for diagnosis of ACS, MI, and assessment of reinfarction, which must be matched with the cutoff point of three selected in the original study using Biosite Triahge cardiac panel. However, initial normal CK-MB levels of above-mentioned patients with abnormally high troponin levels of 0.259 and 0.204 μg/L were 2.37 and 3.4 ng/mL, respectively (both were male). We also aim to conduct a similar study in a multicenter setting using troponin as the main marker. We hope that future studies regarding this and other clinical prediction rules would provide an appropriate tool to help clinicians make confident decisions when facing the challenge of dealing with a patient with apparently low-risk chest pain.

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