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Commentary

Commentary My initial impression of the findings in the current case—a classic, early, and rapid increase of the myocardial-specific cardiac troponin I (cTnI)2—was that they represented a spontaneous reperfusion of a type 1 non-ST segment elevation myocardial infarction, analogous to a rapid flushing out of a clogged drain (coronary artery) with chemicals. The initial 3.5-fold high-sensitivity cTnI increase above the 99th percentile at 2-h post-index chest pain demonstrates the early diagnostic sensitivity of high-sensitivity cTnI assays. The 70-fold further increase at 8 h (4017 ng/L) supports reperfusion. In this light, the initial case finding of normal coronaries at angiography (a snapshot in time postreperfusion) was expected based on the large concentration and rapid increase of cTnI. However, an alternative explanation of such a large increase in cTnI in only 8 h, accompanied by persistent chest pain, is persistent occlusion of a large artery. Eventually in this case, an occlusion was indeed confirmed in a branch of the anterior descending coronary artery. No studies to date have carefully examined the mechanism of cTnI clearance following an acute myocardial infarction. Furthermore, it should be noted that, in the case of reperfusion especially, the amount of tissue damage or infarct size cannot be easily or accurately determined on the basis of the amount of washed-out cTnI concentration from the necrotic tissue; this could be determined only at autopsy. I would surmise this patient to be fortunate to have had resolution of her chest pain, and possibly reperfusion, minimizing her infarct size and likely resulting in a better short-term prognosis. 2 Nonstandard abbreviation cTnI cardiac troponin I. " Author Contributions:All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article. " Author Disclosures or Potential Conflicts of Interest:Upon manuscript submission, the author completed the author disclosure form. Disclosures and/or potential conflicts of interest: " Employment or Leadership: F.S. Apple, Clinical Chemistry, AACC. " Consultant or Advisory Role: F.S. Apple, HyTest, Metanomics, and Philips Healthcare Incubator. " Stock Ownership: None declared. " Honoraria: F.S. Apple, Instrumentation Laboratory. " Research Funding: Abbott Diagnostics, Beckman Coulter, Alere, Roche Diagnostics, and Siemens Healthcare. " Expert Testimony: None declared. " Patents: None declared. © 2017 The American Association for Clinical Chemistry This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model) http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical Chemistry Oxford University Press

Commentary

Apple, Fred, S
Clinical Chemistry , Volume 63 (10) – Oct 1, 2017
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Publisher
Oxford University Press
Copyright
© 2017 The American Association for Clinical Chemistry
ISSN
0009-9147
eISSN
1530-8561
DOI
10.1373/clinchem.2016.270033
Publisher site
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Abstract

My initial impression of the findings in the current case—a classic, early, and rapid increase of the myocardial-specific cardiac troponin I (cTnI)2—was that they represented a spontaneous reperfusion of a type 1 non-ST segment elevation myocardial infarction, analogous to a rapid flushing out of a clogged drain (coronary artery) with chemicals. The initial 3.5-fold high-sensitivity cTnI increase above the 99th percentile at 2-h post-index chest pain demonstrates the early diagnostic sensitivity of high-sensitivity cTnI assays. The 70-fold further increase at 8 h (4017 ng/L) supports reperfusion. In this light, the initial case finding of normal coronaries at angiography (a snapshot in time postreperfusion) was expected based on the large concentration and rapid increase of cTnI. However, an alternative explanation of such a large increase in cTnI in only 8 h, accompanied by persistent chest pain, is persistent occlusion of a large artery. Eventually in this case, an occlusion was indeed confirmed in a branch of the anterior descending coronary artery. No studies to date have carefully examined the mechanism of cTnI clearance following an acute myocardial infarction. Furthermore, it should be noted that, in the case of reperfusion especially, the amount of tissue damage or infarct size cannot be easily or accurately determined on the basis of the amount of washed-out cTnI concentration from the necrotic tissue; this could be determined only at autopsy. I would surmise this patient to be fortunate to have had resolution of her chest pain, and possibly reperfusion, minimizing her infarct size and likely resulting in a better short-term prognosis. 2 Nonstandard abbreviation cTnI cardiac troponin I. " Author Contributions:All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article. " Author Disclosures or Potential Conflicts of Interest:Upon manuscript submission, the author completed the author disclosure form. Disclosures and/or potential conflicts of interest: " Employment or Leadership: F.S. Apple, Clinical Chemistry, AACC. " Consultant or Advisory Role: F.S. Apple, HyTest, Metanomics, and Philips Healthcare Incubator. " Stock Ownership: None declared. " Honoraria: F.S. Apple, Instrumentation Laboratory. " Research Funding: Abbott Diagnostics, Beckman Coulter, Alere, Roche Diagnostics, and Siemens Healthcare. " Expert Testimony: None declared. " Patents: None declared. © 2017 The American Association for Clinical Chemistry This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

Journal

Clinical Chemistry – Oxford University Press

Published: Oct 1, 2017

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