Does This Patient Have Acute Myocardial Infarction?
A 58-year-old female patient with a history of myocardial infarction (MI)  and multiple episodes of cardiomyositis presented with signs and symptoms of acute coronary syndrome (ACS). An electrocardiogram showed Q-waves that were attributed to her previous MI. Her first cardiac troponin I (cTnI) was <0.04 ng/mL but she progressed to ST-elevation acute MI while her cTnI remained <0.04 ng/mL for 69 h postadmission. cTnI by a different assay showed a rise and fall of cTnI concentration (Table 1).
1. What can cause false-negative cTn results in otherwise confirmed MI?
2. How can you prove a false-negative cTnI in this patient and determine the cause?
The answers are below.
False-negative results can be caused by posttranslational modification of an epitope of the cTn molecule or the presence of autoantibodies that block reagent--antibody binding in the immunoassay (1-3).
Testing using a cTnI assay from a different vendor can confirm the false-negative result (Table 1) and mixing studies can prove the presence of an anti-troponin autoantibody. In this case, mixing of the patient's samples with an interference-free patient pool, containing 0.32 ng/mL cTnI, confirmed the presence of blocking autoantibodies.
Author Contributions: All authors confirmed they have contributed to the intellectual content of this paper and have met the following3 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.
Authors' Disclosures or Potential Conflicts of Interest: No authors declared any potential conflicts of interest.
(1.) Panteghini M. Selection of antibodies and epitopes for cardiac troponin immunoassays: should we revise our evidence-based beliefs? Clin Chem 2005;51:803-4.
(2.) Eriksson S, Halenius H, Pulkki K, Hellman J, Pettersson K. Negative interference in cardiac troponin I immunoassays by circulating troponin autoantibodies. Clin Chem 2005;51:839-47.
(3.) Savukoski T, Twarda A, Hellberg S, Ristiniemi N, Wittfooth S, Sinisalo J, etal. Epitope specificity and IgG subclass distribution of autoantibodies to cardiac troponin. Clin Chem 2013;59:512-8.
Geza S. Bodor  *
 VA Eastern Colorado Health Care System, Pathology and Laboratory Medicine Service 113, Denver, CO.
* Address correspondence to the author at: University of Colorado, Denver, Department of Pathology, Aurora, CO 80045-0508. E-mail email@example.com.
Received September 20, 2016; accepted October 17, 2016.
 Nonstandard abbreviations: MI, myocardial infarction; ACS, acute coronary syndrome; cTnI, cardiac troponin I.
Table 1. Patient's laboratory results (assay A) with results from the comparison assay (assay B). Neat sample, 50:50 Mix, ng/mL assay A, ng/mL Time since admission, Assay A Assay B Expected (a) Measured h:min Admission 0.0 0.0 0.16 0.0 1:49 0.0 0.4 (b) 0.16 0.0 12:29 0.0 7.3 (b) 0.16 QNS [c] 20:39 0.0 5.7 (b) 0.16 0.0 44:40 0.0 1.9 (b) 0.16 QNS 68:55 0.0 1.1 (b) 0.16 Not done 50:50 Mix, assay B, ng/mL Time since admission, Expected Measured h:min Admission 0.16 0.15 1:49 0.36 0.25 12:29 3.81 QNS 20:39 3.01 3.14 44:40 1.11 QNS 68:55 0.71 Not done (a) Expected concentrations were calculated from the measured cTnI concentration in the neat sample and the concentration of the patient pool (0.32 ng/mL). (b) Positive for AMI. [c] QNS, quantity notsufficient to do mixing study.
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|Title Annotation:||the Clinical Chemist: What Is Your Guess?|
|Author:||Bodor, Geza S.|
|Date:||Jan 1, 2017|
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