These 2 cases stress the importance of carefully integrating laboratory results and clinical findings for the accurate diagnosis of acute myocardial infarction (AMI). Such integration is even more crucial when the new high-sensitivity cardiac troponin assays are used. Although these new assays have improved diagnostic and prognostic accuracy compared with current assays, they increase the risk of improper interpretation of results.
In case 1, the cardiac troponin T (cTnT) concentration and the clinical signs and symptoms are concordant with a diagnosis of AMI. The angiography examination revealed no coronary artery lesions, however, and the echocardiogram showed no wall-motion abnormalities. In contrast, cardiac MRI documented a small area of infarction, and a type 2 AMI (produced by coronary vasospasm or vasoconstriction) was diagnosed. Cardiac troponin measurements can sensitively detect myocardial damage regardless of its origin, but such measurements cannot unequivocally distinguish type 2 AMI from type 1 (which is produced by coronary lesions). Type 2 AMI does not require aggressive antithrombotic therapies. Owing to the MRI results, the patient was not exposed to a therapy with potentially adverse effects.
Case 2 highlights the challenge that high-sensitivity cardiac troponin assays pose when they are used to evaluate acute coronary syndromes. A female patient presented with atypical symptoms and an undetectable contemporary cTnT concentration, but she did have a value in the high-sensitivity cTnT assay that was higher than the sex-specific 99th-percentile reference value. In the absence of serial increases in the high-sensitivity cTnT assay, her diagnosis was stable coronary disease, not type 1 AMI. This case illustrates how high-sensitivity cardiac troponin assays can produce an increase in patients “positive” for cardiac troponin. A correct clinical classification is of utmost importance in these patients; however, we should consider that the influences of age, sex, and existing cardiovascular risk factors on the 99th-percentile reference value of high-sensitivity cardiac troponin assays are not yet fully known. Additionally, the absolute or relative change that defines a clinically important increasing or decreasing pattern in the cardiac troponin concentration measured with high-sensitivity assays remains to be defined. These issues require urgent clarification to ensure the optimal use of high-sensitivity cardiac troponin assays in clinical scenarios similar to case 2.
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.
Authors' Disclosures or Potential Conflicts of Interest: Upon manuscript submission, all authors completed the Disclosures of Potential Conflict of Interest form. Potential conflicts of interest:
Employment or Leadership: None declared.
Consultant or Advisory Role: J. Ordonez-Llanos, Abbott Diagnostics and Roche Diagnostics.
Stock Ownership: None declared.
Honoraria: J. Ordonez-Llanos, Abbott Diagnostics and Roche Diagnostics.
Research Funding: J. Ordonez-Llanos, Abbott Diagnostics and Roche Diagnostics.
Expert Testimony: None declared.
- Received for publication October 12, 2011.
- Accepted for publication October 18, 2011.
- © 2012 The American Association for Clinical Chemistry