The following post was written several years ago. Although more recent developments have changed the field of clinical laboratory science since the original posting, the information contained was deemed to be of historical interest.

There have been a multiplicity of recent articles in both acute coronary syndromes and heart failure indicating that high sensitivity assays for cardiac troponin provide additional diagnostic and prognostic information but may do so at the cost of specificity for the underlying diagnosis. The pros and cons of such assays are described below.

First, a definition of high sensitivity assays is needed. The only one thus far proposed is by Apple who suggests that a definition based on the number of normal subjects who have detectable values. His classification is enclosed. In his analysis, of the presently available assays in the U.S., only the Beckman assay was better than a class 1, at class 2. Other research only assays were at class 3 or 4.

The Upside

Initial clinical experience with these assays is limited but increasing rapidly. In patients with acute coronary syndromes, they provide for an earlier diagnosis (often on admission) and include more patients at risk for events. These assays appear to provide between an 8 and 10% increase in the number of patients detected. In addition, the data support the idea that these assays will also be very valuable in defining the short and long term risk in patients with heart failure. Finally, these assays are very likely to unmask additional causes of cardiac injury and in the long run will probably be used to detect the development of structural heart disease since values seem to rise when structural heart disease is present.

The Downside

It is clear that with these high sensitivity assays that a larger percentage of elevations in troponin will be due to disease processes other than acute ischemic heart disease which may be problematic to clinicians. Some of these may be chronic due to structural heart disease and some acute due to processes like pulmonary emboli or sepsis. In addition, many more of the elevations associated with ischemic heart disease may reflect possibly stable disease or fixed disease or endothelial dysfunction with supply-demand imbalance and not necessarily acute plaque related events. The idea of using a rising and/or falling pattern has been suggested to distinguish the chronic elevations from the acute ones and there is some support for such an approach but the exact metrics for defining that pattern have not been totally defined. In addition, this technique may not work well if patients present late after the onset of symptoms or when the onset of symptoms is unknown. Finally, minor analytical problems which with less sensitive assays rarely cause diagnostic confusion might be more of a problem with such high sensitivity approaches. Fro example, it appears that with some high sensitive assays, there are differences between men and women.


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  4. Jaffe AS and Apple FS. High-Sensitivity Cardiac Troponin: Hype, Help, and Reality. Clinical Chemistry; 2010; 56: 342 - 344.
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