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Spontaneous Circulation: Maleficent Troponins

Bruen, Charles MD

doi: 10.1097/01.EEM.0000461014.30707.93
Spontaneous Circulation

Dr. Bruenis a fellow in critical care medicine and emergency cardiology at Hennepin County Medical Center in Minneapolis. He has special interest in stabilization, resuscitation, hemodynamic evaluation, and emergency cardiovascular care. Visit his website, http://resusreview.com, follow him @resusreview, and read his past columns athttp://bit.ly/SponCirc.

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We have convinced ourselves that more exacting biomarker tests will provide us dichotomous yes/no answers, answers without all of the uncertainty of clinical picture. Troponins have turned on us, however, and emergency physicians and cardiologists are quickly learning to hate their previous friend. Clinical chemists devised ways to measure troponins at lower and lower levels, and we started to find patients with positive troponin levels who were not having acute coronary syndrome. Deciphering the meaning of a positive troponin is becoming less clear.

So what defines a high-sensitivity test? The important point to remember is that we are talking about analytical sensitivity, not clinical sensitivity. It is the sensitivity of detecting troponin, not how useful that measurement is to answer our clinical question if the patient is having a myocardial infarction. Two criteria have been established for an assay to be labeled high-sensitivity. First, it must be able to measure a detectable value for 50 percent of healthy individuals; this is called the limit of detection. The second criterion is coefficient of variation (CV), the analytical impression at the 99% percentile. Most contemporary tests are about 20%, and in general high-sensitivities are much better. The lower sensitivity is important, but the more precise CV may actually be the more clinically useful criterion because it makes the troponin measurements more easily repeated, especially at the lower values. Figure 1 provides a visualization of the assay criteria.

Elevated troponins can occur by type 1 (plaque rupture with thrombus formation) or type 2 (supply demand imbalance) myocardial infarctions, but also by nonischemic mechanisms that cause direct myocardial injury. Unfortunately, distinguishing between type 1 MI, type 2 MI, and nonischemic myocardial injury can be challenging, especially in the presence of coronary artery disease. There is a level-dependent increasing risk for adverse outcomes, but the elevation itself does not provide any etiology. Clinical context is very important, and the entirety of the clinical presentation (history, physical exam, ECG, imaging, and angiography) matters in determining the diagnosis.

The dynamic rise and fall of troponins on serial measurement can help establish that there has been an acute myocardial injury, rather than a baseline troponin elevation as may be seen in renal failure. A diagnosis of type 2 MI should be considered only when there is clinical evidence of an acute imbalance. Nonischemic mechanisms should be evident from the history. Advanced imaging such as cardiac MRI may be useful in cases where the diagnosis remains uncertain.

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More on Troponins

Find Dr. Bruen's complete discussion of troponins in the EMN iPad app and in the Spontaneous Circulation blog on www.EM-News.com, where the app can also be downloaded for free.

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