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Fred S Apple, Commentary, Clinical Chemistry, Volume 63, Issue 10, 1 October 2017, Pages 1573–1574, https://doi.org/10.1373/clinchem.2016.270033
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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.
