Commentary

The case report details a phenomenon now becoming more appreciated. With early iterations of the cTnT assay, there was cross-reactivity between the tag antibody and skeletal muscle protein that led to false positive increases in patients with renal failure. A more specific tag seemed to solve the problem. However, reports continued to suggest that some patients with skeletal muscle disease and no overt cardiovascular disease had cTnT increases potentially from skeletal muscle. This is difficult to prove because one could argue, as in the case presented, that there could be diffuse myocardial involvement not detected by MRI, which requires confluent necrosis before a signal can be appreciated. On the other hand, a recent report in Circulation Cardiovascular Genetics (1) describes a large cohort of patients with Pompe disease, most of which had increased cTnT. It included measurement of the cTnT mRNA from affected skeletal muscle and a mass spectrometry analysis, suggesting that there were fragments from cTnT as well. These data, along with the data showing protein binding of the antibodies used in the cTnT assay to a 39.5-kDa protein from skeletal muscle, make a strong case that there are proteins in diseased skeletal muscle that are capable of causing increases of cTnT. How common this is only time will tell, but for now clinicians should be astute to the fact that patients with skeletal muscle disease can have increased cTnT. These increases may be even more common with the high sensitivity assay. To date, the numbers of cases where there has been a rising and/or falling pattern of cTnT, where there could be confusion with acute myocardial injury, have been rare but that does not mean they could not occur in individuals with skeletal muscle disease and critical illness.

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