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. 2019 Nov 8;9:16304. doi: 10.1038/s41598-019-52671-y

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Surrogate markers of neutrophil extracellular traps. (A) Double-stranded DNA (dsDNA, n = 83, femoral 581.7 [519.8–672.7] versus culprit site 692.7 [552.7–888.0] ng/ml) and (B) citrullinated histone 3 levels (citH3, n = 87, femoral 233 [156.5–545.6] versus culprit site 380.5 [173.8–820.3] ng/ml) were significantly increased at the culprit site of STEMI patients. Enzymatic infarct size expressed as the creatine phosphokinase isoform MB area under the curve (CK-MB AUC) correlated with (C) double-stranded DNA (dsDNA, n = 65, r_s = 0.409, p < 0.001) and (D) citrullinated histone 3 (citH3, n = 65, r_s = 0.315, p < 0.01). Significance ****p < 0.0001.