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• W3198808393 abstract "HomeCirculationVol. 144, No. 9Letter by Sandoval and Jaffe Regarding Article, “Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin After Brief Induced Coronary Artery Balloon Occlusion in Humans” Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBLetter by Sandoval and Jaffe Regarding Article, “Temporal Release of High-Sensitivity Cardiac Troponin T and I and Copeptin After Brief Induced Coronary Artery Balloon Occlusion in Humans” Yader Sandoval, MD Allan S. JaffeMD Yader SandovalYader Sandoval Cardiovascular Department, Mayo Clinic, Rochester, MN. Search for more papers by this author and Allan S. JaffeAllan S. Jaffe Cardiovascular Department, Mayo Clinic, Rochester, MN. Search for more papers by this author Originally published30 Aug 2021https://doi.org/10.1161/CIRCULATIONAHA.121.054861Circulation. 2021;144:e168To the Editor:We have been intrigued by the observations of Árnadóttir and colleagues1 since we saw the abstract of their data at the 2018 European Society of Cardiology in Munich. They raise several interesting issues, most of which were discussed by the accompanying editorial comments, which were excellent. The results could scare clinicians about the clinical sensitivity of these assays. One issue of importance that helps ease some concerns that was not adequately addressed is the role of transient occlusion and reperfusion on the kinetics of cardiac troponin (cTn) release. Regardless of the mechanisms, there clearly is release of cTn after transient occlusion of a coronary artery. However, in this situation, the magnitude of the peak value is accentuated by the abrupt robust reperfusion that occurs due to reactive hyperemia, which, by washing out cTn, accentuates the magnitude of the changes. Clinicians understand this from observing the effects of reperfusion and physiologic studies confirm that in the human coronary circulation, flow can increase 4- to 5-fold.2 Although it was not done, had the authors continued to measure cTn, it is likely that the area under the time–concentration curve would be small despite such an apparent marked peak increase. This phenomenon is likely an important reason why atrial pacing3 and small doses of dobutamine4 even in normal patients cause detectable rises in high-sensitivity cTn as well when there are widely patent coronary arteries. It is also likely the reason that concentrations increase and come down so rapidly after exercise and with pulmonary embolism. On the other hand, when ischemic heart disease is present, the magnitude of release may be blunted because of less robust reperfusion but the area under the time–concentration curve will be much larger in that situation. Recognizing this important concept may alleviate some of the concerns clinicians may have.The universal definition of myocardial infarction mandates the need for objective evidence of myocardial ischemia (ECG changes, angiographic complications, or “imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischemic etiology”) in addition to biomarker criteria to diagnose a periprocedural myocardial infarction. As reported, these patients lacked those criteria and thus had myocardial injury but not myocardial infarction.5Disclosures Dr Sandoval has previously served on advisory boards for Roche Diagnostics and Abbott Diagnostics and has been a speaker for Abbott Diagnostics, both without personal financial compensation. Dr Jaffe consults for or has consulted for most of the major diagnostic companies, including Abbott, Beckman-Coulter, Siemens, Roche, Radiometer, ET Healthcare, Sphingotec, Amgen, and Novartis. These companies make the troponin assays used in the report commented on.Footnoteshttps://www.ahajournals.org/journal/circReferences1. Árnadóttir Á, Pedersen S, Bo Hasselbalch R, Goetze JP, Friis-Hansen LJ, Bloch-Münster AM, Skov Jensen J, Bundgaard H, Iversen K. Temporal release of high-sensitivity cardiac troponin T and I and copeptin after brief induced coronary artery balloon occlusion in humans.Circulation. 2021; 143:1095–1104. doi: 10.1161/CIRCULATIONAHA.120.046574LinkGoogle Scholar2. Duncker DJ, Canty JM. Coronary blood flow and myocardial ischemia.Zipes D, Libby P. In: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 11th ed. Elsevier; 2019.Google Scholar3. Turer AT, Addo TA, Martin JL, Sabatine MS, Lewis GD, Gerszten RE, Keeley EC, Cigarroa JE, Lange RA, Hillis LD, et al.. Myocardial ischemia induced by rapid atrial pacing causes troponin T release detectable by a highly sensitive assay: insights from a coronary sinus sampling study.J Am Coll Cardiol. 2011; 57:2398–2405. doi: 10.1016/j.jacc.2010.11.066CrossrefMedlineGoogle Scholar4. Siriwardena M, Campbell V, Richards AM, Pemberton CJ. Cardiac biomarker responses to dobutamine stress echocardiography in healthy volunteers and patients with coronary artery disease.Clin Chem. 2012; 58:1492–1494. doi: 10.1373/clinchem.2012.187682CrossrefMedlineGoogle Scholar5. Thygesen K, Alpert JS, Jaffe AS, Chaitman BR, Bax JJ, Morrow DA, White HD; Executive Group on behalf of the Joint European Society of Cardiology (ESC)/American College of Cardiology (ACC)/American Heart Association (AHA)/World Heart Federation (WHF) Task Force for the Universal Definition of Myocardial Infarction. Fourth universal definition of myocardial infarction (2018).Circulation. 2018; 138:e618–e651. doi: 10.1161/CIR.0000000000000617LinkGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetails August 31, 2021Vol 144, Issue 9Article InformationMetrics Download: 122 © 2021 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.121.054861PMID: 34460324 Originally publishedAugust 30, 2021 PDF download" @default.
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