Kinetics of high-sensitivity cardiac troponin T and I differ in patients with ST-segment elevation myocardial infarction treated by primary coronary intervention. Issue 4 (1st August 2016)

• Record Type: Journal Article
• Authors: Laugaudin, Guillaume; Kuster, Nils; Petiton, Amael; Leclercq, Florence; Gervasoni, Richard; Macia, Jean-Christophe; Cung, Thien-Tri; Dupuy, Anne-Marie; Solecki, Kamila; Lattuca, Benoit; Cade, Stéphane; Cransac, Frédéric; Cristol, Jean-Paul; Roubille, François
• Is Part Of: European heart journal. Volume 5:Issue 4(2016)
• Page Start: 354
• Page End: 363
• Publication Date: 2016-08-01
• Subjects: Acute myocardial infarction -- percutaneous coronary intervention -- high-sensitivity troponin -- creatine kinase -- troponin I -- troponin T -- kinetics; 616.1205
• DOI: 10.1177/2048872615585518
• Languages: English
• ISSNs: 2048-8726

Abstract

Abstract: Purpose: Cardiac biomarkers including troponins are the cornerstone of the biological definition of acute myocardial infarction. New high-sensitivity cardiac assays determining troponin T (hs-cTnT) as well as I ((hs-cTnI) from Abbott and s-cTnI from Siemens) raise concerns because of their unclear kinetics following the peak. Aims: This study aims to compare kinetics of creatine kinases, hs-cTnT, hs-cTnI and s-cTnI in patients with ST-segment elevation myocardial infarction (STEMI) treated by percutaneous coronary intervention. Methods: We prospectively studied 106 consecutive patients admitted in our institution for STEMI and treated by percutaneous coronary intervention. We evaluated for all the patients simultaneously kinetics of creatine kinases, hs-cTnT (Roche) and two different cTnIs (hs-cTnI from Abbott and s-cTnI from Siemens). Modelling of kinetics was realized using mixed effects with cubic splines. Results: Kinetics of markers showed a first peak at 10.7h (8.0–12.0) for creatine kinases, 11.8h (10.4–13.3) for hs-cTnT (Roche); 11.8h (10.7–11.8) for hs-cTnI from Abbott and 10.2h (8.7–11.6) for s-cTnI from Siemens, respectively. This peak was followed by a nearly log linear decrease for hs-cTnI/s-cTnI and creatine kinases in contrast to hs-cTnT, which appeared with a biphasic shape curve marked by a second peak at 76.9h (69.5–82.8). The analysis of the decrease in percentage of the peak value at 77h showed that hs-cTnT follows a twice lower decrease than other markers. Conclusion: Kinetics of hs-cTnT, hs-cTnI and s-cTnI differ significantly with a linear decrease regarding both cTnI assays contrasting with a biphasic shape curve for hs-cTnT. This is of importance for clinical management of patients in routine settings especially in follow-up after STEMI including the suspicion of reinfarction.