2010
Prospective Evaluation of the Prognostic Implications of Improved Assay Performance With a Sensitive Assay for Cardiac Troponin I
BONACA, Marc; Benjamin SCIRICA; Marc SABATINE; Anthony DALBY; Jindřich ŠPINAR et al.Základní údaje
Originální název
Prospective Evaluation of the Prognostic Implications of Improved Assay Performance With a Sensitive Assay for Cardiac Troponin I
Autoři
BONACA, Marc; Benjamin SCIRICA; Marc SABATINE; Anthony DALBY; Jindřich ŠPINAR; Sabina A MURPHY; Peter JAROLIM; Eugene BRAUNWALD a David A MORROW
Vydání
Journal of The American College of Cardiology, USA, Elsevier Science Inc. 2010, 0735-1097
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
30201 Cardiac and Cardiovascular systems
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 14.293
Označené pro přenos do RIV
Ne
Organizační jednotka
Lékařská fakulta
UT WoS
Klíčová slova anglicky
troponin; prognosis; sensitive; acute coronary syndrome; ACS
Příznaky
Mezinárodní význam
Změněno: 22. 4. 2013 17:08, Soňa Böhmová
Anotace
V originále
Objectives The purpose of this study was to investigate the prognostic implications of low-level increases in cardiac troponin I (cTnI) using a current-generation sensitive assay in patients with suspected acute coronary syndrome (ACS). Background Recent enhancements in troponin assays have enabled resolution of the 99th percentile reference limit at progressively lower concentrations. However, the clinical significance of low-level increases with sensitive assays is still debated. Methods We measured cTnI using a sensitive assay (TnI-Ultra, Siemens Healthcare Diagnostics, Deerfield, Illinois) at baseline in 4,513 patients with non-ST-segment elevation ACS randomly assigned to ranolazine or placebo. We applied decision limits at the 99th percentile reference limit (0.04 mu g/l), the cut point of the predecessor assay (0.1 mu g/l), and 1 equivalent to elevation of creatine kinase-myocardial band (1.5 ng/ml). Results Patients with baseline cTnI >= 0.04 mu g/l (n = 2,924) were at higher risk of death/myocardial infarction (MI) at 30 days than were patients with a negative cTnI (6.1% vs. 2.0%, p < 0.001). After adjusting for the TIMI (Thrombolysis In Myocardial Infarction) risk score, cTnI >= 0.04 mu g/l was associated with a 3-fold (95% confidence interval: 2.0 to 4.4, p < 0.001) higher risk of death/MI at 30 days. Moreover, patients with low-level increases (0.04 mu g/l to <0.1 mu g/l), were at significantly higher risk of death/MI at 30 days (5.0% vs. 2.0%, p = 0.001) and death at 12 months (6.4% vs. 2.4%, p = 0.005) than were patients with cTnI <0.04 mu g/l. Conclusions Low-level increases in cTnI using a sensitive assay identify patients at higher risk of death or MI. These findings support current American College of Cardiology/American Heart Association recommendations defining MI, and the incremental value of newer, more sensitive assays in identifying high-risk patients with ACS.