ORIGINAL PAPER Minor troponin T elevation in patients 6 months after acute myocardial infarction: an observational study Mirja Neizel Æ Henning Steen Æ Grigorios Korosoglou Æ Dirk Lossnitzer Æ Stephanie Lehrke Æ Boris T. Ivandic Æ Hugo A. Katus Æ Evangelos Giannitsis Received: 9 November 2008 / Accepted: 13 February 2009 / Published online: 12 March 2009 Ó Springer-Verlag 2009 Abstract Background Troponin elevation in patients with stable coronary heart disease is associated with adverse outcome and prognosis. However, the mechanism is not yet clearly understood. Our objectives were to examine the prevalence and range of cardiac troponin T (cTnT) in stable patients, 6 months after acute myocardial infarction (AMI) using a new high sensitive cTnT assay and to investigate the association of minor cTnT elevation in these patients to clinical variables, NT-proBNP and cardiac MRI-findings. Study design and methods cTnT was measured in 98 patients 6 months after AMI with a precommercial assay by electrochemiluminescence methods (Roche Diagnos- tics, Mannheim, Germany). cTnT values were correlated with clinical and angiographic variables, NT-proBNP concentrations and with cardiac MRI-findings. Results Minor cTnT concentrations were detectable in 90% of the entire cohort, of whom 16% had cTnT values above the 99th percentile ( [ 12 ng/L). These patients were also significantly older, suffered more frequently from hypertension, had a higher New York Heart Association class and received more often diuretics at follow up. Patients with cTnT elevation had a more impaired left ventricular ejection fraction (P = 0.02) but did not have an increased infarct size (P = 0.73). Conclusions Elevated minor cTnT levels are frequently detectable in patients 6 months after AMI. Increased cTnT level were associated with clinical parameter for heart failure, impaired ejection fraction and higher NT-proBNP levels suggesting that myocardial dysfunction is a main cause for cTnT elevation in these patient group. Keywords High sensitive troponin Á Myocardial infarction Á Cardiac remodeling Á Magnetic resonance imaging Introduction Cardiac troponins are highly sensitive and specific markers of myocardial injury [11]. For detection of acute myocar- dial infarction (AMI), a commercially available troponin assay with a detection limit of 0.01 lg/L is sufficient [11]. However, for clinical risk stratification in patients with stable coronary heart disease, a lower more sensitive detection limit is warranted [30]. Recent data suggest that in these patients, levels of troponin below the diagnostic thresholds for the diagnosis of AMI may be useful for risk assessment [8, 28]. However, current commercial troponin assays are not able to measure precisely at the 99th per- centile. Therefore, the introduction of more sensitive and exclusively cardio-specific assays that meet the precision criteria of the ESC/AHA definition of AMI may open a new diagnostic window. The range and prevalence of persistent minor cTnT levels in asymptomatic patients after AMI is not clear. Persistent cTnT concentration has been discussed to be due to increased left ventricular (LV) myocardial overload or subclinical ischemia which leads to transient changes in cell membrane permeability and leakage of cytosolic tro- ponin [29]. Another explanation may be that apoptotic processes persist for months after AMI leading to elevated levels of cTnT cleavage which is detectable over several weeks [3, 19]. However, the mechanisms of persistent M. Neizel (&) Á H. Steen Á G. Korosoglou Á D. Lossnitzer Á S. Lehrke Á B. T. Ivandic Á H. A. Katus Á E. Giannitsis Medical Clinic III, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany e-mail: m.neizel@gmx.de 123 Clin Res Cardiol (2009) 98:297–304 DOI 10.1007/s00392-009-0002-8