Received on July 31, 2008
Accepted on January 21, 2009

Proteomics and Protein Markers

Antiantibodies to Cardiac Troponin Associate with Higher Initial Concentrations and Longer Release of Troponin I in Acute Coronary Syndrome Patients

¹ Department of Biotechnology, University of Turku, Turku, Finland
² Innotrac Diagnostics Oy, Turku, Finland
³ Division of Cardiology, Cardiovascular Laboratory, Helsinki University Central Hospital, Helsinki, Finland

^* To whom correspondence should be addressed. E-mail: kim.pettersson{at}utu.fi.

BACKGROUND: Cardiac troponin (cTn) is an established marker of myocardial infarction. Pronounced heterogeneity and the minute amounts released into the circulation constitute significant challenges for cTn detection. Recently, autoantibody formation to cTn was shown to be common and to interfere with immunoassay performance. In this study, we investigated cTn autoantibodies and cardiac troponin I (cTnI) in acute coronary syndrome (ACS) patients over a 1-year period after the index event.

METHODS: We used a second-generation cTnI assay designed to reduce the interference of cTn autoantibodies. The assay for cTn autoantibodies used 2 anti-cTnI antibodies to capture the ternary cTnI-complex, enabling unrestricted binding of the autoantibodies, which were detected with a labeled antihuman IgG antibody. We analyzed serum samples from 81 non–ST-elevation ACS patients taken at admission and after 1 week and 3 and 12 months.

RESULTS: We found 14 cTn autoantibody–positive patients (21%) among the 67 cTnI-positive and none among the 14 cTnI-negative patients. Nine were autoantibody-positive at admission, and 5 became positive at 1 week. Autoantibody signals significantly increased in the 1-week and 3-month samples. At all time points, cTnI was significantly increased in the autoantibody-positive group relative to the negative group. Persistent cTnI elevations at 3 and 12 months were seen in the patients already autoantibody positive at admission.

CONCLUSIONS: During ACS, patients with cTn autoantibodies have higher cTnI release and therefore larger myocardial damage than patients without autoantibodies. Their cTnI release also lasts longer, at least months. The possible prognostic impact of these observations must be evaluated in larger clinical cohorts.