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1
Department of Clinical Chemistry, Lasarettet, S-251 87 Helsingborg, Sweden.
2
Department of Clinical Chemistry, University Hospital
Lund, 221 85 Lund, Sweden.
3
Department of Clinical Chemistry, Karolinska Sjukhuset,
171 76 Stockholm, Sweden.
4
Department of Clinical Chemistry and Transfusion
Medicine, Ryhov, S-551 85 Jönköping, Sweden.
5
Medizinische Klinik II, Medizinische Universität
zu Lübeck, 23528 Lübeck, Germany.
a Author for correspondence. Fax 46-42-102109; e-mail willie.gerhardt{at}telia.com
Background: Heparinized plasma samples allow more rapid analysis than serum samples, but preliminary studies showed lower cardiac troponin T (cTnT) results in plasma. We undertook a multicenter study to characterize this effect for cTnT and cardiac troponin I (cTnI).
Methods: Blood samples were collected with and without heparin at five hospitals. cTnT was measured by a "third generation" assay (Elecsys®), and cTnI was measured by a commercial immunoassay (IMMULITE®).
Results: Mean cTnT was 15% lower in heparin sampling tubes than in serum. Measured concentrations of cardiac troponins also decreased with increasing heparin concentrations added to sera. Heparin-induced losses were greater in early than in late phases after onset of chest pain. Addition of heparin (~100 IU/mL) to serial samples from nine acute myocardial infarction patients produced mean cTnT losses of 33% at 112 h after onset of chest pain, 17% at 1348 h, and 7% after 48 h. The changing heparin effects were seen for both cTnT and cTnI during time courses of individual patients with myocardial infarction.
Conclusion: We suggest that binding of heparin to troponins decreases immunoreactivity, especially in early phases of myocardial injury. The resulting losses may depend on the antibodies used in each troponin assay.
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