Effect of coronary thrombolysis on the plasma concentration of osteonectin(SPARC, BM40) in patients with acute myocardial infarction

Citation
Vl. Serebruany et al., Effect of coronary thrombolysis on the plasma concentration of osteonectin(SPARC, BM40) in patients with acute myocardial infarction, J THROMB TH, 10(2), 2000, pp. 197-202
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF THROMBOSIS AND THROMBOLYSIS
ISSN journal
09295305 → ACNP
Volume
10
Issue
2
Year of publication
2000
Pages
197 - 202
Database
ISI
SICI code
0929-5305(200010)10:2<197:EOCTOT>2.0.ZU;2-H
Abstract
Osteonectin is a phosphoglycoprotein exclusively located in bone and platel et alpha-granules. Human platelet-derived osteonectin is released into plas ma after thrombin-induced activation. Recognizing the unique distribution o f the osteonectin pool, we first sought to investigate whether osteonectin could serve as a sensitive marker of platelet activity, and identify patien ts with acute myocardial infarction (AMI). The second objective was to defi ne the effects of thrombolytic therapy in these patients on the plasma conc entrations of osteonectin at prespecified time points following attempted r eperfusion. Osteonectin levels by ELISA were determined in AMI patients bef ore thrombolysis and at 3, 6, 12, and 24 hours thereafter and compared with 12 healthy controls. At baseline, soluble osteonectin plasma levels were s imilar between controls (447.7 +/- 20.6 ng/ml) and AMI patients (425.7 +/- 43.3 ng/mL; p = NS). A significant increase of the soluble osteonectin was observed at 3 hours after thrombolysis (519.4 +/- 26.9 ng/mL; p = 0.03), an d was followed by a decrease to baseline levels at 6 hours after attempted reperfusion. Contrary to expectations, the plasma osteonectin level in our pilot study was not a sensitive marker distinguishing patients with AMI. Th e early peak of soluble osteonectin at 3 hours after thrombolytic therapy i s most likely not related to coronary thrombolysis per se but rather to the phasic changes of platelet activity during myocardial ischemia-reperfusion . The unquestionable platelet origin of this protein and the lack of elevat ed plasma levels of this alpha-granule constituent, challenge the postulate of uniform platelet activation in AMI patients.