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Interleukin 8 released after acute myocardial infarction is mainly bound to erythrocytes
  1. Robbert J de Wintera,
  2. Annemieke Mantenb,
  3. Ype P de Jongb,
  4. Rob Adamsa,
  5. Sander J H van Deventerb,
  6. Kong I Liea
  1. aDepartment of Cardiology, Academic Medical Centre, University of Amsterdam, Netherlands, bDepartment of Haemostasis, Inflammation, Atherosclerosis and Thrombosis Research
  1. Dr de Winter, Department of Cardiology, Room G3-231, Academic Medical Centre, Meibergdreef 9, 1105 AZ Amsterdam, Netherlands.

Abstract

Objective To determine whether rapid clearance of interleukin 8 (IL-8) from plasma through binding to the erythrocyte chemokine receptor may be responsible for failure to detect IL-8 consistently after acute myocardial infarction.

Design Plasma concentrations of IL-8 were measured at frequent intervals in 43 consecutive patients. In 21 of these, erythrocyte bound IL-8 concentrations were also measured. The influence of infarct size, type of treatment, and the presence of early successful reperfusion on IL-8 release was assessed.

Results Peak IL-8 concentrations in plasma were raised in 31 of the 43 patients (68%). Median plasma IL-8 concentrations were 16.0 pg/ml (range 2.4 to 225.0 pg/ml) six hours after the onset of chest pain. Twelve hours after the onset of symptoms, plasma IL-8 concentrations had already returned to normal in 27 patients. In contrast, in 18 of 21 patients (86%), erythrocyte bound IL-8 concentrations were raised at between 6 and 30 hours, with a median peak value of 59.8 pg/ml (range 19 to 148 pg/ml). No correlation between peak creatine kinase MB and peak IL-8 (plasma or erythrocyte bound) was observed. There was a significant difference in peak plasma IL-8 concentrations between patients who underwent direct PTCA (19.4 pg/ml) and those who received conservative treatment (9.9 pg/ml; p = 0.0206), but no correlation with the presence of early successful reperfusion.

Conclusions IL-8 is released in plasma after acute myocardial infarction and subsequently binds to red blood cells, resulting in only a transient rise of plasma IL-8 and a more prolonged increase of erythrocyte bound IL-8.

  • acute myocardial infarction
  • interleukin 8
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