Introduction:
Increases in the number of circulating platelet-leukocyte-complexes (PLC) in patients
with acute myocardial infarction (AMI), compared to those with stabile coronary artery
disease and healthy volunteers, suggested a pathogenic role in the inflammatory
response to myocardial ischemia and reperfusion (I/R). In this experimental work we
challenged this assumption.
Methods:
By generating P-selectin-/- bone marrow chimeras in Bl6 mice we were able to
selectively delete P-selectin in platelets without affecting endothelial P-selectin
resulting in a >70% reduction in circulating PLC. AMI was induced by 35 minutes of
LAD closure followed by 24h of reperfusion.
Results:
The surge in circulating PLC levels 24 hours post myocardial I/R injury was blunted in
P-selectin-/- -chimeras. Nevertheless, we observed no difference in infarct size, tissue
inflammation and long-term ejection fraction between both groups. The number of
rolling, adhering and tissue infiltrating leukocytes remained unaffected despite
impaired PLC formation at the vessel wall as observed by two-colour intravital
microscopy. In contrast, P-selectin dependent PLC formation was relevant for
phagocytosis of bacteria.
Conclusion:
Our results suggest that PLC form in AMI due to conserved response patterns originally
developed to fight bacterial infections that are dispensable for myocardial infarct
healing.

05 - PLATELET-LEUKOCYTE COMPLEX FORMATION IN MYOCARDIAL INFARCTION: A MARKER NOT A PATHOGEN