The aggregation of platelets on the plaque rupture site on the coronary artery 
is reported to cause both acute coronary syndromes (ACS) and acute myocardial 
infarction (AMI). While the inhibition of platelet aggregation by acetyl 
salicylic acid was reported to produce beneficial effects in ACS, it failed to 
do in AMI. The concentration of a stress induced protein (dermcidin isoform-2) 
was much higher in AMI than that in ACS. Incubation of normal platelet rich 
plasma (PRP) with dermcidin showed one high affinity (Kd = 40 nM) and one low 
affinity binding sites (Kd = 333 nM). When normal PRP was incubated with 0.4 μM 
dermcidin, the platelets became resistant to the inhibitory effect of aspirin 
similar to that in the case of AMI. Incubation of PRP from AMI with dermcidin 
antibody restored the sensitivity of the platelets to the aspirin effect. 
Incubation of AMI PRP pretreated with 15 μM aspirin, a stimulator of the NO 
synthesis, resulted in the increased production of NO in the platelets that 
removed the bound dermcidin by 40% from the high affinity binding sites of AMI 
platelets. When the same AMI PRP was retreated with 10 μM aspirin, the 
aggregation of platelets was completely inhibited by NO synthesis.