Background In acute myocardial infarction (AMI), platelets play a key
role in thrombotic processes that limit the patency of the recanalized
, infarct-related coronary artery and contribute to reperfusion injury
. Platelet function in the course of AMI treated by direct percutaneou
s transluminal coronary angioplasty (PTCA) has not been evaluated. Met
hods and Results In 15 patients with anterior AMI, peripheral venous b
lood samples were obtained before and 4, 8, 24, and 48 hours after rec
analization of the occluded artery by PTCA. Fifteen patients who had s
table coronary heart disease and were undergoing elective balloon angi
oplasty served as control subjects. Fibrinogen receptor function and s
urface expression of P-selectin on platelets were determined by flow c
ytometry. In addition, we evaluated generation of platelet-derived mic
roparticles and the effect of systemic plasma from patients with AMI o
n normal platelet function and on platelet adhesion to human endotheli
al cells in culture. We found fibrinogen receptor activity and P-selec
tin expression on circulating platelets 8 hours after direct PTCA are
decreased (P<.01). This coincided with a decrease in peripheral platel
et count (P<.05) and an increase in generation of microparticles (P<.0
02). Twenty-four to 48 hours after PTCA, fibrinogen receptor activity
and P-selectin expression increased again. Systemic plasma obtained be
fore and after direct PTCA sensitized normal platelets to hyperaggrega
te in vitro (P<.002) and stimulated platelet adhesion to endothelial c
ells in culture (P<.01). None of the changes found in AMI were detecta
ble in the control group. Conclusions After transient apparent deactiv
ation of circulating platelets, probably caused by sequestration of hy
peracdtive platelets, the level of platelet activation increases in pa
tients with AMI treated by direct PTCA. These findings underscore the
need for novel antiplatelet strategies in AMI.