Background: The purpose of the present study was to describe infarct size a
nd platelet accumulation when reperfusion injury was combined with a thromb
ogenic lesion in the coronary artery. The left anterior descending artery w
as damaged in 11 pigs and subsequently occluded proximal to the lesion for
50 min, followed by 4 h of reperfusion. Results: The infarct size/area at r
isk was 40 (35-63)%. Infarct size correlated with troponin-T-3 h (p=0.85, p
<0.002), but not with creatine kinase-3 h. Platelet aggregation decreased b
y 34% (p<0.01) at 15 min of reperfusion, but returned to baseline. Platelet
accumulation in the left ventricle was significantly higher in the area at
risk (194 (157-206)%) compared to the right ventricle (137 (120-142)%); p<
0.05). Conclusion: A decreased platelet reactivity and increased accumulati
on of platelets in the area at risk indicates that activated platelets beco
me entrapped in the myocardium. Troponin-T was a better marker of myocardia
l damage than creatine kinase in this in vivo model with pigs.