Key result
In a pig model of ischaemia/reperfusion injury, platelet accumulation was significantly higher in the area at risk compared to the right ventricle (194% vs 137%; p<0.05).
Absolute Event Rate: 194% vs 137%
p-value: p=<0.05
Should not change clinical reperfusion management; leaves open platelet contributions in combined thrombotic-injury models.
BACKGROUND: The purpose of the present study was to describe infarct size and platelet accumulation when reperfusion injury was combined with a thrombogenic lesion in the coronary artery. The left anterior descending artery was 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 risk 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 by 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 accumulation of platelets in the area at risk indicates that activated platelets become entrapped in the myocardium. Troponin-T was a better marker of myocardial damage than creatine kinase in this in vivo model with pigs.
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Ravn et al. (2000) studied Thrombosis and ischaemia/reperfusion injury (n=11). Left anterior descending artery damage and occlusion vs. Right ventricle (for platelet accumulation) was evaluated on Platelet accumulation in the area at risk compared to the right ventricle (p=<0.05). In a pig model of ischaemia/reperfusion injury, platelet accumulation was significantly higher in the area at risk compared to the right ventricle (194% vs 137%; p<0.05).
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