Ja. Barrabes et al., INJURY IN A TRANSIENTLY OCCLUDED CORONARY-ARTERY INCREASES MYOCARDIALNECROSIS - EFFECT OF ASPIRIN, Pflugers Archiv, 432(4), 1996, pp. 663-670
This study tested the hypothesis that intimal injury in a transiently
occluded coronary artery limits myocardial salvage, The effect of inti
mal injury on reactive hyperaemia was investigated in 17 pigs submitte
d to a 30-min occlusion of the left anterior descending coronary arter
y (LAD), not resulting in myocardial infarction. Catheter-induced inti
mal damage increased local platelet deposition (Tc-99m) and reduced hy
peraemia, but did not modify myocardial platelet or polymorphonuclear
leucocyte content (myeloperoxidase activity) after 6 h reperfusion. To
investigate the influence of intimal injury on the extent of myocardi
al necrosis secondary to a more prolonged coronary occlusion, and the
role of platelets on this influence, 52 pigs were submitted to a doubl
e randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. plac
ebo and to coronary intimal injury vs. no coronary damage before a 48-
min occlusion of the LAD and 6 h of reperfusion. After excluding 12 an
imals with reocclusion, coronary intimal injury was associated with la
rger infarcts (triphenyltetrazolium reaction) in animals receiving pla
cebo (36.2+/-7.0% of the area at risk in animals with intimal injury v
s. 10.81+/-3.9% in animals without coronary injury, P=0,006) but not i
n those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at r
isk in animals with and without intimal injury respectively). These re
sults suggest that coronary intimal injury in the reperfused artery ma
y have adverse effects on myocardial salvage by mechanisms other than
reocclusion or embolization of platelet aggregates.