title: Intimal injury in a transiently occluded coronary artery increases myocardial necrosis. Effect of aspirin.
abstract: This study tested the hypothesis that intimal injury in a transiently occluded coronary artery limits myocardial salvage. The effect of intimal injury on reactive hyperaemia was investigated in 17 pigs submitted to a 30-min occlusion of the left anterior descending coronary artery (LAD), not resulting in myocardial infarction. Catheter-induced intimal damage increased local platelet deposition (99mTc) and reduced hyperaemia, 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 myocardial necrosis secondary to a more prolonged coronary occlusion, and the role of platelets on this influence, 52 pigs were submitted to a double randomization (2x2 factorial design) to 250 mg i.v. aspirin vs. placebo 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 animals with reocclusion, coronary intimal injury was associated with larger infarcts (triphenyltetrazolium reaction) in animals receiving placebo (36.2+/-7.0% of the area at risk in animals with intimal injury vs. 10.8+/-3.9% in animals without coronary injury, P=0.006) but not in those receiving aspirin (20.3+/-6.5 vs. 21.7+/-6.5% of the area at risk in animals with and without intimal injury respectively). These results suggest that coronary intimal injury in the reperfused artery may have adverse effects on myocardial salvage by mechanisms other than reocclusion or embolization of platelet aggregates.
authors.affiliation: Servicio de Cardiología, Hospital General Universitario Vall d'Hebron, Pg. Vall d'Hebron 119-129, E-08035 Barcelona, Spain.
authors.forename: J A
authors.initials: JA
authors.lastname: Barrabés
authors.forename: D
authors.initials: D
authors.lastname: Garcia-Dorado
authors.forename: J
authors.initials: J
authors.lastname: Oliveras
authors.forename: M A
authors.initials: MA
authors.lastname: González
authors.forename: M
authors.initials: M
authors.lastname: Ruiz-Meana
authors.forename: J
authors.initials: J
authors.lastname: Solares
authors.forename: A G
authors.initials: AG
authors.lastname: Burillo
authors.forename: R M
authors.initials: RM
authors.lastname: Lidón
authors.forename: M
authors.initials: M
authors.lastname: Antolín
authors.forename: J
authors.initials: J
authors.lastname: Castell
authors.forename: J
authors.initials: J
authors.lastname: Soler-Soler
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D001760:Bleeding Time; D001772:Blood Cell Count / Q000187:drug effects; D003324:Coronary Artery Disease / Q000150:complications / Q000473:pathology*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000473:pathology*; D009203:Myocardial Infarction / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D009336:Necrosis; D009504:Neutrophils / Q000378:metabolism; D010974:Platelet Aggregation / Q000187:drug effects; D012039:Regional Blood Flow / Q000187:drug effects; D013552:Swine; D017539:Tunica Intima / Q000187:drug effects / Q000473:pathology*; D014693:Ventricular Fibrillation / Q000150:complications
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D001241:Aspirin