title: Dynamic intracoronary thrombosis does not cause significant downstream platelet embolization.
abstract: OBJECTIVE
  A mural intracoronary thrombus is a potential source of platelet emboli that may obstruct downstream microvessels, but this phenomenon has not been characterized. The present study aimed to assess the magnitude of myocardial platelet accumulation downstream of a mural intracoronary thrombus and its modification by a concomitant transient coronary occlusion (OC) or by treatment with aspirin.
  
  
  METHODS
  The myocardial content of 99mTc-labelled platelets was analyzed in 26 pigs submitted to intimal injury of the left anterior descending coronary artery (LAD) followed by no intervention (n=6), 25-min OC (n=6), or 48-min OC preceded (n=8) or not (n=6) by intravenous administration of 250 mg aspirin.
  
  
  RESULTS
  After 2 h, 24 animals had had 12+/-1 cyclic flow reductions (CFRs) reflecting dynamic LAD thrombosis. Myocardial platelet content in the inferior region was similar among groups. Platelet content in the LAD region was not significantly different to that in the inferior region (129+/-19%, P=NS) in the no intervention group, but was increased following OC (172+/-20 and 312+/-71% after 25- and 48-min OC, respectively, P<0.05). Pre-treatment with aspirin lessened the number of CFRs but did not reduce platelet accumulation in LAD myocardium (483+/-148%). Myocardial platelet accumulation was not associated with the magnitude of platelet deposition in the LAD nor with the number of CFRs, but was correlated with myeloperoxidase activity (r=0.91, P<0.001) and with infarct size (r=0.52, P=0.05). Histological analysis frequently showed sparse platelets or small platelet or leukoplatelet aggregates in small vessels, but arteriolar emboli were rare. In none of seven additional experiments coronary angiography showed obstructions of arterial branches during CFRs.
  
  
  CONCLUSIONS
  The magnitude of platelet embolization from a mural intracoronary thrombus into downstream myocardium is small despite the presence of repetitive CFRs.
authors.affiliation: Servicio de Cardiología, Hospital General Universitari Vall d'Hebron, Barcelona, Spain.
authors.forename: J A
authors.initials: JA
authors.lastname: Barrabés
authors.forename: D
authors.initials: D
authors.lastname: Garcia-Dorado
authors.forename: B
authors.initials: B
authors.lastname: Soriano
authors.forename: J
authors.initials: J
authors.lastname: Solares
authors.forename: Y
authors.initials: Y
authors.lastname: Puigfel
authors.forename: L
authors.initials: L
authors.lastname: Trobo
authors.forename: A
authors.initials: A
authors.lastname: Garcia-Lafuente
authors.forename: J
authors.initials: J
authors.lastname: Soler-Soler
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D001241:Aspirin / Q000627:therapeutic use; D003328:Coronary Thrombosis / Q000097:blood* / Q000188:drug therapy / Q000473:pathology; D004195:Disease Models, Animal; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010477:Perfusion; D009195:Peroxidase / Q000378:metabolism; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D011897:Random Allocation; D013552:Swine
chemical_list: D010975:Platelet Aggregation Inhibitors; D009195:Peroxidase; D001241:Aspirin