title: Effect of glycoprotein IIb/IIIa receptor blockade on recovery of coronary flow and left ventricular function after the placement of coronary-artery stents in acute myocardial infarction.
abstract: BACKGROUND
  Apart from its established effects on vessel patency after percutaneous coronary revascularization, glycoprotein IIb/IIIa receptor blockade by abciximab may improve myocardial perfusion by inhibition of the interaction of platelets and platelet aggregates with the microvasculature. We investigated the effect of abciximab with stent placement in acute myocardial infarction.
  
  
  RESULTS
  In a prospective randomized trial, patients undergoing stenting in acute myocardial infarction within 48 hours after onset of symptoms were randomly assigned to receive either standard-dose heparin or abciximab plus low-dose heparin. Immediately after the procedure and at 14-day angiographic follow-up, we assessed flow velocity in the recanalized vessel with the Doppler wire and regional wall motion by the centerline method. End points were changes in papaverine-induced peak flow velocities and in wall motion indices. We assigned 98 patients to standard heparin and 102 to abciximab. We obtained 152 paired flow measurements and 151 paired left ventricular function studies. Residual stenoses of the treated lesions did not differ between the 2 groups. Improvement of peak flow velocity (mean [95% CI]: 18.1 cm/s [13.6 to 22.6 cm/s], n=80, versus 10.4 cm/s [5.4 to 15.4 cm/s], n=72, P=0.024) and wall motion index (0.44 SD/chord [0.29 to 0.59 SD/chord], n=79 versus 0. 15 SD/chord [0.00 to 0.30 SD/chord], n=72, P=0.007) was significantly greater in patients assigned to abciximab than in those on heparin alone. At follow-up, the abciximab group had a higher global left ventricular ejection fraction than the heparin group (62% [59% to 65%] versus 56% [53% to 59%], P=0.003).
  
  
  CONCLUSIONS
  Abciximab had important effects beyond the maintenance of large-vessel patency. It improved the recovery of microvascular perfusion and concomitantly enhanced the recovery of contractile function in the area at risk.
authors.affiliation: Deutsches Herzzentrum and 1. Medizinische Klinik der Technischen Universität München, Munich, Germany. neumann@dhm.mhn.de
authors.forename: F J
authors.initials: FJ
authors.lastname: Neumann
authors.forename: R
authors.initials: R
authors.lastname: Blasini
authors.forename: C
authors.initials: C
authors.lastname: Schmitt
authors.forename: E
authors.initials: E
authors.lastname: Alt
authors.forename: J
authors.initials: J
authors.lastname: Dirschinger
authors.forename: M
authors.initials: M
authors.lastname: Gawaz
authors.forename: A
authors.initials: A
authors.lastname: Kastrati
authors.forename: A
authors.initials: A
authors.lastname: Schömig
mesh_terms: D000077284:Abciximab; D000368:Aged; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D001783:Blood Flow Velocity / Q000187:drug effects; D017023:Coronary Angiography; D005260:Female; D006493:Heparin / Q000627:therapeutic use; D006801:Humans; D007140:Immunoglobulin Fab Fragments / Q000494:pharmacology / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000188:drug therapy* / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000379:methods*; D010208:Papaverine / Q000494:pharmacology; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors* / Q000627:therapeutic use*; D011446:Prospective Studies; D016037:Single-Blind Method; D015607:Stents; D016896:Treatment Outcome; D016277:Ventricular Function, Left / Q000187:drug effects*
chemical_list: D000911:Antibodies, Monoclonal; D007140:Immunoglobulin Fab Fragments; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D006493:Heparin; D010208:Papaverine; D000077284:Abciximab