title: Effects of glycoprotein IIb/IIIa inhibition on microvascular flow after coronary reperfusion. A quantitative myocardial contrast echocardiography study.
abstract: OBJECTIVE
  We assessed the effect of glycoprotein IIb/IIIa inhibition (GPI) on microvascular flow after coronary occlusion/reperfusion using quantitative myocardial contrast echocardiography (QMCE).
  
  
  BACKGROUND
  Platelets may play a major role in the dissociation of epicardial artery recanalization and tissue-level reperfusion, referred to as the "no-reflow phenomenon." Therefore, GPI might improve myocardial reperfusion, distinct from its effects on epicardial patency.T METHOD: hree-hour occlusion of the left anterior descending coronary artery (LAD) was followed by 3-h reperfusion in 16 open-chest dogs: 8 controls and 8 given a continuous infusion of the GPI tirofiban, starting 45 min before LAD reopening. Perfusion of the LAD bed was quantified by the rate of intensity rise (b) by QMCE; myocardial blood flow (MBF) was assessed by fluorescent microspheres.
  
  
  RESULTS
  No differences in b or MBF were observed within the risk area between the control and GPI groups at baseline or occlusion. However, b and MBF were higher in GPI dogs than in controls during reperfusion, despite similar epicardial flow (p < 0.05 at 30, 60, and 90 min; p = NS at 180 min). Infarct area size was significantly reduced in GPI dogs compared with non-treated dogs (26.9 +/- 10.5% vs. 49.0 +/- 11.1% of at-risk area, respectively).
  
  
  CONCLUSIONS
  As demonstrated by QMCE, GPI improves microvascular flow and reduces the infarct area after coronary occlusion/reperfusion, independent of epicardial flow. These data demonstrate the usefulness of QMCE in assessing microvascular flow, provide novel evidence for the role of platelets in the early phase of reperfusion injury, and show that GPI is of value in preserving microvascular perfusion after coronary reperfusion.
authors.affiliation: Division of Cardiology, University of California at San Diego, San Diego, California 92103-8411, USA.
authors.forename: Hideki
authors.initials: H
authors.lastname: Kunichika
authors.forename: Ori
authors.initials: O
authors.lastname: Ben-Yehuda
authors.forename: Stephane
authors.initials: S
authors.lastname: Lafitte
authors.forename: Naomi
authors.initials: N
authors.lastname: Kunichika
authors.forename: Barry
authors.initials: B
authors.lastname: Peters
authors.forename: Anthony N
authors.initials: AN
authors.lastname: DeMaria
mesh_terms: D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D004452:Echocardiography / Q000379:methods*; D008833:Microcirculation / Q000187:drug effects*; D023421:Models, Animal; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology; D015425:Myocardial Reperfusion / Q000379:methods; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology*; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000037:antagonists & inhibitors*; D015427:Reperfusion Injury / Q000188:drug therapy / Q000503:physiopathology; D000077466:Tirofiban; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000494:pharmacology*
chemical_list: D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D014443:Tyrosine; D000077466:Tirofiban