Levine et al 2011 ACCF/AHA/SCAI PCI Guideline e609 with anti-IIa activity should be administered be- cause of the risk of catheter thrombosis.651,652 (Level of Evidence: C) Fondaparinux, a pentasaccharide, is an indirect factor Xa inhibitor but has no effect on thrombin. On the basis of reports of catheter thrombosis when fondaparinux is used alone during primary PCI,651,652 the writing committee rec- ommends that an anticoagulant with anti-IIa activity be used in patients undergoing PCI.651,652 One study suggested that clinical outcomes were better when fondaparinux was re- placed during PCI by a standard dose of UFH (85 U/kg, 60 U/kg with GP IIb/IIIa inhibitors) rather than by a low dose 5.7.5. No-Reflow Pharmacological Therapies: Recommendation Class IIa 1. Administration of an intracoronary vasodilator (adenosine, calcium channel blocker, or nitroprus- side) is reasonable to treat PCI-related no-reflow that occurs during primary or elective PCI.674 689 (Level of Evidence: B) See Online Data Supplement 25 for additional data regarding no-reflow therapies. No-reflow is a broad term used to describe 2 distinct entities. The first is interventional no-reflow attributed to vasospasm and downstream embolization of debris dislodged during PCI, usually in the setting of atherectomy, thrombus, or degenerated SVGs. The second entity is suboptimal reperfusion of an infarct artery, attributed to endothelial injury in addition to embolization and vasospasm. Angio- graphic no-reflow is the most obvious sequela of the same pathophysiology that produces abnormal TIMI frame counts and TIMI blush scores, so these measures are often used interchangeably. The principal clinical sequela of no-reflow is myonecrosis. Efforts to prevent no-reflow overlap with strategies to reduce MI size and prevent periprocedural MI. In the setting of MI, several drugs have been shown to reduce the incidence of no-reflow. 