Pharmaceutical Interventions for the Management of No-Reflow

Tim A. Fischell, MD

J Invasive Cardiol. 2008;20(7):374-379. 

In This Article


Percutaneous coronary intervention (PCI) for atherosclerotic coronary artery disease is an effective therapy for restoring vessel caliber and improving blood flow to ischemic myocardium. At least 1.25 million PCIs are performed annually in the United States, and it has been estimated that nearly 2 million procedures are performed annually worldwide.[1] The growth in the number of PCIs has occurred in tandem with technological refinements and advances in peri- and postprocedural medication, which have reduced procedural risk, improved success rates and dramatically changed the prognosis of patients with acute coronary syndromes.[2,3,4,5,6,7,8]

The no-reflow and slow-reflow phenomena[9] are poorly understood complications of PCI in which reduced coronary flow persists despite the intraprocedural removal of the occlusive lesion from the epicardial coronary artery or arteries. In as many as 2% of patients without acute myocardial infarction (AMI) who undergo PCI, restoration of normal anterograde myocardial blood flow (myocardial "blush") is unsuccessful due to microcirculatory dysfunction and/or mechanical obstruction; this failure – slow- or no-reflow – occurs in the absence of postprocedural angiographic evidence of an encroaching luminal lesion (e.g., evolving dissection) or evidence of macroscopic distal embolization.[10,11,12] The no-reflow phenomenon is encountered most frequently among patients undergoing PCI of saphenous vein grafts (SVGs) and in patients with AMI who undergo thrombolysis or mechanical intervention. In these populations, the incidence of slow- or no-reflow may be greater than 30%.[12,13,14]

The no-reflow phenomenon following PCI is associated with significant cardiac consequences due to myocardial ischemia caused by inadequate distal microvascular flow and poor myocardial perfusion. Despite widely patent epicardial vessel lumens, no-reflow can be associated with angina and ischemic ST-segment changes in these patients.[10] Consequently, angiographic or contrast-enhanced echocardiographic demonstration of open epicardial vessels may not be a reliable indicator of successful myocardial reperfusion in AMI patients with no-reflow and residual perfusion defects in the risk area.[15] No-reflow predicts a poor functional recovery and impaired ventricular remodeling, and its persistence – despite attempted treatment – is associated with a high incidence of ongoing or recurrent acute coronary syndrome (ACS) as well as increased short-term mortality.[11,13,15,16]


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