Pharmaceutical Interventions for the Management of No-Reflow

Tim A. Fischell, MD

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

In This Article

Pertinent Management of Angiographic No-reflow

Various strategies target abnormalities that directly or indirectly contribute to the no-reflow phenomenon and cell death. Nonpharmaceutical approaches to reduce the risk of microemboli include the use of distal protection devices to sequester effluent material subsequent to balloon deflation,[28,29] angioscopy to assess prospectively the presence of unfavorable intracoronary (IC) morphology and possibly identify patients most likely to warrant distal protection,[30] and the continuing technical refinement of catheters. Soluble, highly potent vasoactive factors released by interventions in degenerated grafts may elude containment and therefore represent a considerable challenge to mechanical distal protection.[26,31] Whether angiographic no-reflow is susceptible to an advanced medical device technology solution is unclear.[11]

In contrast, pharmacologic adjuncts to PCI capable of impeding platelet aggregation or directly reducing microvascular spasm have attracted great interest, given the importance of both processes in the development of no-reflow pathophysiology, and the current availability of several medications for clinical use. A range of pharmacologic adjuncts have been evaluated to limit no-reflow, including adenosine, diltiazem, nicardipine, verapamil, nitroprusside, glycoprotein antiplatelet medications, soluble factor antagonists, anti-endothelins and others. Most await large-scale, randomized, controlled trials to confirm their roles and define optimal regimens ( Table 2 ).


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