Italo Porto, Vaishali Ashar and Andrew R.J. Mitchell Pages 95 - 100 ( 6 )
Angiographic no reflow is a recognized phenomenon during percutaneous coronary intervention (PCI). It usually follows successful lesion dilation and, by definition, it represents a reduction in epicardial coronary blood flow in the absence of identifiable dissection, obstruction or distal vessel cut off (indicative of distal embolisation). No reflow appears to be more commonly associated with PCI for acute myocardial infarction and PCI for saphenous vein graft occlusions. While the exact mechanism of no reflow is unknown, theoretical causes include local humoral and microembolic effects leading to microcirculatory dysfunction. As the process is multifactorial, various therapeutic strategies are required in different situations. The present day pharmacological management involves the use of vasodilators including nitrates, verapamil, papaverine, adenosine, nicardipine and sodium nitroprusside, but interestingly a vasoconstrictor like epinephrine may also have a role. Glycoprotein IIb/IIIa platelet receptors antagonist have shown a powerful de-thrombotic effect, and the intracoronary administration appears to be particularly promising. We review the pathogenesis of a reduced epicardial flow during PCI and focus on those drugs that have been studied for the treatment of no reflow. Although no double blind, randomized trial has been conducted to assess any of these agents, or to determine the appropriate dosage, we try to identify some useful conclusions from the published evidence.
No reflow, percutaneous coronary intervention, vasodilator, myocardial infarction, glycoprotein IIbIIIa antagonist
Department of Cardiology,John Radcliffe Hospital, Oxford, OX3 9DU, United Kingdom.