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Embolization and coronary no-reflow are rare but important complications during percutaneous coronary intervention (PCI). Recognition and treatment are important in that they may reduce or prevent myocardial necrosis and serious subsequent complications. Additionally, nonclinical events may occur as a result of this phenomenon, and prevention where possible becomes important. Macroembolization usually is due to macro-particles and/or blood clots that may occur during intervention of patients with acute coronary syndromes. No-reflow may occur due to the embolization of micro-particulate matter as debris from coronary lesions, activation of platelets, and/or release of vasoactive substances that may modulate distal vasculature. No-reflow is defined as the reduction of coronary flow in the absence of a proximal occlusive lesion with resultant myocardial ischemia. In PCI of native coronary vessels in absence of acute coronary syndromes, no-reflow may be due to microvascular spasm and/or platelet microemboli. When PCI is performed in thrombotic lesions, such as in acute coronary syndromes, no-reflow may be due to distal embolization of thrombus. During saphenous vein graft intervention and rotational atherectomy, it is most often related to embolization of degenerated plaque elements including thrombotic and atherosclerotic debris. Any or all of these mechanisms can occur simultaneously.

A number of strategies have been available as adjuncts to reduce embolization, but many have been shown to be ineffective and are no longer available. Many are mentioned here for an historical perspective.


The problem of embolization of plaque material during percutaneous catheter angioplasty and stenting has been recognized since the early development of balloon angioplasty. Shortly after the introduction of balloon angioplasty in an experimental model of angioplasty, effluent debris was collected and analyzed by histologic and polarized light microscopic examinations for gross debris and cholesterol.1 This study is often widely cited as showing no evidence for significant embolization during balloon angioplasty. Microscopically visible atherosclerotic debris was present in 12% of procedures, and thin-layer chromatography showed evidence of cholesterol embolization in 25%. These findings of atherosclerotic debris in between 12% and 25% of treated vessels is completely in line with clinical studies that followed in patients over the next 2 decades.

Both particle size and amount of the embolic material are important. Small amounts of 15-μm particles have been shown to cause patchy ischemia, while increased numbers of particles can cause decrease in flow. When particles are larger, in the 100 to 300 μm range, a relatively few particles can reduce flow.


Clinical studies have found evidence for embolization associated with PCI procedures. In the stent era, embolization has been detected in about 20% of simple native vessel stent implantation procedures based on the occurrence of creatine phosphokinase-MB (CPK-MB) enzyme release only. For example, in the STARS trial, patients with type A lesions who had completely uncomplicated, successful stenting with a single stent were evaluated. In ...

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