Primary Percutaneous Coronary Intervention

Devices to Prevent No-Reflow Phenomenon

Tatyana Weitsman; David Meerkin


Interv Cardiol. 2013;5(3):289-300. 

In This Article

Abstract and Introduction


Primary percutaneous coronary intervention, where available, has become the therapy of choice in myocardial reperfusion during ST-elevation myocardial infarction. However, in a significant proportion of patients, owing to a high thrombus burden, myocardial perfusion is not fully achieved in the epicardial vessel. This phenomenon has been attributed predominantly to the distal embolization of thrombus particles and atherosclerotic plaque debris resulting in an association with poorer short- and long-term outcomes, including heart failure and death. Pharmacological measures, such as adequate antiplatelet therapy, glycoprotein IIb/IIIa antagonists and coronary vasodilators, have been employed with the aim of reducing this phenomenon, with limited success. This clinical need has led to the development of devices dedicated to evacuating or trapping thrombus during intervention to reduce the risk of distal embolization during percutaneous coronary intervention. Controversies regarding the benefits that have been achieved with the use of these devices and additional novel approaches, such as the mesh covered stent, will be discussed in this article.


The superiority of primary percutaneous coronary intervention (PPCI) over conventional thrombolytic treatment for ST-elevation myocardial infarction (STEMI) has been demonstrated in randomized controlled trials (RCTs). This has resulted in it becoming the treatment of choice when available.[1–3] PPCI aims to restore normal coronary arterial perfusion and is successful in most cases. However, in up to 40% of patients, normal perfusion is not completely achieved despite successful treatment of the occlusive culprit lesion, as evidenced by reduced thrombolysis in myocardial infarction (TIMI) flow, failure of ST-segment resolution (STR) and poor myocardial blush grade (MBG).[4]

This phenomenon, known as no or slow reflow in its most pronounced manifestations, has been associated with adverse clinical outcomes and has been attributed to a combination of distal embolization of plaque debris, vasoconstriction and reperfusion injury.[5,6] Several STEMI studies demonstrated that percutaneous coronary intervention (PCI) resulted in approximately 15% distal embolization rate.[7,8] Microembolization may lead to the occlusion of arterioles in the microcirculation, thus impairing end myocardial perfusion, whereas embolization of larger atherosclerotic particles can lead to the occlusion of prearterioles and side branches.[9,10] The resulting capillary edema, along with endothelial dysfunction and leukocyte activation, leads to impaired oxygen delivery and eventually to myocardial cell necrosis.[11] It is, therefore, not surprising that in patients with no reflow, infarct sizes are larger, early postinfarction complications are more common and longer-term outcomes, such as left ventricular function and survival, are worse.[12–15] According to the TYPHOON STEMI trial, 7.5–14.3% of patients with acute myocardial infarction (MI) treated with primary PCI experience major adverse cardiac events (MACEs), including cardiac death, heart attack and restenting of the artery.[16]