The primary mechanism of no-reflow is likely due to distal embolization of atheromatous and thrombotic debris dislodged by balloon inflation or stent implantation.^[1][2] During PCI, microthrombi and small particles of plaques are thought to be showered downstream, occluding small arteries, arterioles, and collateral microvasculature. Analysis of the aspirate obtained from patients without no-reflow revealed a greater amount of atheromatous plaques and significantly more platelet and fibrin complex, macrophages, and cholesterolcrystals than those who experienced no-reflow. The 30-day mortality was significantly higher (27.5%) in patients with no-reflow phenomenon than in patients with normal coronary blood flow after PCI (5.3%, P < 0.001). Predictors of no-reflow include a higher plaque burden, thrombus, lipid pools by IVUS, higher lesion elastic membrane cross-sectional area, pre-infarction angina, and TIMI flow grade 0 on the initial coronary angiogram, among other factors.

Other pathophysiologic mechanisms include:

• Release of active tissue factor from the dislodged plaque^[3]
• Vasoconstriction secondary to serotonin, adenosine diphosphate, thromboxane A2, released by the embolized platelet-rich atheromatous material^[4]
• Reperfusion injury from the release of oxygen free radicals during inflammation
• Myocardial necrosis and stunning
• Microvascular damage^[5]
• Microvascular plugging with platelets or leukocytes
• Endothelial swelling and tissue edema compressing vasculature

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