Pathogenesis of no/slow-reflow phenomenon following percutaneous coronary intervention (PCI) in patients with acute coronary syndrome and ST-segment elevation (STEMI) requires constant and in-depth study. It is known that no-reflow phenomenon is com plex and can be triggered by combination of the following factors: 1) distal embolism of infarct-related coronary artery; 2) myocardial ischemic damage in appropriate coronary basin; 3) myocardial reperfusion injury; 4) genetic predisposition to microvascular damage. The risk of no-reflow or slow-reflow phenomenon is present at any stage of PCI. Most often, no-reflow phenomenon occurs due to distal embolism following balloon inflation during pre-dilatation or stent implantation. Distal embolism of infarct-related coronary artery due to fragmentation and migration of atherothrombotic conglomerate during PCI is sufficiently studied. Endovascular prevention of slow/no-reflow phenomenon took place in different years of development of endovascular surgery, and some ones are used now. At various times, surgeons used mesh-covered stents, manual and rheolytic thrombaspiration, protection by filter traps, proximal protection from distal embolism by temporary occlusion of infarct-related coronary artery. However, manual thromboaspiration currently occupies its niche, and indications for this procedure are limited. Intravenous administration of platelet glycoprotein IIB/IIIA receptor inhibitors is the most effective and common pharmacological method for the treatment and prevention of no-reflow or slow-reflow phenomenon. Some authors suppose that direct stenting of infarct-related coronary artery without pre-dilatation reduces the risk of distal embolism. That is why this strategy may be preferable for revascularization in STEMI patients to reduce the risk of microvascular embolization. © 2024, Media Sphera Publishing Group. All rights reserved.