The pathophysiology of the no-reflow phenomenon in primary PCI for STEMI involves reperfusion injury, oxidative stress, and microvascular obstruction, highlighting potential new therapeutic approaches.
The no-reflow phenomenon in STEMI patients undergoing primary PCI is driven by reperfusion injury, microvascular obstruction, and distal embolization, suggesting potential benefits for adjunctive therapies like thrombus aspiration and post-conditioning.
The no-reflow phenomenon occurs in about one third of the patients treated with primary PCI for acute ST segment elevation myocardial infarction. Our understanding of its pathophysiology has expanded considerably: in addition of the effect of prolonged ischaemia also reperfusion injury contributes significantly to the microvascular damage in the perfusion territory of the infarct-related coronary artery. Lethal reperfusion injury to both the endothelial cells and the cardiomyocytes is mainly related to the effects of oxidative stress and the energy paradox. Paradoxical vasoconstriction caused by endothelial dysfunction, plugging of the capillaries by endothelial blebs and by packed neutrophils and mechanical compression by myocardial oedema all related to the reperfusion injury lead to microvascular obstruction. Iatrogenic embolization of thrombus and/or plaque material during coronary intervention adds further to the development of the no-reflow phenomenon. New insights in the pathophysiology open the way to a new therapeutic approach of the no-reflow phenomenon: preventing embolization during primary coronary intervention by using adjunctive thrombus aspiration before stent deployment and reducing the reperfusion injury by post-conditioning.
Christiaan Vrints (Mon,) conducted a review in no-reflow phenomenon in acute ST segment elevation myocardial infarction. The pathophysiology of the no-reflow phenomenon in primary PCI for STEMI involves reperfusion injury, oxidative stress, and microvascular obstruction, highlighting potential new therapeutic approaches.
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