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Bare metal or drug-eluting stent versus drug-coated balloon in non-ST-elevation myocardial infarction: the randomised PEPCAD NSTEMI trial Optical Coherence Tomography Predictors for Recurrent Restenosis After Paclitaxel-Coated Balloon Angioplasty for Drug-Eluting Stent Restenosis Fractional Flow Reserve–Guided PCI as Compared with Coronary Bypass Surgery Evolution of the Crush Technique for Bifurcation Stenting Treating Bifurcation Lesions: The Result Overcomes the Technique Applications of left ventricular strain measurements to patients undergoing chemotherapy Chronic Total Occlusion Interventions: Update on Current Tips and Tricks Comparison of new-generation drug-eluting stents versus drug-coated balloon for in-stent restenosis: a meta-analysis of randomised controlled trials Sustainable Antirestenosis Effect With a Low-Dose Drug-Coated Balloon: The ILLUMENATE European Randomized Clinical Trial 2-Year Results Multicentre, randomized comparison of two-stent and provisional stenting techniques in patients with complex coronary bifurcation lesions: the DEFINITION II trial
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Original Research2008 Aug;4(2):181-3.

JOURNAL：EuroIntervention. Article Link

Management of two major complications in the cardiac catheterisation laboratory: the no-reflow phenomenon and coronary perforations

Muller O, Windecker S, Cuisset T et al. Keywords: complication; no-reflow phenomenon; coronary perforation

ABSTRACT

The no-reflow phenomenon has been defined in 2001 by Eeckhout and Kern as inadequate myocardial perfusion through a given segment of the coronary circulation without angiographic evidence of mechanical vessel obstruction1. Rates of cardiac death and non-fatal cardiac events are increased in patients with compared to those without no-reflow2,3. The term “no reflow” encompasses the slow-flow, slow-reflow, no-flow and low-flow phenomenon. Its incidence depends on the clinical setting, ranging from as low as 2% in elective native coronary percutaneous coronary interventions (PCI) to 20% in saphenous venous graft (SVG) PCI and up to 26% in acute myocardial infarction (AMI) mechanical reperfusion4-6. Depending on the clinical setting, the mechanism of the no-reflow phenomenon differs. Distal embolisation and ischaemic-reperfusion cell injury prevail in patients with AMI, microvascular spasm and embolisation of aggregated platelets occur in native coronary PCI, whereas embolisation of degenerated plaque elements, including thrombotic and atherosclerotic debris are encountered during SVG PCI7. The no-reflow phenomenon is classified according to its pathophysiology with potential implications for its treatment in the categories provided in Table 1.


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