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Impact of Coronary Lesion Complexity in Percutaneous Coronary Intervention: One-Year Outcomes From the Large, Multicentre e-Ultimaster Registry Management of Percutaneous Coronary Intervention Complications: Algorithms From the 2018 and 2019 Seattle Percutaneous Coronary Intervention Complications Conference Thin Composite-Wire-Strut Zotarolimus-Eluting Stents Versus Ultrathin-Strut Sirolimus-Eluting Stents in BIONYX at 2 Years Overall and Cause-Specific Mortality in Randomized Clinical Trials Comparing Percutaneous Interventions With Coronary Bypass Surgery: A Meta-analysis Appropriate Use Criteria and Health Status Outcomes Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN-CTO Registry European Bifurcation Club White Paper on Stenting Techniques for Patients With Bifurcated Coronary Artery Lesions Syncope After Percutaneous Coronary Intervention Mortality Differences Associated With Treatment Responses in CANTOS and FOURIER: Insights and Implications Prospective Elimination of Distal Coronary Sinus to Left Atrial Connection for Atrial Fibrillation Ablation (PRECAF) Randomized Controlled Trial Invasive Coronary Physiology After Stent Implantation: Another Step Toward Precision Medicine

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.