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Current treatment of significant left main coronary artery disease: A review Two-year outcomes following unprotected left main stenting with first vs new-generation drug-eluting stents: the FINE registry. EuroIntervention. Mechanisms of in-stent restenosis after drug-eluting stent implantation: intravascular ultrasound analysis The Science Underlying COVID-19: Implications for the Cardiovascular System Anthracycline-induced cardiotoxicity: A multicenter randomised trial comparing two strategies for guiding prevention with enalapril: The International CardioOncology Society-one trial Impact of Intravascular Ultrasound on Long-Term Clinical Outcomes in Patients With Acute Myocardial Infarction Risk of Coronary Obstruction and Feasibility of Coronary Access After Repeat Transcatheter Aortic Valve Replacement With the Self-Expanding Evolut Valve: A Computed Tomography Simulation Study Comparison of 1-Year Pre- And Post-Transcatheter Aortic Valve Replacement Hospitalization Rates: A Population-Based Cohort Study Randomized study to evaluate sirolimus-eluting stents implanted at coronary bifurcation lesions Defining a new standard for IVUS optimized drug eluting stent implantation: the PRAVIO study
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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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