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Frailty in Older Adults Undergoing Aortic Valve Replacement: The FRAILTY-AVR Study In vitro flow and optical coherence tomography comparison of two bailout techniques after failed provisional stenting for bifurcation percutaneous coronary interventions Polymer-based or Polymer-free Stents in Patients at High Bleeding Risk 2019 Guidelines on Diabetes, Pre-Diabetes and Cardiovascular Diseases developed in collaboration with the EASD ESC Clinical Practice Guidelines Impact of SYNTAX Score on 10-Year Outcomes After Revascularization for Left Main Coronary Artery Disease Safety and efficacy of the bioabsorbable polymer everolimus-eluting stent versus durable polymer drug-eluting stents in high-risk patients undergoing PCI: TWILIGHT-SYNERGY Inhibition of Platelet Aggregation After Coronary Stenting in Patients Receiving Oral Anticoagulation Adenosine and adenosine receptor-mediated action in coronary microcirculation Left Main Percutaneous Coronary Intervention Versus Coronary Artery Bypass Grafting in Patients With Prior Cerebrovascular Disease: Results From the EXCEL Trial A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling

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.