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A Meta-Analysis of Contemporary Lesion Modification Strategies During Percutaneous Coronary Intervention in 244,795 Patients From 22 Studies Drug-Coated Balloon Treatment for Femoropopliteal Artery Disease: The IN.PACT Global Study De Novo In-Stent Restenosis Imaging Cohort Coronary Artery Calcium Is Associated with Left Ventricular Diastolic Function Independent of Myocardial Ischemia Can the Vanishing Stent Reappear? Fix the Technique, or Fix the Device? Aggressive lipid-lowering therapy after percutaneous coronary intervention – for whom and how? Rotational Atherectomy Followed by Drug-Coated Balloon Dilation for Left Main In-Stent Restenosis in the Setting of Acute Coronary Syndrome Complicated with Right Coronary Chronic Total Occlusion SGLT2 Inhibitors in Patients With Heart Failure With Reduced Ejection Fraction: A Meta-Analysis of the EMPEROR-Reduced and DAPA-HF Trials Disrupting Fellow Education Through Group Texting: WhatsApp in Fellow Education? AIM2-driven inflammasome activation in heart failure Coronary Angiography after Cardiac Arrest — The Right Timing or the Right Patients?

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.