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Percutaneous Coronary Intervention for Chronic Total Occlusion—The Michigan Experience: Insights From the BMC2 Registry From Early Pharmacology to Recent Pharmacology Interventions in Acute Coronary Syndromes Epidemiology and Clinical Outcomes of Patients With Inflammatory Bowel Disease Presenting With Acute Coronary Syndrome The Prognostic Significance of Periprocedural Infarction in the Era of Potent Antithrombotic Therapy: The PRAGUE-18 Substudy Transition of Macrophages to Fibroblast-Like Cells in Healing Myocardial Infarction Linking Spontaneous Coronary Artery Dissection, Cervical Artery Dissection, and Fibromuscular Dysplasia: Heart, Brain, and Kidneys Comparative Effectiveness of β-Blocker Use Beyond 3 Years After Myocardial Infarction and Long-Term Outcomes Among Elderly Patients Pharmacotherapy in the Management of Anxiety and Pain During Acute Coronary Syndromes and the Risk of Developing Symptoms of Posttraumatic Stress Disorder Intensive Care Utilization in Stable Patients With ST-Segment Elevation Myocardial Infarction Treated With Rapid Reperfusion Percutaneous coronary intervention for coronary bifurcation disease: 11th consensus document from the European Bifurcation Club

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.