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The association between body mass index and obesity with survival in pulmonary arterial hypertension Major trials in coronary intervention from 2018 In-Hospital Coronary Revascularization Rates and Post-Discharge Mortality Risk in Non–ST-Segment Elevation Acute Coronary Syndrome Ticagrelor versus Clopidogrel in Patients with STEMI Treated with Fibrinolytic Therapy: TREAT Trial Chronic total occlusion intervention of the non-infarct-related artery in acute myocardial infarction patients: the Korean multicenter chronic total occlusion registry An EAPCI Expert Consensus Document on Ischaemia with Non-Obstructive Coronary Arteries in Collaboration with European Society of Cardiology Working Group on Coronary Pathophysiology & Microcirculation Endorsed by Coronary Vasomotor Disorders International Study Group Association Between Collateral Circulation and Myocardial Viability Evaluated by Cardiac Magnetic Resonance Imaging in Patients With Coronary Artery Chronic Total Occlusion Galectin-3 Levels and Outcomes After Myocardial Infarction: A Population-Based Study Epinephrine Versus Norepinephrine for Cardiogenic Shock After Acute Myocardial Infarction Early versus delayed invasive intervention in acute coronary syndromes

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.