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A Test in Context: E/A and E/e' to Assess Diastolic Dysfunction and LV Filling Pressure Geometry as a Confounder When Assessing Ventricular Systolic Function: Comparison Between Ejection Fraction and Strain Long-Term Outcomes in Women and Men Following Percutaneous Coronary Intervention Basic Biology of Oxidative Stress and the Cardiovascular System: Part 1 of a 3-Part Series A Combination of Allogeneic Stem Cells Promotes Cardiac Regeneration Heart Failure With Preserved, Borderline, and Reduced Ejection Fraction: 5-Year Outcomes Pulmonary Artery Pressure-Guided Management of Patients With Heart Failure and Reduced Ejection Fraction Association Between Living in Food Deserts and Cardiovascular Risk 2016 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure Burden of 30-Day Readmissions After Percutaneous Coronary Intervention in 833,344 Patients in the United States: Predictors, Causes, and Cost

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.