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Nonculprit Stenosis Evaluation Using Instantaneous Wave-Free Ratio in Patients With ST-Segment Elevation Myocardial Infarction PCI Strategies in Patients with Acute Myocardial Infarction and Cardiogenic Shock Intraluminal Intensity of Blood Speckle on Intravascular Ultrasound, a Novel Predictor of Periprocedural Myocardial Injury After Coronary Stenting Characterization of the Average Daily Ischemic and Bleeding Risk After Primary PCI for STEMI Transcatheter Aortic-Valve Replacement with a Balloon-Expandable Valve in Low-Risk Patients Ranolazine in High-Risk Patients With Implanted Cardioverter-Defibrillators - The RAID Trial Comparison of Outcomes of Patients With ST-Segment Elevation Myocardial Infarction Treated by Primary Percutaneous Coronary Intervention Analyzed by Age Groups (<75, 75 to 85, and >85 Years); (Results from the Bremen STEMI Registry) Location of the culprit coronary lesion and its association with delay in door-to-balloon time (from a multicenter registry of primary percutaneous coronary intervention) Fine particulate air pollution and hospital admissions and readmissions for acute myocardial infarction in 26 Chinese cities Door to Balloon Time: Is There a Point That Is Too Short?

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.