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Right ventricular expression of NT-proBNP adds predictive value to REVEAL score in patients with pulmonary arterial hypertension One-Year Outcomes of Orbital Atherectomy of Long, Diffusely Calcified Coronary Artery Lesions In vivo comparison of lipid-rich plaque on near-infrared spectroscopy with histopathological analysis of coronary atherectomy specimens Coronary Calcification and Long-Term Outcomes According to Drug-Eluting Stent Generation Clinical Characteristics and Long-Term Outcomes of Rotational Atherectomy-J2T Multicenter Registry Orbital atherectomy for the treatment of small (2.5mm) severely calcified coronary lesions: ORBIT II sub-analysis Trends in Usage and Clinical Outcomes of Coronary Atherectomy: A Report From the National Cardiovascular Data Registry CathPCI Registry North American Expert Review of Rotational Atherectomy Procedural Success and Outcomes With Increasing Use of Enabling Strategies for Chronic Total Occlusion Intervention Incidence and Standardized Definitions of Mitral Valve Leaflet Adverse Events After Transcatheter Mitral Valve Repair: the EXPAND Study
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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.


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