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Overall and Cause-Specific Mortality in Randomized Clinical Trials Comparing Percutaneous Interventions With Coronary Bypass Surgery: A Meta-analysis Long-Term Prognostic Implications of Previous Silent Myocardial Infarction in Patients Presenting With Acute Myocardial Infarction Efficacy and Safety of Stents in ST-Segment Elevation Myocardial Infarction Major infections after bypass surgery and stenting for multivessel coronary disease in the randomised SYNTAX trial Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement From the American Heart Association A Meta-Analysis of Contemporary Lesion Modification Strategies During Percutaneous Coronary Intervention in 244,795 Patients From 22 Studies Long-Term Follow-Up of Complete Versus Lesion-Only Revascularization in STEMI and Multivessel Disease: The CvLPRIT Trial Dynamic Myocardial Ultrasound Localization Angiography Transcatheter Mitral-Valve Repair in Patients with Heart Failure Routinely reported ejection fraction and mortality in clinical practice: where does the nadir of risk lie?
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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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