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The Regulation of Pulmonary Vascular Tone by Neuropeptides and the Implications for Pulmonary Hypertension Percutaneous Closure of the Left Atrial Appendage Versus Warfarin Therapy for Prevention of Stroke in Patients With Atrial Fibrillation: A Randomised Non-Inferiority Trial Association Between Malignant Mitral Valve Prolapse and Sudden Cardiac Death: A Review Prevalence of potential drug-drug interactions in cancer patients treated with oral anticancer drugs Benefits with drug-coated balloon as compared to a conventional revascularization strategy for the treatment of coronary and non-coronary arterial disease: a comprehensive meta-analysis of 45 randomized trials Optical Coherence Tomography to Assess Proximal Side Optimization Technique in Crush Stenting Thrombotic Risk and Antithrombotic Strategies After Transcatheter Mitral Valve Replacement Transcatheter Interventions for Tricuspid Valve Disease: What to Do and Who to Do it On Initial experience with percutaneous mitral valve repair in patients with cardiac amyloidosis Italian Society of Interventional Cardiology (GIse) Registry Of Transcatheter Treatment of Mitral Valve RegurgitaTiOn (GIOTTO): Impact of Valve Disease Etiology and Residual Mitral Regurgitation after MitraClip Implantation
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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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