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From organic and inorganic phosphates to valvular and vascular calcifications The impact of intravascular ultrasound guidance during drug eluting stent implantation on angiographic outcomes Accuracy of Fractional Flow Reserve Derived From Coronary Angiography Long-term outcome of prosthesis-patient mismatch after transcatheter aortic valve replacement Simple Electrocardiographic Measures Improve Sudden Arrhythmic Death Prediction in Coronary Disease The Evolution of β-Blockers in Coronary Artery Disease and Heart Failure (Part 1/5) The Utility of Rapid Atrial Pacing Immediately Post-TAVR to Predict the Need for Pacemaker Implantation High-risk plaque detected on coronary CT angiography predicts acute coronary syndromes independent of significant stenosis in acute chest pain: results from the ROMICAT-II trial Cardiac Structural Changes After Transcatheter Aortic Valve Replacement: Systematic Review and Meta-Analysis of Cardiovascular Magnetic Resonance Studies Prognostic implications of baseline 6‐min walk test performance in intermediate risk patients undergoing transcatheter aortic valve replacement
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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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