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Mortality after coronary artery bypass grafting versus percutaneous coronary intervention with stenting for coronary artery disease: a pooled analysis of individual patient data Lysed Erythrocyte Membranes Promote Vascular Calcification: Possible Role of Erythrocyte-Derived Nitric Oxide Low shear stress induces endothelial reactive oxygen species via the AT1R/eNOS/NO pathway Fate of post-procedural malapposition of everolimus-eluting polymeric bioresorbable scaffold and everolimus-eluting cobalt chromiummetallic stent in human coronary arteries: sequential assessment with optical coherence tomography in ABSORB Japan trial A randomized trial of bifurcation stenting technique in chronic total occlusions percutaneous coronary intervention Left main coronary artery compression in pulmonary hypertension Optical coherence tomography and C-reactive protein in risk stratification of acute coronary syndromes Diagnostic accuracy of fractional flow reserve from anatomic CT angiography Volumetric characterization of human coronary calcification by frequency-domain optical coherence tomography Fractional Flow Reserve–Guided PCI for Stable Coronary Artery Disease
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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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