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A Combined Optical Coherence Tomography and Intravascular Ultrasound Study on Plaque Rupture, Plaque Erosion, and Calcified Nodule in Patients With ST-Segment Elevation Myocardial Infarction: Incidence, Morphologic Characteristics, and Outcomes After Percutaneous Coronary Intervention Clinical impact of PCSK9 inhibitor on stabilization and regression of lipid-rich coronary plaques: a near-infrared spectroscopy study Negative Risk Markers for Cardiovascular Events in the Elderly Comparison of safety and periprocedural complications of transfemoral aortic valve replacement under local anaesthesia: minimalist versus complete Heart Team Prognostic implications of baseline 6‐min walk test performance in intermediate risk patients undergoing transcatheter aortic valve replacement Incidence and Outcomes of Surgical Bailout During TAVR : Insights From the STS/ACC TVT Registry The Evolution of β-Blockers in Coronary Artery Disease and Heart Failure (Part 1/5) Colchicine Reduces Cardiovascular Events in Chronic Coronary Disease Impact of Positive and Negative Lesion Site Remodeling on Clinical Outcomes : Insights From PROSPECT From organic and inorganic phosphates to valvular and vascular calcifications
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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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