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Intravascular Ultrasound-Guided Versus Angiography-Guided Implantation of Drug-Eluting Stent in All-Comers: The ULTIMATE trial Mediterranean Diet and the Association Between Air Pollution and Cardiovascular Disease Mortality Risk In patients with stable coronary heart disease, low-density lipoprotein-cholesterol levels < 70 mg/dL and glycosylated hemoglobin A1c < 7% are associated with lower major cardiovascular events Coronary calcification in the diagnosis of coronary artery disease Clinical Risk Factors and Atherosclerotic Plaque Extent to Define Risk for Major Events in Patients Without Obstructive Coronary Artery Disease: The Long-Term Coronary Computed Tomography Angiography CONFIRM Registry Bioprosthetic valve oversizing is associated with increased risk of valve thrombosis following TAVR Minimizing Permanent Pacemaker Following Repositionable Self-Expanding Transcatheter Aortic Valve Replacement Health Status after Transcatheter vs. Surgical Aortic Valve Replacement in Low-Risk Patients with Aortic Stenosis Bridging the Gap Between Epigenetic and Genetic in PAH The Role of Vascular Imaging in Guiding Routine Percutaneous Coronary Interventions: A Meta-Analysis of Bare Metal Stent and Drug-Eluting Stent Trials
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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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