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De-escalation of antianginal medications after successful chronic total occlusion percutaneous coronary intervention: Frequency and relationship with health status Combining IVUS and Optical Coherence Tomography for More Accurate Coronary Cap Thickness Quantification and Stress/Strain Calculations: A Patient-Specific Three-Dimensional Fluid-Structure Interaction Modeling Approach Changes in One-Year Mortality in Elderly Patients Admitted with Acute Myocardial Infarction in Relation with Early Management The HACD4 haplotype as a risk factor for atherosclerosis in males Prospective Elimination of Distal Coronary Sinus to Left Atrial Connection for Atrial Fibrillation Ablation (PRECAF) Randomized Controlled Trial The Impact of Proximal Vessel Tortuosity on the Outcomes of Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From a Contemporary Multicenter Registry Association of the PHACTR1/EDN1 Genetic Locus With Spontaneous Coronary Artery Dissection Eruptive Calcified Nodules as a Potential Mechanism of Acute Coronary Thrombosis and Sudden Death Long-term Survival following Multivessel Revascularization in Patients with Diabetes (FREEDOM Follow-On Study) Acute Noncardiac Organ Failure in Acute Myocardial Infarction With Cardiogenic Shock
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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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