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Association of White Matter Hyperintensities and Cardiovascular Disease: The Importance of Microcirculatory Disease 2019 ESC/EAS Guidelines for the management of dyslipidaemias: lipid modification to reduce cardiovascular risk: The Task Force for the management of dyslipidaemias of the European Society of Cardiology (ESC) and European Atherosclerosis Society (EAS) Surgical ineligibility and mortality among patients with unprotected left main or multivessel coronary artery disease undergoing percutaneous coronary intervention Transcatheter Aortic Valve Replacement in Low-Risk Patients With Symptomatic Severe Bicuspid Aortic Valve Stenosis Left Ventricular Hypertrophy and Clinical Outcomes Over 5 Years After TAVR: An Analysis of the PARTNER Trials and Registries Ticagrelor versus clopidogrel in patients with acute coronary syndromes Cardiac surgery following transcatheter aortic valve replacement The contribution of tissue-grouped BMI-associated gene sets to cardiometabolic-disease risk: a Mendelian randomization study Thrombotic Versus Bleeding Risk After Transcatheter Aortic Valve Replacement: JACC Review Topic of the Week Balloon Aortic Valvuloplasty as a Bridge to Aortic Valve Replacement: A Contemporary Nationwide Perspective
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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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