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Age-Related Characteristics and Outcomes of Patients With Heart Failure With Preserved Ejection Fraction Atherosclerotic plaque with ultrasonic attenuation affects coronary reflow and infarct size in patients with acute coronary syndrome: an intravascular ultrasound study Sex- and Race-Related Differences in Characteristics and Outcomes of Hospitalizations for Heart Failure With Preserved Ejection Fraction Primary Prevention of Heart Failure in Women Mechanical circulatory support devices for acute right ventricular failure Myocardial bridging: contemporary understanding of pathophysiology with implications for diagnostic and therapeutic strategies Timing of Intervention in Aortic Stenosis Burden of Cardiovascular Diseases in China, 1990-2016: Findings From the 2016 Global Burden of Disease Study Guideline‐Directed Medical Therapy for Patients With Heart Failure With Midrange Ejection Fraction: A Patient‐Pooled Analysis From the KorHF and KorAHF Registries In-stent neoatherosclerosis: a final common pathway of late stent failure
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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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