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Efficacy of Ertugliflozin on Heart Failure–Related Events in Patients With Type 2 Diabetes Mellitus and Established Atherosclerotic Cardiovascular Disease Results of the VERTIS CV Trial Unexpectedly Low Natriuretic Peptide Levels in Patients With Heart Failure Major Bleeding Rates in Atrial Fibrillation Patients on Single, Dual, or Triple Antithrombotic Therapy Association of Left Ventricular Systolic Function With Incident Heart Failure in Late Life Atrial Fibrillation and the Prognostic Performance of Biomarkers in Heart Failure Guideline‐Directed Medical Therapy for Patients With Heart Failure With Midrange Ejection Fraction: A Patient‐Pooled Analysis From the KorHF and KorAHF Registries Mediterranean Diet and the Association Between Air Pollution and Cardiovascular Disease Mortality Risk Short- versus long-term duration of dual-antiplatelet therapy after coronary stenting: a randomized multicenter trial Heart Failure With Mid-Range (Borderline) Ejection Fraction: Clinical Implications and Future Directions Dapagliflozin and Cardiovascular Outcomes in Type 2 Diabetes
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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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