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The Current State of Left Main Percutaneous Coronary Intervention Genetics and Causality of Triglyceride-Rich Lipoproteins in Atherosclerotic Cardiovascular Disease sST2 Predicts Outcome in Chronic Heart Failure Beyond NT−proBNP and High-Sensitivity Troponin T Glucose-lowering Drugs or Strategies, Atherosclerotic Cardiovascular Events, and Heart Failure in People With or at Risk of Type 2 Diabetes: An Updated Systematic Review and Meta-Analysis of Randomised Cardiovascular Outcome Trials Potential protective mechanisms of green tea polyphenol EGCG against COVID-19 Prevention of Bleeding in Patients with Atrial Fibrillation Undergoing PCI Radial Versus Femoral Access for Rotational Atherectomy: A UK Observational Study of 8622 Patients Effect of empagliflozin on exercise ability and symptoms in heart failure patients with reduced and preserved ejection fraction, with and without type 2 diabetes The outcomes of intravascular ultrasound-guided drug-eluting stent implantation among patients with complex coronary lesions: a comprehensive meta-analysis of 15 clinical trials and 8,084 patients Limitations of Repeat Revascularization as an Outcome Measure

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.