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Effect of Medication Co-payment Vouchers on P2Y12 Inhibitor Use and Major Adverse Cardiovascular Events Among Patients With Myocardial Infarction: The ARTEMIS Randomized Clinical Trial Prevalence of Coronary Vasospasm Using Coronary Reactivity Testing in Patients With Spontaneous Coronary Artery Dissection Evaluation and Management of Nonculprit Lesions in STEMI Association of Acute Procedural Results with Long-term Outcomes After CTO-PCI Coronary CT Angiography in Patients With Non-ST-Segment Elevation Acute Coronary Syndrome Canadian spontaneous coronary artery dissection cohort study: in-hospital and 30-day outcomes Step-by-step manual for planning and performing bifurcation PCI: a resource-tailored approach Rotational atherectomy and new-generation drug-eluting stent implantation Clinical Characteristics and Outcomes of STEMI Patients With Cardiogenic Shock and Cardiac Arrest Relation of prior statin and anti-hypertensive use to severity of disease among patients hospitalized with COVID-19: Findings from the American Heart Association’s COVID-19 Cardiovascular Disease Registry

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.