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Mild Hypothermia in Cardiogenic Shock Complicating Myocardial Infarction - The Randomized SHOCK-COOL Trial Inflammatory Bowel Disease and Acute Coronary Syndromes: From Pathogenesis to the Fine Line Between Bleeding and Ischemic Risk Prognostic Value of SYNTAX Score in Patients With Infarct-Related Cardiogenic Shock: Insights From the CULPRIT-SHOCK Trial Subcutaneous Selatogrel Inhibits Platelet Aggregation in Patients With Acute Myocardial Infarction Complete Revascularization During Primary Percutaneous Coronary Intervention Reduces Death and Myocardial Infarction in Patients With Multivessel Disease-Meta-Analysis and Meta-Regression of Randomized Trials Evaluation and Management of Nonculprit Lesions in STEMI Circulating MicroRNAs and Monocyte-Platelet Aggregate Formation in Acute Coronary Syndrome Use of Mechanical Circulatory Support Devices Among Patients With Acute Myocardial Infarction Complicated by Cardiogenic Shock Short Sleep Duration, Obstructive Sleep Apnea, Shiftwork, and the Risk of Adverse Cardiovascular Events in Patients After an Acute Coronary Syndrome Classic crush and DK crush stenting techniques

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.