CBS 2019
CBSMD教育中心
English

科学研究

科研文章

荐读文献

Relationship Between Hospital Surgical Aortic Valve Replacement Volume and Transcatheter Aortic Valve Replacement Outcomes Infective Endocarditis After Transcatheter Aortic Valve Replacement Adenosine and adenosine receptor-mediated action in coronary microcirculation Decline in Left Ventricular Ejection Fraction During Follow-Up in Patients With Severe Aortic Stenosis Differences between the left main and other bifurcations Ascending Aortic Length and Risk of Aortic Adverse Events: The Neglected Dimension New-onset atrial fibrillation after PCI and CABG for left main disease: insights from the EXCEL trial and additional studies Comparative effectiveness analysis of percutaneous coronary intervention versus coronary artery bypass grafting in patients with chronic kidney disease and unprotected left main coronary artery disease Surgical ineligibility and mortality among patients with unprotected left main or multivessel coronary artery disease undergoing percutaneous coronary intervention Active SB-P Versus Conventional Approach to the Protection of High-Risk Side Branches: The CIT-RESOLVE Trial

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.