CBS 2019
CBSMD教育中心
中 文

推荐文献

Abstract

Recommended Article

Inflammation: A New Target For CAD Treatment and Prevention Blood CSF1 and CXCL12 as Causal Mediators of Coronary Artery Disease Temporal trends in percutaneous coronary interventions thru the drug eluting stent era: Insights from 18,641 procedures performed over 12-year period Use of Risk Assessment Tools to Guide Decision-Making in the Primary Prevention of Atherosclerotic Cardiovascular Disease A Special Report From the American Heart Association and American College of Cardiology Predicting the 10-Year Risks of Atherosclerotic Cardiovascular Disease in Chinese Population: The China-PAR Project (Prediction for ASCVD Risk in China) Incidence, Treatment, and Outcomes of Coronary Perforation During Chronic Total Occlusion Percutaneous Coronary Intervention ACC临床简报:新型冠状病毒对心脏的影响(2019-nCoV) Correction of a pathogenic gene mutation in human embryos

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.