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Complex PCI procedures: challenges for the interventional cardiologist Management of Asymptomatic Severe Aortic Stenosis: Evolving Concepts in Timing of Valve Replacement A Controlled Trial of Rivaroxaban After Transcatheter Aortic-Valve Replacement Comparison of Early Surgical or Transcatheter Aortic Valve Replacement Versus Conservative Management in Low-Flow, Low-Gradient Aortic Stenosis Using Inverse Probability of Treatment Weighting: Results From the TOPAS Prospective Observational Cohort Study Anticoagulation After Surgical or Transcatheter Bioprosthetic Aortic Valve Replacement Balloon Aortic Valvuloplasty as a Bridge to Aortic Valve Replacement: A Contemporary Nationwide Perspective A Review of the Role of Breast Arterial Calcification for Cardiovascular Risk Stratification in Women Association of Coronary Artery Calcium With Long-term, Cause-Specific Mortality Among Young Adults Pulmonary arterial hypertension in congenital heart disease: an epidemiologic perspective from a Dutch registry Expansion or contraction of stenting in coronary artery disease?
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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.


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