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The Tricuspid Annular Plane Systolic Excursion to Systolic Pulmonary Artery Pressure Index: Association With All-Cause Mortality in Patients With Moderate or Severe Tricuspid Regurgitation Five-Year Clinical Outcomes After Drug-Eluting Stent Implantation Following Rotational Atherectomy for Heavily Calcified Lesions Orbital atherectomy for the treatment of small (2.5mm) severely calcified coronary lesions: ORBIT II sub-analysis Risk of Atrial Fibrillation According to Cancer Type: A Nationwide Population-Based Study Incidence and Standardized Definitions of Mitral Valve Leaflet Adverse Events After Transcatheter Mitral Valve Repair: the EXPAND Study Pathophysiology, diagnosis and new therapeutic approaches for ischemic mitral regurgitation An artificial intelligence-enabled ECG algorithm for the identification of patients with atrial fibrillation during sinus rhythm: a retrospective analysis of outcome prediction Novel Transcatheter Mitral Valve Prosthesis for Patients With Severe Mitral Annular Calcification Outcomes of TTVI in Patients With Pacemaker or Defibrillator Leads: Data From the TriValve Registry Cardio-Oncology Services: rationale, organization, and implementation: A report from the ESC Cardio-Oncology council
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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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