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Anatomical Attributes of Clinically Relevant Diagonal Branches in Patients with Left Anterior Descending Coronary Artery Bifurcation Lesions The Impact of Coronary Physiology on Contemporary Clinical Decision Making Echocardiographic Screening for Pulmonary Hypertension in Congenital Heart Disease Noninvasive Screening for Pulmonary Hypertension by Exercise Testing in Congenital Heart Disease Spontaneous Coronary Artery Dissection: Pathophysiological Insights From Optical Coherence Tomography Three-Year Outcomes of the DKCRUSH-V Trial Comparing DK Crush With Provisional Stenting for Left Main Bifurcation Lesions Double-Kissing Culotte Technique for Coronary Bifurcation Stenting - Technical evaluation and comparison with conventional double stenting techniques Prognostic Implications of Plaque Characteristics and Stenosis Severity in Patients With Coronary Artery Disease Clinical use of intracoronary imaging. Part 1: guidance and optimization of coronary interventions. An expert consensus document of the European Association of Percutaneous Cardiovascular Interventions: Endorsed by the Chinese Society of Cardiology Physiological Stratification of Patients With Angina Due to Coronary Microvascular Dysfunction
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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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