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Clinician’s Guide to Reducing Inflammation to Reduce Atherothrombotic Risk Proportion and Morphological Features of Restenosis Lesions With Acute Coronary Syndrome in Different Timings of Target Lesion Revascularization After Sirolimus-Eluting Stent Implantation Appropriate Use Criteria and Health Status Outcomes Following Chronic Total Occlusion Percutaneous Coronary Intervention: Insights From the OPEN-CTO Registry Impact of Coronary Lesion Complexity in Percutaneous Coronary Intervention: One-Year Outcomes From the Large, Multicentre e-Ultimaster Registry Intensive Care Utilization in Stable Patients With ST-Segment Elevation Myocardial Infarction Treated With Rapid Reperfusion Pharmacotherapy in the Management of Anxiety and Pain During Acute Coronary Syndromes and the Risk of Developing Symptoms of Posttraumatic Stress Disorder The Prognostic Significance of Periprocedural Infarction in the Era of Potent Antithrombotic Therapy: The PRAGUE-18 Substudy A Test in Context: E/A and E/e' to Assess Diastolic Dysfunction and LV Filling Pressure Linking Spontaneous Coronary Artery Dissection, Cervical Artery Dissection, and Fibromuscular Dysplasia: Heart, Brain, and Kidneys Genetic dysregulation of endothelin-1 is implicated in coronary microvascular dysfunction

Original Research2011 Aug;32(16):2059-66.

JOURNAL:Eur Heart J. Article Link

Impact of plaque components on no-reflow phenomenon after stent deployment in patients with acute coronary syndrome: a virtual histology-intravascular ultrasound analysis

Hong YJ, Jeong MH, Choi YH et al. Keywords: coronary disease, stents, plaque, ultrasonics

ABSTRACT


AIMS We used virtual histology-intravascular ultrasound (VH-IVUS) to evaluate the relation between coronary plaque characteristics and no-reflow in acute coronary syndrome (ACS) patients.


METHODS AND RESULTS - A total of 190 consecutive ACS patients were imaged using VH-IVUS and analysed retrospectively. Angiographic no-reflow was defined as TIMI flow grade 0, 1, and 2 after stenting. Virtual histology-intravascular ultrasound classified the colour-coded tissue into four major components: fibrotic, fibro-fatty, dense calcium, and necrotic core (NC). Thin-cap fibroatheroma (TCFA) was defined as focal, NC-rich (≥10% of the cross-sectional area) plaques being in contact with the lumen in a plaque burden≥40%. Of the 190 patients studied at pre-stenting, no-reflow was observed in 24 patients (12.6%) at post-stenting. The absolute and %NC areas at the minimum lumen sites (1.6±1.2 vs. 0.9±0.8 mm2, P<0.001, and 24.5±14.3 vs. 16.1±10.6%, P=0.001, respectively) and the absolute and %NC volumes (30±24 vs. 16±17 mm3, P=0.001, and 22±11 vs. 14±8%, P<0.001, respectively) were significantly greater, and the presence of at least one TCFA and multiple TCFAs within culprit lesions (71 vs. 36%, P=0.001, and 38 vs. 15%, P=0.005, respectively) was significantly more common in the no-reflow group compared with the normal-reflow group. In the multivariable analysis, %NC volume was the only independent predictor of no-reflow (odds ratio=1.126; 95% CI 1.045-1.214, P=0.002).

CONCLUSION - In ACS patients, post-stenting no-reflow is associated with plaque components defined by VH-IVUS analysis with larger NC and more TCFAs.