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Superficial Calcium Fracture After PCI as Assessed by OCT Transthoracic echocardiography for the evaluation of children and adolescents with suspected or confirmed pulmonary hypertension. Expert consensus statement on the diagnosis and treatment of paediatric pulmonary hypertension. The European Paediatric Pulmonary Vascular Disease Network, endorsed by ISHLT and D6PK Long-Term Clinical Outcomes and Optimal Stent Strategy in Left Main Coronary Bifurcation Stenting Self-expandable sirolimus-eluting stents compared to second-generation drug-eluting stents for the treatment of the left main: A propensity score analysis from the SPARTA and the FAILS-2 registries Medical Therapy for CTEPH: Is There Still Space for More? Autologous CD34+ Stem Cell Therapy Increases Coronary Flow Reserve and Reduces Angina in Patients With Coronary Microvascular Dysfunction Sotatercept for the Treatment of Pulmonary Arterial Hypertension Machine Learning Using CT-FFR Predicts Proximal Atherosclerotic Plaque Formation Associated With LAD Myocardial Bridging Dual Antiplatelet Therapy after PCI in Patients at High Bleeding Risk Pancoronary Plaque Characteristics in STEMI Caused by Culprit Plaque Erosion Versus Rupture: 3-Vessel OCT Study

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.