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From Subclinical Atherosclerosis to Plaque Progression and Acute Coronary Events Timing of Intervention in Aortic Stenosis Minimizing Permanent Pacemaker Following Repositionable Self-Expanding Transcatheter Aortic Valve Replacement From Focal Lipid Storage to Systemic Inflammation Bioprosthetic valve oversizing is associated with increased risk of valve thrombosis following TAVR Aliskiren, Enalapril, or Aliskiren and Enalapril in Heart Failure Coronary plaque redistribution after stent implantation is determined by lipid composition: A NIRS-IVUS analysis Sex- and Race-Related Differences in Characteristics and Outcomes of Hospitalizations for Heart Failure With Preserved Ejection Fraction Suture- or Plug-Based Large-Bore Arteriotomy Closure: A Pilot Randomized Controlled Trial Health Status after Transcatheter vs. Surgical Aortic Valve Replacement in Low-Risk Patients with Aortic Stenosis
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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.
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