Association between continuous variables was assessed by Pearson’s correlation coefficient and linear regression. Outliers were removed using the median absolute deviation method (threshold 3.5). Model diagnostics were performed by inspecting residual and Q–Q plots to test model assumptions. Potential confounding factors were included in multivariable regression analyses to assess robustness of the main study findings. Adjustment of P values for multiple comparisons was performed using the Bonferroni method. All plaque anatomical, geometric, compositional or PSS measurements were analysed by LME on frame-based data in each patient unless otherwise indicated. Statistical analysisĪs each plaque had multiple VH-IVUS frames, linear mixed-effects (LME) models were used to account for hierarchical data structure and clustering in individual patients undergoing different treatments, and results presented as mean ± standard error (SE). 16 Maximum principal stress in the peri-luminal region was used to indicate critical mechanical conditions within the structure. Vessel geometry and plaque composition were extracted and 2D dynamic FEA simulations performed as described previously ( Supplementary material online). A total of 4933 frames with <30% stenosis or containing significant side branches or immediately adjacent to bifurcations were excluded from finite element analysis (FEA) due to violating the plane strain assumption for 2-dimensional (2D) solid modelling. 22 Biomechanical analysisĮach vessel generated an average of 169 (136–212) (median, interquartile range) baseline and follow-up VH-IVUS frames (total = 10 517 frames). We also calculated lumen aspect ratio (ratio between maximum/minimum diameter of ellipse) to measure lumen eccentricity, lumen curvature (computed using the radius of the circle determined by the point of interest and 2 adjacent points) to measure lumen angulation, lumen irregularity (variation in luminal angulation), and lumen roughness (lumen surface evenness in respect to curvature) ( Supplemental material online, Figure S1). Matching was confirmed by two analysts and showed good reproducibility (see Supplementary material online). Frames were rotated using anatomical landmarks and lumen shape matching for circumferential alignment. side branches, stenosis, calcification/large lipid cores). Lumen and external elastic membrane (EEM) areas, plaque area (PA, defined as plaque and media = EEM − lumen areas), PB (defined as 100% × PA/EEM area), and plaque composition were calculated between baseline and follow-up.īaseline and follow-up VH-IVUS frames were co-registered longitudinally using anatomical landmarks (e.g.
Incontrol intensity software#
Data were analysed offline using echoPlaque 4.0 (Indec Medical, San Jose, USA) and QIVUS software (Medis, Leiden, Netherlands). All images underwent quality control assessment by experienced investigators blinded to clinical data at Emory Cardiovascular Imaging and Biomechanical Core Laboratory (control and atorvastatin) or Cardialysis B.V., Rotterdam (rosuvastatin). Radiofrequency data were captured on the R-wave using ECG-triggered acquisition. Images were acquired with phased-array 20-MHz Eagle Eye catheters (Volcano Corp., Rancho Cordova, USA) using 0.5-mm/s automated motorized pullback. Virtual-histology intravascular ultrasound 20, 21 We analysed only left anterior descending arteries as US studies included only these arteries. 19 Atorvastatin-treated patients presented with either stable angina or ACS with moderate lesions, while rosuvastatin-treated patients presented with ST-segment elevation myocardial infarction, with study of moderate lesions in non-culprit vessels. 4, 5 Lipid-lowering with statins and proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors reduce MACE by 25–40%, 1, 2, 6 despite modest reductions in lumen stenosis 7 and 0.80].
1, 2 In particular, patients presenting with acute coronary syndrome (ACS) demonstrate multiple vulnerable plaques and simultaneous plaque ruptures in non-culprit vessels, 3 confirming the multifocal nature of unstable atherosclerosis, and prospective studies show that 50% of future MACE occur in non-culprit vessels. Atherosclerosis, Plaque architecture, Plaque structural stress, Virtual-histology intravascular ultrasound Introductionĭespite current optimal medical and interventional management, patients with coronary artery disease (CAD) have significant risk of future major adverse cardiovascular events (MACE).
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