Author + information
- Christos V. Bourantas, MD, PhD,
- Stella-Lida Papadopoulou, MD,
- Patrick W. Serruys, MD, PhD,
- Antonis Sakellarios, MSc,
- Pieter H. Kitslaar, MSc,
- Paschalis Bizopoulos, MSc,
- Chrysafios Girasis, MD, PhD,
- Yao-Jun Zhang, MD, PhD,
- Ton de Vries, MSc,
- Eric Boersma, PhD, MSc,
- Michail I. Papafaklis, MD, PhD,
- Katerina K. Naka, MD, PhD,
- Dimitrios I. Fotiadis, PhD,
- Gregg W. Stone, MD,
- Johan H.C. Reiber, PhD,
- Lampros K. Michalis, MD,
- Pim J. de Feyter, MD, PhD and
- Hector M. Garcia-Garcia, MD, PhD∗ ()
- ↵∗Thoraxcenter, Erasmus MC, z120 Dr Molewaterplein 40, 3015 GD Rotterdam, the Netherlands
Intravascular imaging-based natural history studies of atherosclerosis have provided insight into atherosclerotic evolution and demonstrated that local hemodynamic factors, plaque burden, and the composition of the atheroma regulate plaque growth and determine vulnerable plaque formation (1,2). However, intravascular imaging is time consuming, is associated with a risk of complications, and does not allow complete assessment of plaque pathophysiology. Recent reports suggest that multislice computed tomography (MSCT) provides useful prognostic information and permits reliable quantification of luminal dimensions and plaque burden, characterization of the composition of the plaque, coronary reconstruction blood flow simulation, and estimation of the local endothelial shear stress (ESS) (3). However, the potential of MSCT in identifying lesions that are prone to progress is undetermined.
The present analysis processed data from the patients enrolled in the PROSPECT-MSCT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree-MSCT) study in order to investigate the value of MSCT-derived variables in predicting plaque evolution (4). PROSPECT-MSCT recruited 32 patients with an acute coronary syndrome, who were enrolled in the PROSPECT study, and underwent MSCT imaging at baseline (after percutaneous coronary intervention of the culprit lesions responsible for the acute coronary syndrome), and at 3-year follow-up. The MSCT data at baseline were used to estimate the luminal dimensions, plaque burden, and composition (3); reconstruct coronary anatomy; and perform blood flow simulation (1). The studied vessels were divided into 3-mm subsegments, and the baseline MSCT-derived plaque characteristics and predominant ESS (defined as the minimum averaged ESS in an arc of 90°) in each 3-mm subsegment were used to identify predictors associated with the changes in the luminal dimensions and atheroma burden and composition at follow-up (1). We define as significant disease progression an increase >21.6% of the plaque area at follow-up. This cutoff was selected based on the intraobserver variability (>2 standard deviations) of the expert who performed the analysis of the MSCT data (5).
The baseline characteristics of the studied population have been presented elsewhere (5). Fifty-eight coronary arteries (median length 41.3 [25.4 to 55.4] mm, 735 3-mm subsegments) that did not contain a treated culprit lesion were included in the analysis. The MSCT-derived variables associated with a reduction in luminal dimensions, an increase in plaque area and burden, and an increase in the necrotic core component are shown in Table 1. The plaque burden and composition appeared as independent predictor in most of the multivariate analyses. Low ESS was independently associated with the changes in lumen area and plaque burden, it was associated with the changes in the necrotic core component in the univariate, but not in the multivariate analysis, and it did not appear to affect the changes in plaque area.
At 3-year follow-up, 176 (23.9%) segments exhibited >21.6% increase in plaque area. Low ESS, plaque and burden, increasing % fibrofatty tissue component, and a decreasing % fibrotic tissue component appeared as predictors of disease progression. In the multivariate model only, decreasing plaque burden (odds ratio: 1.72; 95% confidence interval: 1.10 to 2.70; p = 0.018) and decreasing % fibrotic tissue component (odds ratio: 1.41; 95% confidence interval: 1.04 to 1.91; p = 0.026) were independently associated with plaque progression. The accuracy of the model created from the independent predictors of disease progression was 59.0%. The sensitivity, specificity, positive and negative predictive values, and the positive and negative likelihood ratios were 70.5%, 54.9%, 33.0%, 85.5%, 1.56, and 0.54, respectively.
The present analysis for the first time investigated the potential value of MSCT-derived plaque characteristics in identifying lesions that are likely to progress at 3-year follow-up. We found that: 1) low ESS and increased baseline lumen area were predictors of lumen decrease at follow-up; 2) decreased plaque area and burden were independently associated with an increase in plaque area at follow-up; 3) low ESS and decreased plaque area and burden and increased calcific tissue component were independently related with an increase in plaque burden at follow-up; and 4) a low plaque area and burden and an increased fibrofatty and fibrous tissue component were independently related to an increase in the necrotic core at follow-up. Interestingly, the results reported in this study are very similar to those presented in other invasive-based imaging studies (1,5). However, MSCT is a noninvasive modality, able to provide a holistic assessment of plaque burden and composition, and allows reconstruction of the entire coronary tree including coronary bifurcations. These unique features render it an attractive alternative for the study of atherosclerotic evolution. Our analysis showed that MSCT-derived variables had a moderate accuracy in detecting lesions that are likely to progress at follow-up. The potential value of this modality in the detection of vulnerable, prone-to-rupture plaques requires further investigation in the context of a large-scale natural history study of atherosclerosis.
Please note: Dr. Bourantas is funded by the Hellenic Cardiological Society, Athens, Greece. Mr. de Vries is an employee of Cardialysis BV. Dr. Stone is a consultant for Abbott Vascular, Volcano Corporation, and InfraReDx. Dr. Reiber has a part-time appointment as Professor of Medical Imaging at the Leiden University Medical Center (LUMC); and is the CEO and has equity in Medis medical imaging systems. Mr. Kitslaar has a research appointment at the LUMC; and is an employee of Medis medical imaging systems. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose. David Bluemke, MD, served as Guest Editor for this paper.
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