Author + information
- Pedro de Araújo Gonçalves, MD, PhD,
- Mauro Echavarria-Pinto, MD and
- Hector M. Garcia-Garcia, MD, PhD∗ ()
- ↵∗Thoraxcenter – Erasmus Medical Center, z120 Dr Molewaterplein 40, 3015 GD Rotterdam, the Netherlands
We read with interest the paper by Park et al. (1) concerning the association between certain atherosclerotic plaque characteristics (APCs), depicted by coronary computed tomography angiography (CTA) and the presence of ischemia by invasive fractional flow reserve (FFR). The study addressed the important issue of whether flow limiting lesions (FFR <0.80) have high-risk morphological plaque characteristics as assessed by coronary CTA.
In recent years, we have witnessed impressive technical improvements in coronary CTA temporal resolution and volume coverage, with associated reductions in scan time, contrast, and radiation doses, but these improvements have not been accompanied by significant changes in spatial resolution. This is of utmost importance when dealing with advanced coronary atherosclerosis imaging, as in this case of the reported coronary plaque features. We should be cautious and take into consideration the limitations already faced by invasive imaging modalities with a significantly higher spatial resolution. Coronary plaque characterization, namely, the identifications of features of vulnerability, has been the focus of extensive research using different coronary imaging modalities, such as intravascular ultrasound (IVUS), IVUS virtual histology, and optical coherence tomography, and although these allow for a better understanding of the footprints of the vulnerable plaque, their positive predictive value for major adverse cardiac events is still modest, as depicted by the PROSPECT (Providing Regional Observations to Study Predictors of Events in the Coronary Tree), VIVA (Viability Imaging in Volumetric Angiography), and ATHEROREMO (The European Collaborative Project on Inflammation and Vascular Wall Remodeling in Atherosclerosis - Intravascular Ultrasound Study) studies (2). In addition, there have been previous studies that correlated IVUS virtual histology characteristics and invasive FFR that failed to show any difference in plaque morphology between FFR <0.80 and their counterpart's lesions (3).
Limitations in coronary CTA spatial resolution might also influence the interobserver reproducibility of this APC, which was not reported by the investigators. Because this advanced coronary CTA plaque features requires very high image quality and expertise in post-processing and interpretation, what was the percentage of patients from the participating centers who were excluded from this study due to low image quality?
Another important limitation preventing the generalization of these findings is related to the threshold (<30 HU in the current study) for low attenuation plaque (LAP), because this has been shown to be largely influenced by lumen attenuation, which, in turn, is related to different contrast and scanning protocols (4). Therefore, it is difficult to establish thresholds for the definition of LAP that can be widely adopted. The definition of remodeling used by the investigators (“…maximal lesion vessel diameter divided by proximal reference vessel…PR defined as…≥1.1.”) can also be challenged. How reliable is the measurement of vessel diameter when the outer limits of the plaque are not easy to discern? Why did the investigators only use the proximal reference diameter (and not the mean), especially in the lengthy lesions (approximately 30 mm) when tapering of the vessel could be present, and why was a 1.1 cutoff used instead of 1.05?
If APCs have a significant influence on the likelihood that a certain lesion causes ischemia, how can we integrate these results with those from FFR-CT, which already has a good correlation with invasive FFR assessment, and does not take into consideration some of these APC-like positive remodeling and LAP?
Finally, the finding of a 17% rate of ischemia among nonobstructive (<50% stenosis) coronary CTA lesions is remarkable. This high rate of false-negative lesions might explain the worse than expected prognosis of patients with nonobstructive CAD, but who had high disease burden, because this has been recently demonstrated by our group and others using coronary atherosclerotic burden scores (5).
Please note: The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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