Author + information
- Gauravpal S. Gill, MD and
- Hector M. Garcia-Garcia, MD, PhD∗ ( )()
- ↵∗Section of Interventional Cardiology, MedStar Washington Hospital Center, 110 Irving Street, NW, Suite 4B-1, Washington, DC 20010
We eagerly read the report by Lee et al. (1) that found slower rate of total and noncalcified percentage of atheroma volume (PAV) progression and a faster progression of calcified PAV in statin-taking patients without history of coronary artery disease who underwent coronary computed tomography angiography at an interscan interval ≥2 years when compared with statin-naïve patients. To gain an understanding of the results, some questions remain unanswered.
This report conflicts with other progression/regression trials for the following reasons: 1) the percentage of stenosis severity does not correlate with the baseline percentage of PAV because, per the Glagov phenomenon, PAV >40% starts encroaching the lumen. Therefore, 13% diameter stenosis should correspond to a PAV much >40%. Indeed, most progression/regression clinical trials have baseline PAV of ∼40%. 2) The observed annual change in PAV in patients taking statins is not only going in the direction of progression (instead of regression), but it is also much larger than any previous report.
In the interscan interval, 8.1% of patients underwent revascularization (surgical and percutaneous) with a significantly higher number of patients belonging to statin-taking group (n = 96) than the statin-naïve group (n = 6) (p = 0.001), which contradicts the slower high-risk plaque progression in the statin-taking group. Also, the number of lesions in the statin-taking patients with diameter stenosis ≥50% is reported as 76 at follow-up, which is lower than the number of revascularizations in the group during the interscan period.
Inclusion of lesions that were revascularized in the interscan period may have further confounded the results if these segments have been excluded in the analysis.
Intensity, duration, and type of statin therapy were not indicated in the study although they are important factors as prior studies have shown data that change in atheroma size is not constant with different statins.
The number of patients starting therapy during the interscan period is significantly high (38.8%), and the exclusion of data for their time of initiation of therapy can have an impact on annualized change in PAV.
Lastly, we feel the inclusion of absolute data for external elastic membrane, lumen, and plaque volumes should be included. Stenosis severity percentage in the population is clinically insignificant, so the results of this study therefore cannot be generalized to a population with clinically significant disease.
Please note: Both authors have reported that they have no relationships relevant to the contents of this paper to disclose.
- 2018 American College of Cardiology Foundation