Cited by 571Lipoproteins and Cardiovascular HealthCoronary Interventions and DiagnosticsCardiac Imaging and Diagnostics

Impact of Statins on Serial Coronary Calcification During Atheroma Progression and Regression

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Puri, Rishi, Nicholls, Stephen J., Shao, Mingyuan, Kataoka, Yu, Uno, Kiyoko, Kapadia, Samir R., Tuzcu, E. Murat, Nissen, Steven E.·2015·Journal of the American College of Cardiology

Abstract

Background Statins can regress coronary atheroma and lower clinical events. Although pre-clinical studies suggest procalcific effects of statins in vitro, it remains unclear if statins can modulate coronary atheroma calcification in vivo. Objectives This study compared changes in coronary atheroma volume and calcium indices (CaI) in patients receiving high-intensity statin therapy (HIST), low-intensity statin therapy (LIST), and no-statin therapy. Methods In a post-hoc patient-level analysis of 8 prospective randomized trials using serial coronary intravascular ultrasound, serial changes in coronary percent atheroma volume (PAV) and CaI were measured across matched coronary segments in patients with coronary artery disease. Results Following propensity-weighted adjustment for differences in baseline and changes in clinical, laboratory, and ultrasonic characteristics, HIST (n = 1,545) associated with PAV regression from baseline (-0.6 ± 0.1%; p < 0.001), whereas both LIST (n = 1,726) and no-statin therapy (n = 224) associated with PAV progression (+0.8 ± 0.1% and +1.0 ± 0.1%; p < 0.001, respectively; p < 0.001 for both HIST vs. LIST and HIST vs. no-statin; p = 0.35 for LIST vs. no-statin). Significant increases in CaI from baseline were noted across all groups (median [interquartile range] HIST, +0.044 [0.0-0.12]; LIST, +0.038 [0.0-0.11]; no-statin, +0.020 [0.0-0.10]; p < 0.001 for all), which could relate to statin intensity (p = 0.03 for LIST vs. no-statin; p = 0.007 for HIST vs. no-statin; p = 0.18 for HIST vs. LIST). No correlations were found between changes in CaI and on-treatment levels of atherogenic and antiatherogenic lipoproteins, and C-reactive protein, in either of the HIST groups or the no-statin group. Conclusions Independent of their plaque-regressive effects, statins promote coronary atheroma calcification. These findings provide insight as to how statins may stabilize plaque beyond their effects on plaque regression.

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Cited by

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Authors
Puri, R., Nicholls, S. J., Shao, M., Kataoka, Y., Uno, K., Kapadia, S. R., Tuzcu, E. M., & Nissen, S. E.
Affiliations
  • Cleveland Clinic (US)
  • South Australian Health and Medical Research Institute (AU)
Corresponding author
Nissen, Steven E.
Venue
Journal of the American College of Cardiology
Publisher
Elsevier BV
Published
2015-04
Volume
65
Issue
13
Pages
1273-1282
ISSN
0735-1097 (ISSN-L)
OpenAlex
W2121363804
Cited by
571
References
1
Citations by year
2026: 32 · 2025: 30 · 2024: 44 · 2023: 49 · 2022: 56 · 2021: 69 · 2020: 66 · 2019: 50 · 2018: 57 · 2017: 39 · 2016: 58 · 2015: 20
FWCI
58.46
Type
journal article
Language
en
Open access
Locations
  • Journal of the American College of Cardiology (publishedVersion)
  • PubMed (publishedVersion)
  • Adelaide Research & Scholarship (AR&S) (University of Adelaide) (submittedVersion)
  • Institutional Repositories DataBase (IRDB) (submittedVersion)
Funders
  • Amgen
  • Eli Lilly and Company
  • Pfizer
  • AstraZeneca
  • Anthera
  • Novo Nordisk
  • Esperion Therapeutics
Topics
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
  • Health Sciences › Medicine › Surgery › Coronary Interventions and Diagnostics
  • Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
Keywords
statins, high-intensity statin therapy, coronary artery disease, intravascular ultrasound, plaque stabilization, lipoproteins, C-reactive protein, atheroma progression, atheroma regression
MeSH terms
Aged, Calcium, Coronary Artery Disease, Coronary Vessels, Female, Humans, Male, Middle Aged, Prospective Studies, Ultrasonography, Interventional, Disease Progression, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Plaque, Atherosclerotic, Vascular Calcification

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