Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition

Alexander R. Van Rosendael; Inge J. Van Den Hoogen; Umberto Gianni; Xiaoyue Ma; Sara W. Tantawy; A. Maxim Bax; Yao Lu; Daniele Andreini; Mouaz H. Al-Mallah; Matthew J. Budoff; Filippo Cademartiri; Kavitha Chinnaiyan; Jung Hyun Choi; Edoardo Conte; Hugo Marques; Pedro De Araújo Gonçalves; Ilan Gottlieb; Martin Hadamitzky; Jonathon A. Leipsic; Erica Maffei; Gianluca Pontone; Sanghoon Shin; Yong Jin Kim; Byoung Kwon Lee; Eun Ju Chun; Ji Min Sung; Sang Eun Lee; Renu Virmani; Habib Samady; Yu Sato; Peter H. Stone; Daniel S. Berman; Jagat Narula; Ron Blankstein; James K. Min; Fay Y. Lin; Leslee J. Shaw; Jeroen J. Bax; Hyuk Jae Chang

doi:10.1001/jamacardio.2021.3055

Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition

Alexander R. Van Rosendael, Inge J. Van Den Hoogen, Umberto Gianni, Xiaoyue Ma, Sara W. Tantawy, A. Maxim Bax, Yao Lu, Daniele Andreini, Mouaz H. Al-Mallah, Matthew J. Budoff, Filippo Cademartiri, Kavitha Chinnaiyan, Jung Hyun Choi, Edoardo Conte, Hugo Marques, Pedro De Araújo Gonçalves, Ilan Gottlieb, Martin Hadamitzky, Jonathon A. Leipsic, Erica MaffeiGianluca Pontone, Sanghoon Shin, Yong Jin Kim, Byoung Kwon Lee, Eun Ju Chun, Ji Min Sung, Sang Eun Lee, Renu Virmani, Habib Samady, Yu Sato, Peter H. Stone, Daniel S. Berman, Jagat Narula, Ron Blankstein, James K. Min, Fay Y. Lin, Leslee J. Shaw, Jeroen J. Bax, Hyuk Jae Chang

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

25 Citations (Scopus)

Abstract

Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P =.001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P <.001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P =.24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium..

Original language	English
Pages (from-to)	1257-1266
Number of pages	10
Journal	JAMA Cardiology
Volume	6
Issue number	11
DOIs	https://doi.org/10.1001/jamacardio.2021.3055
Publication status	Published - 2021 Nov

Bibliographical note

Funding Information:
reported receiving grants from the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea funded by the Ministry of Science and ICT during the conduct of the study. Dr Budoff reported receiving grants from General Electric outside the submitted work. Dr Chinnaiyan reported receiving grants from HeartFlow outside the submitted work and being on the medical advisory board of HeartFlow. Dr Leipsic reported receiving grants from Abbott, Boston Scientific, Core Lab, Edwards LifeSciences, and Medtronic; receiving personal fees from HeartFlow and from Circle CVI during the conduct of the study; and receiving personal fees from Philips and from GE Healthcare outside the submitted work. Dr Virmani reported receiving grants from 480 Biomedical, 4C Medical, 4Tech Inc, Accumedical, Alivas, Amgen, Biosensors, Cardiac Implants, Canon U.S.A., Claret Medical, Concept Medical, Cordis, DuNing Inc, Endotronix, Emboline, Endotronix, Envision Scientific, Gateway, Leducq Foundation, Lifetech, Limflo, MedAlliance, Mercator, Mitra assist, Microport Medical, Microvention, Mitraalign, the National Institutes of Health, NIPRO, NAMSA, Nanova, Neovasc, Phenox, Novogate, Occulotech, Protembis, Profusa, Shockwave, Qool, Senseonics, Symic, Spectranetics, and Vesper; and receiving personal fees from Abbott Vascular, Boston Scientific, Celonova, Cook Medical, CSI, Edwards LifeSciences, Lutonix/Bard, Medtronic, OrbusNeich Medical, ReCor Medical, Sinomed Medical, Surmodics, Terumo, W.L. Gore, and Xeltis outside the submitted work. Dr Samady reported receiving grants from Medtronic; receiving personal fees from Abbott and from Philips during the conduct of the study; and being a co-founder and equity holder in Covanos outside the submitted work. Dr Blankstein reported receiving grants from Amgen and from Astellas Inc; and receiving personal fees from Amgen outside the submitted work. Dr Min reported having an equity interest and being an employee of Cleerly Inc; and being a medical advisory board member of Arineta during the conduct of the study. Dr Lin reported receiving grants from GE Healthcare outside the submitted work. Dr Shaw reported having an equity interest in Cleerly Inc and being a scientific advisory board member for Covanos Inc. No other disclosures were reported.

Funding Information:
Funding/Support: This work was supported by the Leading Foreign Research Institute Recruitment Program through grant 2012027176 from the National Research Foundation of Korea funded by the Ministry of Science and ICT. The study was also funded in part by gifts from the Dalio Institute of Cardiovascular Imaging and the Michael Wolk Heart Foundation.

Publisher Copyright:
© 2021 American Medical Association. All rights reserved.

All Science Journal Classification (ASJC) codes

Cardiology and Cardiovascular Medicine

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10.1001/jamacardio.2021.3055

Cite this

Van Rosendael, A. R., Van Den Hoogen, I. J., Gianni, U., Ma, X., Tantawy, S. W., Bax, A. M., Lu, Y., Andreini, D., Al-Mallah, M. H., Budoff, M. J., Cademartiri, F., Chinnaiyan, K., Choi, J. H., Conte, E., Marques, H., De Araújo Gonçalves, P., Gottlieb, I., Hadamitzky, M., Leipsic, J. A., ... Chang, H. J. (2021). Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition. JAMA Cardiology, 6(11), 1257-1266. https://doi.org/10.1001/jamacardio.2021.3055

@article{f16e730579754a2e9e2899558fc8a568,

title = "Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition",

abstract = "Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P =.001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P <.001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P =.24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium..",

author = "{Van Rosendael}, {Alexander R.} and {Van Den Hoogen}, {Inge J.} and Umberto Gianni and Xiaoyue Ma and Tantawy, {Sara W.} and Bax, {A. Maxim} and Yao Lu and Daniele Andreini and Al-Mallah, {Mouaz H.} and Budoff, {Matthew J.} and Filippo Cademartiri and Kavitha Chinnaiyan and Choi, {Jung Hyun} and Edoardo Conte and Hugo Marques and {De Ara{\'u}jo Gon{\c c}alves}, Pedro and Ilan Gottlieb and Martin Hadamitzky and Leipsic, {Jonathon A.} and Erica Maffei and Gianluca Pontone and Sanghoon Shin and Kim, {Yong Jin} and Lee, {Byoung Kwon} and Chun, {Eun Ju} and Sung, {Ji Min} and Lee, {Sang Eun} and Renu Virmani and Habib Samady and Yu Sato and Stone, {Peter H.} and Berman, {Daniel S.} and Jagat Narula and Ron Blankstein and Min, {James K.} and Lin, {Fay Y.} and Shaw, {Leslee J.} and Bax, {Jeroen J.} and Chang, {Hyuk Jae}",

note = "Funding Information: reported receiving grants from the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea funded by the Ministry of Science and ICT during the conduct of the study. Dr Budoff reported receiving grants from General Electric outside the submitted work. Dr Chinnaiyan reported receiving grants from HeartFlow outside the submitted work and being on the medical advisory board of HeartFlow. Dr Leipsic reported receiving grants from Abbott, Boston Scientific, Core Lab, Edwards LifeSciences, and Medtronic; receiving personal fees from HeartFlow and from Circle CVI during the conduct of the study; and receiving personal fees from Philips and from GE Healthcare outside the submitted work. Dr Virmani reported receiving grants from 480 Biomedical, 4C Medical, 4Tech Inc, Accumedical, Alivas, Amgen, Biosensors, Cardiac Implants, Canon U.S.A., Claret Medical, Concept Medical, Cordis, DuNing Inc, Endotronix, Emboline, Endotronix, Envision Scientific, Gateway, Leducq Foundation, Lifetech, Limflo, MedAlliance, Mercator, Mitra assist, Microport Medical, Microvention, Mitraalign, the National Institutes of Health, NIPRO, NAMSA, Nanova, Neovasc, Phenox, Novogate, Occulotech, Protembis, Profusa, Shockwave, Qool, Senseonics, Symic, Spectranetics, and Vesper; and receiving personal fees from Abbott Vascular, Boston Scientific, Celonova, Cook Medical, CSI, Edwards LifeSciences, Lutonix/Bard, Medtronic, OrbusNeich Medical, ReCor Medical, Sinomed Medical, Surmodics, Terumo, W.L. Gore, and Xeltis outside the submitted work. Dr Samady reported receiving grants from Medtronic; receiving personal fees from Abbott and from Philips during the conduct of the study; and being a co-founder and equity holder in Covanos outside the submitted work. Dr Blankstein reported receiving grants from Amgen and from Astellas Inc; and receiving personal fees from Amgen outside the submitted work. Dr Min reported having an equity interest and being an employee of Cleerly Inc; and being a medical advisory board member of Arineta during the conduct of the study. Dr Lin reported receiving grants from GE Healthcare outside the submitted work. Dr Shaw reported having an equity interest in Cleerly Inc and being a scientific advisory board member for Covanos Inc. No other disclosures were reported. Funding Information: Funding/Support: This work was supported by the Leading Foreign Research Institute Recruitment Program through grant 2012027176 from the National Research Foundation of Korea funded by the Ministry of Science and ICT. The study was also funded in part by gifts from the Dalio Institute of Cardiovascular Imaging and the Michael Wolk Heart Foundation. Publisher Copyright: {\textcopyright} 2021 American Medical Association. All rights reserved.",

year = "2021",

month = nov,

doi = "10.1001/jamacardio.2021.3055",

language = "English",

volume = "6",

pages = "1257--1266",

journal = "JAMA Cardiology",

issn = "2380-6583",

publisher = "American Medical Association",

number = "11",

}

Van Rosendael, AR, Van Den Hoogen, IJ, Gianni, U, Ma, X, Tantawy, SW, Bax, AM, Lu, Y, Andreini, D, Al-Mallah, MH, Budoff, MJ, Cademartiri, F, Chinnaiyan, K, Choi, JH, Conte, E, Marques, H, De Araújo Gonçalves, P, Gottlieb, I, Hadamitzky, M, Leipsic, JA, Maffei, E, Pontone, G, Shin, S, Kim, YJ, Lee, BK, Chun, EJ, Sung, JM, Lee, SE, Virmani, R, Samady, H, Sato, Y, Stone, PH, Berman, DS, Narula, J, Blankstein, R, Min, JK, Lin, FY, Shaw, LJ, Bax, JJ & Chang, HJ 2021, 'Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition', JAMA Cardiology, vol. 6, no. 11, pp. 1257-1266. https://doi.org/10.1001/jamacardio.2021.3055

TY - JOUR

T1 - Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition

AU - Van Rosendael, Alexander R.

AU - Van Den Hoogen, Inge J.

AU - Gianni, Umberto

AU - Ma, Xiaoyue

AU - Tantawy, Sara W.

AU - Bax, A. Maxim

AU - Lu, Yao

AU - Andreini, Daniele

AU - Al-Mallah, Mouaz H.

AU - Budoff, Matthew J.

AU - Cademartiri, Filippo

AU - Chinnaiyan, Kavitha

AU - Choi, Jung Hyun

AU - Conte, Edoardo

AU - Marques, Hugo

AU - De Araújo Gonçalves, Pedro

AU - Gottlieb, Ilan

AU - Hadamitzky, Martin

AU - Leipsic, Jonathon A.

AU - Maffei, Erica

AU - Pontone, Gianluca

AU - Shin, Sanghoon

AU - Kim, Yong Jin

AU - Lee, Byoung Kwon

AU - Chun, Eun Ju

AU - Sung, Ji Min

AU - Lee, Sang Eun

AU - Virmani, Renu

AU - Samady, Habib

AU - Sato, Yu

AU - Stone, Peter H.

AU - Berman, Daniel S.

AU - Narula, Jagat

AU - Blankstein, Ron

AU - Min, James K.

AU - Lin, Fay Y.

AU - Shaw, Leslee J.

AU - Bax, Jeroen J.

AU - Chang, Hyuk Jae

N1 - Funding Information: reported receiving grants from the Leading Foreign Research Institute Recruitment Program through the National Research Foundation of Korea funded by the Ministry of Science and ICT during the conduct of the study. Dr Budoff reported receiving grants from General Electric outside the submitted work. Dr Chinnaiyan reported receiving grants from HeartFlow outside the submitted work and being on the medical advisory board of HeartFlow. Dr Leipsic reported receiving grants from Abbott, Boston Scientific, Core Lab, Edwards LifeSciences, and Medtronic; receiving personal fees from HeartFlow and from Circle CVI during the conduct of the study; and receiving personal fees from Philips and from GE Healthcare outside the submitted work. Dr Virmani reported receiving grants from 480 Biomedical, 4C Medical, 4Tech Inc, Accumedical, Alivas, Amgen, Biosensors, Cardiac Implants, Canon U.S.A., Claret Medical, Concept Medical, Cordis, DuNing Inc, Endotronix, Emboline, Endotronix, Envision Scientific, Gateway, Leducq Foundation, Lifetech, Limflo, MedAlliance, Mercator, Mitra assist, Microport Medical, Microvention, Mitraalign, the National Institutes of Health, NIPRO, NAMSA, Nanova, Neovasc, Phenox, Novogate, Occulotech, Protembis, Profusa, Shockwave, Qool, Senseonics, Symic, Spectranetics, and Vesper; and receiving personal fees from Abbott Vascular, Boston Scientific, Celonova, Cook Medical, CSI, Edwards LifeSciences, Lutonix/Bard, Medtronic, OrbusNeich Medical, ReCor Medical, Sinomed Medical, Surmodics, Terumo, W.L. Gore, and Xeltis outside the submitted work. Dr Samady reported receiving grants from Medtronic; receiving personal fees from Abbott and from Philips during the conduct of the study; and being a co-founder and equity holder in Covanos outside the submitted work. Dr Blankstein reported receiving grants from Amgen and from Astellas Inc; and receiving personal fees from Amgen outside the submitted work. Dr Min reported having an equity interest and being an employee of Cleerly Inc; and being a medical advisory board member of Arineta during the conduct of the study. Dr Lin reported receiving grants from GE Healthcare outside the submitted work. Dr Shaw reported having an equity interest in Cleerly Inc and being a scientific advisory board member for Covanos Inc. No other disclosures were reported. Funding Information: Funding/Support: This work was supported by the Leading Foreign Research Institute Recruitment Program through grant 2012027176 from the National Research Foundation of Korea funded by the Ministry of Science and ICT. The study was also funded in part by gifts from the Dalio Institute of Cardiovascular Imaging and the Michael Wolk Heart Foundation. Publisher Copyright: © 2021 American Medical Association. All rights reserved.

PY - 2021/11

Y1 - 2021/11

N2 - Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P =.001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P <.001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P =.24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium..

AB - Importance: The density of atherosclerotic plaque forms the basis for categorizing calcified and noncalcified morphology of plaques. Objective: To assess whether alterations in plaque across a range of density measurements provide a more detailed understanding of atherosclerotic disease progression. Design, Setting, and Participants: This cohort study enrolled 857 patients who underwent serial coronary computed tomography angiography 2 or more years apart and had quantitative measurements of coronary plaques throughout the entire coronary artery tree. The study was conducted from 2013 to 2016 at 13 sites in 7 countries. Main Outcomes and Measures: The main outcome was progression of plaque composition of individual coronary plaques. Six plaque composition types were defined on a voxel-level basis according to the plaque attenuation (expressed in Hounsfield units [HU]): low attenuation (-30 to 75 HU), fibro-fatty (76-130 HU), fibrous (131-350 HU), low-density calcium (351-700 HU), high-density calcium (701-1000 HU), and 1K (>1000 HU). The progression rates of these 6 compositional plaque types were evaluated according to the interaction between statin use and baseline plaque volume, adjusted for risk factors and time interval between scans. Plaque progression was also examined based on baseline calcium density. Analysis was performed among lesions matched at baseline and follow-up. Data analyses were conducted from August 2019 through March 2020. Results: In total, 2458 coronary lesions in 857 patients (mean [SD] age, 62.1 [8.7] years; 540 [63.0%] men; 548 [63.9%] received statin therapy) were included. Untreated coronary lesions increased in volume over time for all 6 compositional types. Statin therapy was associated with volume decreases in low-attenuation plaque (β, -0.02; 95% CI, -0.03 to -0.01; P =.001) and fibro-fatty plaque (β, -0.03; 95% CI, -0.04 to -0.02; P <.001) and greater progression of high-density calcium plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001) and 1K plaque (β, 0.02; 95% CI, 0.01-0.03; P <.001). When analyses were restricted to lesions without low-attenuation plaque or fibro-fatty plaque at baseline, statin therapy was not associated with a change in overall calcified plaque volume (β, -0.03; 95% CI, -0.08 to 0.02; P =.24) but was associated with a transformation toward more dense calcium. Interaction analysis between baseline plaque volume and calcium density showed that more dense coronary calcium was associated with less plaque progression. Conclusions and Relevance: The results suggest an association of statin use with greater rates of transformation of coronary atherosclerosis toward high-density calcium. A pattern of slower overall plaque progression was observed with increasing density. All findings support the concept of reduced atherosclerotic risk with increased densification of calcium..

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Association of Statin Treatment with Progression of Coronary Atherosclerotic Plaque Composition

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