Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome

Alexander R. Van Rosendael; Jagat Narula; Fay Y. Lin; Inge J. Van Den Hoogen; Umberto Gianni; Omar Al Hussein Alawamlh; Patricia C. Dunham; Jessica M. Penã; Sang Eun Lee; Daniele Andreini; Filippo Cademartiri; Kavitha Chinnaiyan; Benjamin J.W. Chow; Edoardo Conte; Ricardo C. Cury; Gudrun Feuchtner; Martin Hadamitzky; Yong Jin Kim; Jonathon Leipsic; Erica Maffei; Hugo Marques; Pedro De Araújo Goncąlves; Fabian Plank; Gianluca Pontone; Gilbert L. Raff; Todd C. Villines; Harald G. Weirich; Subhi J. Al'Aref; Lohendran Baskaran; Iksung Cho; Ibrahim Danad; Donghee Han; Ran Heo; Ji Hyun Lee; Asim Rivzi; Wijnand J. Stuijfzand; Heidi Gransar; Yao Lu; Ji Min Sung; Hyung Bok Park; Habib Samady; Peter H. Stone; Renu Virmani; Matthew J. Budoff; Daniel S. Berman; Hyuk Jae Chang; Jeroen J. Bax; James K. Min; Leslee J. Shaw

doi:10.1001/jamacardio.2019.5315

Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome

Alexander R. Van Rosendael, Jagat Narula, Fay Y. Lin, Inge J. Van Den Hoogen, Umberto Gianni, Omar Al Hussein Alawamlh, Patricia C. Dunham, Jessica M. Penã, Sang Eun Lee, Daniele Andreini, Filippo Cademartiri, Kavitha Chinnaiyan, Benjamin J.W. Chow, Edoardo Conte, Ricardo C. Cury, Gudrun Feuchtner, Martin Hadamitzky, Yong Jin Kim, Jonathon Leipsic, Erica MaffeiHugo Marques, Pedro De Araújo Goncąlves, Fabian Plank, Gianluca Pontone, Gilbert L. Raff, Todd C. Villines, Harald G. Weirich, Subhi J. Al'Aref, Lohendran Baskaran, Iksung Cho, Ibrahim Danad, Donghee Han, Ran Heo, Ji Hyun Lee, Asim Rivzi, Wijnand J. Stuijfzand, Heidi Gransar, Yao Lu, Ji Min Sung, Hyung Bok Park, Habib Samady, Peter H. Stone, Renu Virmani, Matthew J. Budoff, Daniel S. Berman, Hyuk Jae Chang, Jeroen J. Bax, James K. Min, Leslee J. Shaw

Department of Internal Medicine

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

52 Citations (Scopus)

Abstract

Importance: Plaque morphologic measures on coronary computed tomography angiography (CCTA) have been associated with future acute coronary syndrome (ACS). However, the evolution of calcified coronary plaques by noninvasive imaging is not known. Objective: To ascertain whether the increasing density in calcified coronary plaque is associated with risk for ACS. Design, Setting, and Participants: This multicenter case-control cohort study included individuals enrolled in ICONIC (Incident Coronary Syndromes Identified by Computed Tomography), a nested case-control study of patients drawn from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry, which included 13 study sites in 8 countries. Patients who experienced core laboratory-verified ACS after baseline CCTA (n = 189) and control individuals who did not experience ACS after baseline CCTA (n = 189) were included. Patients and controls were matched 1:1 by propensity scores for age; male sex; presence of hypertension, hyperlipidemia, and diabetes; family history of premature coronary artery disease (CAD); current smoking status; and CAD severity. Data were analyzed from November 2018 to March 2019. Exposures: Whole-heart atherosclerotic plaque volume was quantitated from all coronary vessels and their branches. For patients who underwent invasive angiography at the time of ACS, culprit lesions were coregistered to baseline CCTA lesions by a blinded independent reader. Low-density plaque was defined as having less than 130 Hounsfield units (HU); calcified plaque, as having more than 350 HU and subcategorized on a voxel-level basis into 3 strata: 351 to 700 HU, 701 to 1000 HU, and more than 1000 HU (termed 1K plaque). Main Outcomes and Measures: Association between calcium density and future ACS risk. Results: A total of 189 patients and 189 matched controls (mean [SD] age of 59.9 [9.8] years; 247 [65.3%] were male) were included in the analysis and were monitored during a mean (SD) follow-up period of 3.9 (2.5) years. The overall mean (SD) calcified plaque volume (>350 HU) was similar between patients and controls (76.4 [101.6] mm³ vs 99.0 [156.1] mm³; P =.32), but patients who experienced ACS exhibited less 1K plaque (>1000 HU) compared with controls (3.9 [8.3] mm³ vs 9.4 [23.2] mm³; P =.02). Individuals within the highest quartile of 1K plaque exhibited less low-density plaque, as a percentage of total plaque, when compared with patients within the lower 3 quartiles (12.6% [10.4%] vs 24.9% [20.6%]; P <.001). For 93 culprit precursor lesions detected by CCTA, the volume of 1K plaque was lower compared with the maximally stenotic lesion in controls (2.6 [7.2] mm³ vs 7.6 [20.3] mm³; P =.01). The per-patient and per-lesion results were similar between the 2 groups when restricted to myocardial infarction cases. Conclusions and Relevance: Results of this study suggest that, on a per-patient and per-lesion basis, 1K plaque was associated with a lower risk for future ACS and that measurement of 1K plaque may improve risk stratification beyond plaque burden.

Original language	English
Pages (from-to)	282-290
Number of pages	9
Journal	JAMA Cardiology
Volume	5
Issue number	3
DOIs	https://doi.org/10.1001/jamacardio.2019.5315
Publication status	Published - 2020 Mar

Bibliographical note

Funding Information:
Alawamlh reported receiving grants from the National Institutes of Health (NIH) during the conduct of the study. Dr Chinnaiyan reported receiving grants from Heartflow Inc outside the submitted work and being an unpaid medical advisory board member of HeartFlow. Dr Chow reported holding the Saul and Edna Goldfarb Chair in cardiac imaging research, receiving research support from CV Diagnostix and Ausculsciences as well as educational support from TeraRecon Inc, and holding equity interest in GE Healthcare. Dr Cury reported receiving personal fees from Cleerly Inc and GE Healthcare outside the submitted work. Dr Hadamitzky reported receiving nonfinancial support from Siemens Healthineers outside the submitted work. Dr Leipsic reported receiving personal fees from HeartFlow and grants from GE Healthcare outside the submitted work. Dr Pontone reported receiving grants and personal fees from GE Healthcare, grants and personal fees from Bracco, and grants from HeartFlow outside the submitted work. Dr Raff reported receiving grants from Blue Cross Blue Shield of Michigan during the conduct of the study and grants from HeartFlow Inc outside the submitted work. Dr Stuijfzand reported receiving grants from the NIH; Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning; and Dalio Institute of Cardiovascular Imaging during the conduct of the study. Dr Samady reported serving on the scientific advisory board of Philips, holding equity interest in Covanos Inc, and receiving research grants from Medtronic, Abbott Vascular, and Philips. Dr Budoff reported receiving grants from GE Healthcare during the conduct of the study. Dr Berman reported receiving software royalties from Cedars-Sinai Medical Center. Dr Bax reported receiving departmental grants and other from Medtronic as well as grants from Biotronik, Boston Scientific, Abbott, Edwards Lifescience, and GE Healthcare during the conduct of the study. Dr Min reported receiving funding from the Dalio Foundation, NIH, and GE Healthcare; serving on the scientific advisory board of Arineta and GE Healthcare; and holding equity interest in Cleerly Inc. No other disclosures were reported.

Funding Information:
Funding/Support: This study was funded by grant HL115150 from the NIH and by the Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning.

Publisher Copyright:
© 2019 American Medical Association. All rights reserved.

All Science Journal Classification (ASJC) codes

Cardiology and Cardiovascular Medicine

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1001/jamacardio.2019.5315

Cite this

Van Rosendael, A. R., Narula, J., Lin, F. Y., Van Den Hoogen, I. J., Gianni, U., Al Hussein Alawamlh, O., Dunham, P. C., Penã, J. M., Lee, S. E., Andreini, D., Cademartiri, F., Chinnaiyan, K., Chow, B. J. W., Conte, E., Cury, R. C., Feuchtner, G., Hadamitzky, M., Kim, Y. J., Leipsic, J., ... Shaw, L. J. (2020). Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome. JAMA Cardiology, 5(3), 282-290. https://doi.org/10.1001/jamacardio.2019.5315

@article{d59902a068994e8dba2b618f99d19b2d,

title = "Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome",

abstract = "Importance: Plaque morphologic measures on coronary computed tomography angiography (CCTA) have been associated with future acute coronary syndrome (ACS). However, the evolution of calcified coronary plaques by noninvasive imaging is not known. Objective: To ascertain whether the increasing density in calcified coronary plaque is associated with risk for ACS. Design, Setting, and Participants: This multicenter case-control cohort study included individuals enrolled in ICONIC (Incident Coronary Syndromes Identified by Computed Tomography), a nested case-control study of patients drawn from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry, which included 13 study sites in 8 countries. Patients who experienced core laboratory-verified ACS after baseline CCTA (n = 189) and control individuals who did not experience ACS after baseline CCTA (n = 189) were included. Patients and controls were matched 1:1 by propensity scores for age; male sex; presence of hypertension, hyperlipidemia, and diabetes; family history of premature coronary artery disease (CAD); current smoking status; and CAD severity. Data were analyzed from November 2018 to March 2019. Exposures: Whole-heart atherosclerotic plaque volume was quantitated from all coronary vessels and their branches. For patients who underwent invasive angiography at the time of ACS, culprit lesions were coregistered to baseline CCTA lesions by a blinded independent reader. Low-density plaque was defined as having less than 130 Hounsfield units (HU); calcified plaque, as having more than 350 HU and subcategorized on a voxel-level basis into 3 strata: 351 to 700 HU, 701 to 1000 HU, and more than 1000 HU (termed 1K plaque). Main Outcomes and Measures: Association between calcium density and future ACS risk. Results: A total of 189 patients and 189 matched controls (mean [SD] age of 59.9 [9.8] years; 247 [65.3%] were male) were included in the analysis and were monitored during a mean (SD) follow-up period of 3.9 (2.5) years. The overall mean (SD) calcified plaque volume (>350 HU) was similar between patients and controls (76.4 [101.6] mm3 vs 99.0 [156.1] mm3; P =.32), but patients who experienced ACS exhibited less 1K plaque (>1000 HU) compared with controls (3.9 [8.3] mm3 vs 9.4 [23.2] mm3; P =.02). Individuals within the highest quartile of 1K plaque exhibited less low-density plaque, as a percentage of total plaque, when compared with patients within the lower 3 quartiles (12.6% [10.4%] vs 24.9% [20.6%]; P <.001). For 93 culprit precursor lesions detected by CCTA, the volume of 1K plaque was lower compared with the maximally stenotic lesion in controls (2.6 [7.2] mm3 vs 7.6 [20.3] mm3; P =.01). The per-patient and per-lesion results were similar between the 2 groups when restricted to myocardial infarction cases. Conclusions and Relevance: Results of this study suggest that, on a per-patient and per-lesion basis, 1K plaque was associated with a lower risk for future ACS and that measurement of 1K plaque may improve risk stratification beyond plaque burden.",

author = "{Van Rosendael}, {Alexander R.} and Jagat Narula and Lin, {Fay Y.} and {Van Den Hoogen}, {Inge J.} and Umberto Gianni and {Al Hussein Alawamlh}, Omar and Dunham, {Patricia C.} and Pen{\~a}, {Jessica M.} and Lee, {Sang Eun} and Daniele Andreini and Filippo Cademartiri and Kavitha Chinnaiyan and Chow, {Benjamin J.W.} and Edoardo Conte and Cury, {Ricardo C.} and Gudrun Feuchtner and Martin Hadamitzky and Kim, {Yong Jin} and Jonathon Leipsic and Erica Maffei and Hugo Marques and {De Ara{\'u}jo Gonc{\c a}lves}, Pedro and Fabian Plank and Gianluca Pontone and Raff, {Gilbert L.} and Villines, {Todd C.} and Weirich, {Harald G.} and Al'Aref, {Subhi J.} and Lohendran Baskaran and Iksung Cho and Ibrahim Danad and Donghee Han and Ran Heo and Lee, {Ji Hyun} and Asim Rivzi and Stuijfzand, {Wijnand J.} and Heidi Gransar and Yao Lu and Sung, {Ji Min} and Park, {Hyung Bok} and Habib Samady and Stone, {Peter H.} and Renu Virmani and Budoff, {Matthew J.} and Berman, {Daniel S.} and Chang, {Hyuk Jae} and Bax, {Jeroen J.} and Min, {James K.} and Shaw, {Leslee J.}",

note = "Funding Information: Alawamlh reported receiving grants from the National Institutes of Health (NIH) during the conduct of the study. Dr Chinnaiyan reported receiving grants from Heartflow Inc outside the submitted work and being an unpaid medical advisory board member of HeartFlow. Dr Chow reported holding the Saul and Edna Goldfarb Chair in cardiac imaging research, receiving research support from CV Diagnostix and Ausculsciences as well as educational support from TeraRecon Inc, and holding equity interest in GE Healthcare. Dr Cury reported receiving personal fees from Cleerly Inc and GE Healthcare outside the submitted work. Dr Hadamitzky reported receiving nonfinancial support from Siemens Healthineers outside the submitted work. Dr Leipsic reported receiving personal fees from HeartFlow and grants from GE Healthcare outside the submitted work. Dr Pontone reported receiving grants and personal fees from GE Healthcare, grants and personal fees from Bracco, and grants from HeartFlow outside the submitted work. Dr Raff reported receiving grants from Blue Cross Blue Shield of Michigan during the conduct of the study and grants from HeartFlow Inc outside the submitted work. Dr Stuijfzand reported receiving grants from the NIH; Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning; and Dalio Institute of Cardiovascular Imaging during the conduct of the study. Dr Samady reported serving on the scientific advisory board of Philips, holding equity interest in Covanos Inc, and receiving research grants from Medtronic, Abbott Vascular, and Philips. Dr Budoff reported receiving grants from GE Healthcare during the conduct of the study. Dr Berman reported receiving software royalties from Cedars-Sinai Medical Center. Dr Bax reported receiving departmental grants and other from Medtronic as well as grants from Biotronik, Boston Scientific, Abbott, Edwards Lifescience, and GE Healthcare during the conduct of the study. Dr Min reported receiving funding from the Dalio Foundation, NIH, and GE Healthcare; serving on the scientific advisory board of Arineta and GE Healthcare; and holding equity interest in Cleerly Inc. No other disclosures were reported. Funding Information: Funding/Support: This study was funded by grant HL115150 from the NIH and by the Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning. Publisher Copyright: {\textcopyright} 2019 American Medical Association. All rights reserved.",

year = "2020",

month = mar,

doi = "10.1001/jamacardio.2019.5315",

language = "English",

volume = "5",

pages = "282--290",

journal = "JAMA Cardiology",

issn = "2380-6583",

publisher = "American Medical Association",

number = "3",

}

Van Rosendael, AR, Narula, J, Lin, FY, Van Den Hoogen, IJ, Gianni, U, Al Hussein Alawamlh, O, Dunham, PC, Penã, JM, Lee, SE, Andreini, D, Cademartiri, F, Chinnaiyan, K, Chow, BJW, Conte, E, Cury, RC, Feuchtner, G, Hadamitzky, M, Kim, YJ, Leipsic, J, Maffei, E, Marques, H, De Araújo Goncąlves, P, Plank, F, Pontone, G, Raff, GL, Villines, TC, Weirich, HG, Al'Aref, SJ, Baskaran, L, Cho, I, Danad, I, Han, D, Heo, R, Lee, JH, Rivzi, A, Stuijfzand, WJ, Gransar, H, Lu, Y, Sung, JM, Park, HB, Samady, H, Stone, PH, Virmani, R, Budoff, MJ, Berman, DS, Chang, HJ, Bax, JJ, Min, JK & Shaw, LJ 2020, 'Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome', JAMA Cardiology, vol. 5, no. 3, pp. 282-290. https://doi.org/10.1001/jamacardio.2019.5315

TY - JOUR

T1 - Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome

AU - Van Rosendael, Alexander R.

AU - Narula, Jagat

AU - Lin, Fay Y.

AU - Van Den Hoogen, Inge J.

AU - Gianni, Umberto

AU - Al Hussein Alawamlh, Omar

AU - Dunham, Patricia C.

AU - Penã, Jessica M.

AU - Lee, Sang Eun

AU - Andreini, Daniele

AU - Cademartiri, Filippo

AU - Chinnaiyan, Kavitha

AU - Chow, Benjamin J.W.

AU - Conte, Edoardo

AU - Cury, Ricardo C.

AU - Feuchtner, Gudrun

AU - Hadamitzky, Martin

AU - Kim, Yong Jin

AU - Leipsic, Jonathon

AU - Maffei, Erica

AU - Marques, Hugo

AU - De Araújo Goncąlves, Pedro

AU - Plank, Fabian

AU - Pontone, Gianluca

AU - Raff, Gilbert L.

AU - Villines, Todd C.

AU - Weirich, Harald G.

AU - Al'Aref, Subhi J.

AU - Baskaran, Lohendran

AU - Cho, Iksung

AU - Danad, Ibrahim

AU - Han, Donghee

AU - Heo, Ran

AU - Lee, Ji Hyun

AU - Rivzi, Asim

AU - Stuijfzand, Wijnand J.

AU - Gransar, Heidi

AU - Lu, Yao

AU - Sung, Ji Min

AU - Park, Hyung Bok

AU - Samady, Habib

AU - Stone, Peter H.

AU - Virmani, Renu

AU - Budoff, Matthew J.

AU - Berman, Daniel S.

AU - Chang, Hyuk Jae

AU - Bax, Jeroen J.

AU - Min, James K.

AU - Shaw, Leslee J.

N1 - Funding Information: Alawamlh reported receiving grants from the National Institutes of Health (NIH) during the conduct of the study. Dr Chinnaiyan reported receiving grants from Heartflow Inc outside the submitted work and being an unpaid medical advisory board member of HeartFlow. Dr Chow reported holding the Saul and Edna Goldfarb Chair in cardiac imaging research, receiving research support from CV Diagnostix and Ausculsciences as well as educational support from TeraRecon Inc, and holding equity interest in GE Healthcare. Dr Cury reported receiving personal fees from Cleerly Inc and GE Healthcare outside the submitted work. Dr Hadamitzky reported receiving nonfinancial support from Siemens Healthineers outside the submitted work. Dr Leipsic reported receiving personal fees from HeartFlow and grants from GE Healthcare outside the submitted work. Dr Pontone reported receiving grants and personal fees from GE Healthcare, grants and personal fees from Bracco, and grants from HeartFlow outside the submitted work. Dr Raff reported receiving grants from Blue Cross Blue Shield of Michigan during the conduct of the study and grants from HeartFlow Inc outside the submitted work. Dr Stuijfzand reported receiving grants from the NIH; Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning; and Dalio Institute of Cardiovascular Imaging during the conduct of the study. Dr Samady reported serving on the scientific advisory board of Philips, holding equity interest in Covanos Inc, and receiving research grants from Medtronic, Abbott Vascular, and Philips. Dr Budoff reported receiving grants from GE Healthcare during the conduct of the study. Dr Berman reported receiving software royalties from Cedars-Sinai Medical Center. Dr Bax reported receiving departmental grants and other from Medtronic as well as grants from Biotronik, Boston Scientific, Abbott, Edwards Lifescience, and GE Healthcare during the conduct of the study. Dr Min reported receiving funding from the Dalio Foundation, NIH, and GE Healthcare; serving on the scientific advisory board of Arineta and GE Healthcare; and holding equity interest in Cleerly Inc. No other disclosures were reported. Funding Information: Funding/Support: This study was funded by grant HL115150 from the NIH and by the Leading Foreign Research Institute Recruitment Program of the National Research Foundation of Korea, Ministry of Science, ICT and Future Planning. Publisher Copyright: © 2019 American Medical Association. All rights reserved.

PY - 2020/3

Y1 - 2020/3

N2 - Importance: Plaque morphologic measures on coronary computed tomography angiography (CCTA) have been associated with future acute coronary syndrome (ACS). However, the evolution of calcified coronary plaques by noninvasive imaging is not known. Objective: To ascertain whether the increasing density in calcified coronary plaque is associated with risk for ACS. Design, Setting, and Participants: This multicenter case-control cohort study included individuals enrolled in ICONIC (Incident Coronary Syndromes Identified by Computed Tomography), a nested case-control study of patients drawn from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry, which included 13 study sites in 8 countries. Patients who experienced core laboratory-verified ACS after baseline CCTA (n = 189) and control individuals who did not experience ACS after baseline CCTA (n = 189) were included. Patients and controls were matched 1:1 by propensity scores for age; male sex; presence of hypertension, hyperlipidemia, and diabetes; family history of premature coronary artery disease (CAD); current smoking status; and CAD severity. Data were analyzed from November 2018 to March 2019. Exposures: Whole-heart atherosclerotic plaque volume was quantitated from all coronary vessels and their branches. For patients who underwent invasive angiography at the time of ACS, culprit lesions were coregistered to baseline CCTA lesions by a blinded independent reader. Low-density plaque was defined as having less than 130 Hounsfield units (HU); calcified plaque, as having more than 350 HU and subcategorized on a voxel-level basis into 3 strata: 351 to 700 HU, 701 to 1000 HU, and more than 1000 HU (termed 1K plaque). Main Outcomes and Measures: Association between calcium density and future ACS risk. Results: A total of 189 patients and 189 matched controls (mean [SD] age of 59.9 [9.8] years; 247 [65.3%] were male) were included in the analysis and were monitored during a mean (SD) follow-up period of 3.9 (2.5) years. The overall mean (SD) calcified plaque volume (>350 HU) was similar between patients and controls (76.4 [101.6] mm3 vs 99.0 [156.1] mm3; P =.32), but patients who experienced ACS exhibited less 1K plaque (>1000 HU) compared with controls (3.9 [8.3] mm3 vs 9.4 [23.2] mm3; P =.02). Individuals within the highest quartile of 1K plaque exhibited less low-density plaque, as a percentage of total plaque, when compared with patients within the lower 3 quartiles (12.6% [10.4%] vs 24.9% [20.6%]; P <.001). For 93 culprit precursor lesions detected by CCTA, the volume of 1K plaque was lower compared with the maximally stenotic lesion in controls (2.6 [7.2] mm3 vs 7.6 [20.3] mm3; P =.01). The per-patient and per-lesion results were similar between the 2 groups when restricted to myocardial infarction cases. Conclusions and Relevance: Results of this study suggest that, on a per-patient and per-lesion basis, 1K plaque was associated with a lower risk for future ACS and that measurement of 1K plaque may improve risk stratification beyond plaque burden.

AB - Importance: Plaque morphologic measures on coronary computed tomography angiography (CCTA) have been associated with future acute coronary syndrome (ACS). However, the evolution of calcified coronary plaques by noninvasive imaging is not known. Objective: To ascertain whether the increasing density in calcified coronary plaque is associated with risk for ACS. Design, Setting, and Participants: This multicenter case-control cohort study included individuals enrolled in ICONIC (Incident Coronary Syndromes Identified by Computed Tomography), a nested case-control study of patients drawn from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry, which included 13 study sites in 8 countries. Patients who experienced core laboratory-verified ACS after baseline CCTA (n = 189) and control individuals who did not experience ACS after baseline CCTA (n = 189) were included. Patients and controls were matched 1:1 by propensity scores for age; male sex; presence of hypertension, hyperlipidemia, and diabetes; family history of premature coronary artery disease (CAD); current smoking status; and CAD severity. Data were analyzed from November 2018 to March 2019. Exposures: Whole-heart atherosclerotic plaque volume was quantitated from all coronary vessels and their branches. For patients who underwent invasive angiography at the time of ACS, culprit lesions were coregistered to baseline CCTA lesions by a blinded independent reader. Low-density plaque was defined as having less than 130 Hounsfield units (HU); calcified plaque, as having more than 350 HU and subcategorized on a voxel-level basis into 3 strata: 351 to 700 HU, 701 to 1000 HU, and more than 1000 HU (termed 1K plaque). Main Outcomes and Measures: Association between calcium density and future ACS risk. Results: A total of 189 patients and 189 matched controls (mean [SD] age of 59.9 [9.8] years; 247 [65.3%] were male) were included in the analysis and were monitored during a mean (SD) follow-up period of 3.9 (2.5) years. The overall mean (SD) calcified plaque volume (>350 HU) was similar between patients and controls (76.4 [101.6] mm3 vs 99.0 [156.1] mm3; P =.32), but patients who experienced ACS exhibited less 1K plaque (>1000 HU) compared with controls (3.9 [8.3] mm3 vs 9.4 [23.2] mm3; P =.02). Individuals within the highest quartile of 1K plaque exhibited less low-density plaque, as a percentage of total plaque, when compared with patients within the lower 3 quartiles (12.6% [10.4%] vs 24.9% [20.6%]; P <.001). For 93 culprit precursor lesions detected by CCTA, the volume of 1K plaque was lower compared with the maximally stenotic lesion in controls (2.6 [7.2] mm3 vs 7.6 [20.3] mm3; P =.01). The per-patient and per-lesion results were similar between the 2 groups when restricted to myocardial infarction cases. Conclusions and Relevance: Results of this study suggest that, on a per-patient and per-lesion basis, 1K plaque was associated with a lower risk for future ACS and that measurement of 1K plaque may improve risk stratification beyond plaque burden.

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JF - JAMA Cardiology

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ER -

Association of High-Density Calcified 1K Plaque with Risk of Acute Coronary Syndrome

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