The importance of nonobstructive plaque characteristics in symptomatic and asymptomatic coronary artery disease
We examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT). 855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronar...
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Published in | Journal of cardiovascular computed tomography Vol. 18; no. 2; pp. 203 - 210 |
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Main Authors | , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
01.03.2024
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Subjects | |
Online Access | Get full text |
ISSN | 1934-5925 1876-861X 1876-861X |
DOI | 10.1016/j.jcct.2024.01.014 |
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Abstract | We examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT).
855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronary syndrome (ACS), and 327 patients with ACS) underwent QCT of proximal coronary segments to assess participant-level plaque volumes of dense calcium, fibrous, fibrofatty, and necrotic core tissue.
Nonobstructive (<50% stenosis) plaque volumes were greater than obstructive plaque volumes, irrespective of population (all p<0.0001): Asymptomatic individuals (mean (95% CI)): 218 [190-250] vs. 16 [12-22] mm3; acute chest pain patients without ACS: 300 [263-341] vs. 51 [41-62] mm3; patients with ACS: 370 [332-412] vs. 159 [139-182] mm3. After multivariable adjustment, nonobstructive fibrous and fibrofatty tissue volumes were greater in acute chest pain patients without ACS compared to asymptomatic individuals (fibrous tissue: 122 [107-139] vs. 175 [155-197] mm3, p<0.01; fibrofatty tissue: 44 [38-50] vs. 71 [63-80] mm3, p<0.01. Necrotic core tissue was greater in ACS patients (29 [26-33] mm3) compared to both asymptomatic individuals (15 [13-18] mm3, p<0.0001) and acute chest pain patients without ACS (21 [18-24] mm3, p<0.05). Nonobstructive dense calcium volumes did not differ between the three populations: 29 [24-36], 29 [23-35], and 41 [34-48] mm3, p>0.3 respectively.
Nonobstructive CAD was the predominant contributor to total atherosclerotic plaque volume in both subclinical and clinically manifested CAD. Nonobstructive fibrous, fibrofatty and necrotic core tissue volumes increased with worsening clinical presentation, while nonobstructive dense calcium tissue volumes did not. |
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AbstractList | We examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT).
855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronary syndrome (ACS), and 327 patients with ACS) underwent QCT of proximal coronary segments to assess participant-level plaque volumes of dense calcium, fibrous, fibrofatty, and necrotic core tissue.
Nonobstructive (<50% stenosis) plaque volumes were greater than obstructive plaque volumes, irrespective of population (all p<0.0001): Asymptomatic individuals (mean (95% CI)): 218 [190-250] vs. 16 [12-22] mm3; acute chest pain patients without ACS: 300 [263-341] vs. 51 [41-62] mm3; patients with ACS: 370 [332-412] vs. 159 [139-182] mm3. After multivariable adjustment, nonobstructive fibrous and fibrofatty tissue volumes were greater in acute chest pain patients without ACS compared to asymptomatic individuals (fibrous tissue: 122 [107-139] vs. 175 [155-197] mm3, p<0.01; fibrofatty tissue: 44 [38-50] vs. 71 [63-80] mm3, p<0.01. Necrotic core tissue was greater in ACS patients (29 [26-33] mm3) compared to both asymptomatic individuals (15 [13-18] mm3, p<0.0001) and acute chest pain patients without ACS (21 [18-24] mm3, p<0.05). Nonobstructive dense calcium volumes did not differ between the three populations: 29 [24-36], 29 [23-35], and 41 [34-48] mm3, p>0.3 respectively.
Nonobstructive CAD was the predominant contributor to total atherosclerotic plaque volume in both subclinical and clinically manifested CAD. Nonobstructive fibrous, fibrofatty and necrotic core tissue volumes increased with worsening clinical presentation, while nonobstructive dense calcium tissue volumes did not. We examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT).BACKGROUNDWe examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT).855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronary syndrome (ACS), and 327 patients with ACS) underwent QCT of proximal coronary segments to assess participant-level plaque volumes of dense calcium, fibrous, fibrofatty, and necrotic core tissue.METHODS855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronary syndrome (ACS), and 327 patients with ACS) underwent QCT of proximal coronary segments to assess participant-level plaque volumes of dense calcium, fibrous, fibrofatty, and necrotic core tissue.Nonobstructive (<50% stenosis) plaque volumes were greater than obstructive plaque volumes, irrespective of population (all p<0.0001): Asymptomatic individuals (mean (95% CI)): 218 [190-250] vs. 16 [12-22] mm3; acute chest pain patients without ACS: 300 [263-341] vs. 51 [41-62] mm3; patients with ACS: 370 [332-412] vs. 159 [139-182] mm3. After multivariable adjustment, nonobstructive fibrous and fibrofatty tissue volumes were greater in acute chest pain patients without ACS compared to asymptomatic individuals (fibrous tissue: 122 [107-139] vs. 175 [155-197] mm3, p<0.01; fibrofatty tissue: 44 [38-50] vs. 71 [63-80] mm3, p<0.01. Necrotic core tissue was greater in ACS patients (29 [26-33] mm3) compared to both asymptomatic individuals (15 [13-18] mm3, p<0.0001) and acute chest pain patients without ACS (21 [18-24] mm3, p<0.05). Nonobstructive dense calcium volumes did not differ between the three populations: 29 [24-36], 29 [23-35], and 41 [34-48] mm3, p>0.3 respectively.RESULTSNonobstructive (<50% stenosis) plaque volumes were greater than obstructive plaque volumes, irrespective of population (all p<0.0001): Asymptomatic individuals (mean (95% CI)): 218 [190-250] vs. 16 [12-22] mm3; acute chest pain patients without ACS: 300 [263-341] vs. 51 [41-62] mm3; patients with ACS: 370 [332-412] vs. 159 [139-182] mm3. After multivariable adjustment, nonobstructive fibrous and fibrofatty tissue volumes were greater in acute chest pain patients without ACS compared to asymptomatic individuals (fibrous tissue: 122 [107-139] vs. 175 [155-197] mm3, p<0.01; fibrofatty tissue: 44 [38-50] vs. 71 [63-80] mm3, p<0.01. Necrotic core tissue was greater in ACS patients (29 [26-33] mm3) compared to both asymptomatic individuals (15 [13-18] mm3, p<0.0001) and acute chest pain patients without ACS (21 [18-24] mm3, p<0.05). Nonobstructive dense calcium volumes did not differ between the three populations: 29 [24-36], 29 [23-35], and 41 [34-48] mm3, p>0.3 respectively.Nonobstructive CAD was the predominant contributor to total atherosclerotic plaque volume in both subclinical and clinically manifested CAD. Nonobstructive fibrous, fibrofatty and necrotic core tissue volumes increased with worsening clinical presentation, while nonobstructive dense calcium tissue volumes did not.CONCLUSIONNonobstructive CAD was the predominant contributor to total atherosclerotic plaque volume in both subclinical and clinically manifested CAD. Nonobstructive fibrous, fibrofatty and necrotic core tissue volumes increased with worsening clinical presentation, while nonobstructive dense calcium tissue volumes did not. We examined obstructive and nonobstructive plaque volumes in populations with subclinical and clinically manifested coronary artery disease (CAD) using quantitative computed tomography (QCT). 855 participants with CAD (274 asymptomatic individuals, 254 acute chest pain patients without acute coronary syndrome (ACS), and 327 patients with ACS) underwent QCT of proximal coronary segments to assess participant-level plaque volumes of dense calcium, fibrous, fibrofatty, and necrotic core tissue. Nonobstructive (<50% stenosis) plaque volumes were greater than obstructive plaque volumes, irrespective of population (all p<0.0001): Asymptomatic individuals (mean (95% CI)): 218 [190-250] vs. 16 [12-22] mm ; acute chest pain patients without ACS: 300 [263-341] vs. 51 [41-62] mm ; patients with ACS: 370 [332-412] vs. 159 [139-182] mm . After multivariable adjustment, nonobstructive fibrous and fibrofatty tissue volumes were greater in acute chest pain patients without ACS compared to asymptomatic individuals (fibrous tissue: 122 [107-139] vs. 175 [155-197] mm , p<0.01; fibrofatty tissue: 44 [38-50] vs. 71 [63-80] mm , p<0.01. Necrotic core tissue was greater in ACS patients (29 [26-33] mm ) compared to both asymptomatic individuals (15 [13-18] mm , p<0.0001) and acute chest pain patients without ACS (21 [18-24] mm , p<0.05). Nonobstructive dense calcium volumes did not differ between the three populations: 29 [24-36], 29 [23-35], and 41 [34-48] mm , p>0.3 respectively. Nonobstructive CAD was the predominant contributor to total atherosclerotic plaque volume in both subclinical and clinically manifested CAD. Nonobstructive fibrous, fibrofatty and necrotic core tissue volumes increased with worsening clinical presentation, while nonobstructive dense calcium tissue volumes did not. |
Author | Fuchs, Andreas Wachtell, Christian Møller, Christina Clemmensen, Peter Hansen, Peter R. Bock-Pedersen, Tina Saunamaki, Kari Bech, Jan Kühl, J. Tobias Mejdahl, Mads Engstrøm, Thomas Trysøe, Kirsten Elming, Marie Dixen, Ulrik Fritz-Hansen, Thomas Schou, Morten Hindsøe, Louise Laursen, Peter Nørkjær Nielsen, Olav Wendelboe Kelbæk, Henning Jurlander, Birgit Nordestgaard, Børge Hansen, Bettina de Knegt, Martina C. Abdulla, Jawdat Norsk, Jakob Jørgensen, Erik Høfsten, Dan E. Smedegaard, Lærke Gislason, Gunnar Bjerre, Andreas Fabricius Hove, Jens D. Knudsen, Andreas Dehlbæk Heitmann, Merete Holmvang, Lene Jensen, Gorm B. Pihl, Christian Haugen, Morten Sigvardsen, Per E. Sørensen, Samuel Kiil Lyngbæk, Stig Kragelund, Charlotte Udholm, Patricia Martens Fornitz, Gitte Gleerup Therkelsen, Susette Elming, Hanne Helquist, Steffen Jensen, Andreas K. Byrne, Christina Petersen, Frans Thrysøe, Kirsten Madsen, Johnny Koertz Køber, Lars V. Linde, Jesper J. Abildgaard, Ulrik Ballegaard, Christian Galatius, Søren Dominguez, Helena Thomsen, Anna Foged Nielsen, Walt |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/38320905$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1093_ehjimp_qyaf014 |
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ContentType | Journal Article |
Contributor | Fuchs, Andreas Wachtell, Christian Møller, Christina Clemmensen, Peter Bock-Pedersen, Tina Saunamaki, Kari Bech, Jan Mejdahl, Mads Linde, Jesper J Pham, Michael H C Trysøe, Kirsten Engstrøm, Thomas Køber, Lars V Elming, Marie Dixen, Ulrik Fritz-Hansen, Thomas Høfsten, Dan E Jensen, Gorm B Schou, Morten Hindsøe, Louise Laursen, Peter Nørkjær Nielsen, Olav Wendelboe Kelbæk, Henning Jurlander, Birgit Nordestgaard, Børge Hansen, Bettina Abdulla, Jawdat Norsk, Jakob Jørgensen, Erik Smedegaard, Lærke Gislason, Gunnar Bjerre, Andreas Fabricius Knudsen, Andreas Dehlbæk Heitmann, Merete Holmvang, Lene Kühl, J Tobias Pihl, Christian Haugen, Morten Sørensen, Samuel Kiil Lyngbæk, Stig Kragelund, Charlotte Udholm, Patricia Martens Fornitz, Gitte Gleerup Therkelsen, Susette Elming, Hanne Helquist, Steffen Byrne, Christina Petersen, Frans Thrysøe, Kirsten Madsen, Johnny Koertz Abildgaard, Ulrik Ballegaard, Christian Galatius, Søren Dominguez, Helena Thomsen, Anna Foged Nielsen, Walter Sørgaard, Mathias Madsen, Jan Kyst Hansen, Peter Riis Sigvardsen, Per E Özc |
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Copyright | 2024 The Authors Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved. |
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CorporateAuthor | The Very Early versus Deferred Invasive Evaluation using Computerized Tomography in Patients with Acute Coronary Syndromes investigators (VERDICT) The Copenhagen General Population Study investigators (CGPS) The Cardiac CT in the Treatment of Acute Chest Pain investigators (CATCH) CGPS, the CATCH, and the VERDICT Investigators Cardiac CT in the Treatment of Acute Chest Pain investigators (CATCH) Copenhagen General Population Study investigators (CGPS) Very Early versus Deferred Invasive Evaluation using Computerized Tomography in Patients with Acute Coronary Syndromes investigators (VERDICT) |
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Keywords | NSTEMI VERDICT Nonobstructive plaque QCT UAP Plaque composition CAD ECG Coronary artery disease ACS BSA CCTA Quantitative computed tomography Computed tomography CATCH CGPS |
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SubjectTerms | Acute Coronary Syndrome Calcium Chest Pain Computed tomography Coronary Angiography - methods Coronary artery disease Coronary Artery Disease - diagnostic imaging Coronary Artery Disease - epidemiology Humans Necrosis Nonobstructive plaque Plaque composition Plaque, Atherosclerotic Predictive Value of Tests Quantitative computed tomography |
Title | The importance of nonobstructive plaque characteristics in symptomatic and asymptomatic coronary artery disease |
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