Stefan B Puchner1, Thomas Mayrhofer2, Jakob Park3, Michael T Lu3, Ting Liu4, Pal Maurovich-Horvat5, Khristine Ghemigian3, Daniel O Bittner6, Jerome L Fleg7, James E Udelson8, Quynh A Truong9, Udo Hoffmann3, Maros Ferencik10. 1. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Department of Biomedical Imaging and Image-Guided Therapy, Medical University of Vienna, Vienna, Austria. 2. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; School of Business Studies, Stralsund University of Applied Sciences, Stralsund, Germany. 3. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA. 4. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Department of Radiology, First Affiliated Hospital of China Medical University, Shenyang, China. 5. MTA-SE Cardiovascular Imaging Research Group, Heart and Vascular Centre, Semmelweis University, Budapest, Hungary. 6. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Friedrich-Alexander University Erlangen-Nürnberg (FAU), Department of Cardiology, University Hospital Erlangen, Germany. 7. Division of Cardiovascular Sciences, National Heart, Lung, and Blood Institute, Bethesda, MD, USA. 8. Division of Cardiology and the Cardio-Vascular Center, Tufts Medical Center, Boston, MA, USA. 9. Department of Radiology and Division of Cardiology, Weill Cornell Medical College, New York, NY, USA. 10. Department of Radiology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Cardiac MR PET CT Program, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA; Knight Cardiovascular Institute, Oregon Health & Science University, Portland, OR, USA. Electronic address: ferencik@ohsu.edu.
Abstract
BACKGROUND AND AIMS: Total coronary artery calcium (CAC) burden is associated with an increased cardiovascular risk, while local CAC may represent stable plaques. We determined differences in relationship of total CAC with acute coronary syndrome (ACS) and local CAC with culprit lesions in patients with suspected ACS. METHODS: We performed computed tomography (CT) for CAC and CT angiography to assess the presence of significant stenosis and high-risk plaque (positive remodeling, low CT attenuation, napkin-ring sign, spotty calcium) in 37 patients with ACS and 223 controls. Total and segmental Agatston scores were measured. Culprit lesions were assessed in subjects with ACS. RESULTS: Patients (n = 260) with vs. without ACS had higher total CAC score (median 229, 25th-75th percentile 75-517 vs. 27, 25th-75th percentile 0-99, p<0.001), higher prevalence of significant stenosis (78% vs. 7%, p<0.001) and high-risk plaque (95% vs. 59%, p<0.001). In those with ACS, culprit (n = 41) vs. non-culprit (n = 200) lesions, had similar segmental CAC score (median 22, 25th-75th percentile 4-71 vs. 14, 25th-75th percentile 0-51; p=0.37), but higher prevalence of significant stenosis (81% vs. 11%, p<0.001) and high-risk plaque (76% vs. 51%, p=0.005). Significant stenosis (odds ratio 40.2, 95%CI 15.6-103.9, p<0.001) and high-risk plaque (odds ratio 3.4, 95%CI 1.3-9.1, p=0.02), but not segmental CAC score (odds ratio 1.0, 95%CI 1.0-1.0, p=0.47), were associated with culprit lesions of ACS. CONCLUSIONS: Total CAC burden was associated with ACS but segmental CAC was not associated with culprit lesions. Our findings suggest that total but not local CAC is a marker of ACS risk and support the hypothesis that extensive local CAC is a marker of plaque stability.
BACKGROUND AND AIMS: Total coronary artery calcium (CAC) burden is associated with an increased cardiovascular risk, while local CAC may represent stable plaques. We determined differences in relationship of total CAC with acute coronary syndrome (ACS) and local CAC with culprit lesions in patients with suspected ACS. METHODS: We performed computed tomography (CT) for CAC and CT angiography to assess the presence of significant stenosis and high-risk plaque (positive remodeling, low CT attenuation, napkin-ring sign, spottycalcium) in 37 patients with ACS and 223 controls. Total and segmental Agatston scores were measured. Culprit lesions were assessed in subjects with ACS. RESULTS:Patients (n = 260) with vs. without ACS had higher total CAC score (median 229, 25th-75th percentile 75-517 vs. 27, 25th-75th percentile 0-99, p<0.001), higher prevalence of significant stenosis (78% vs. 7%, p<0.001) and high-risk plaque (95% vs. 59%, p<0.001). In those with ACS, culprit (n = 41) vs. non-culprit (n = 200) lesions, had similar segmental CAC score (median 22, 25th-75th percentile 4-71 vs. 14, 25th-75th percentile 0-51; p=0.37), but higher prevalence of significant stenosis (81% vs. 11%, p<0.001) and high-risk plaque (76% vs. 51%, p=0.005). Significant stenosis (odds ratio 40.2, 95%CI 15.6-103.9, p<0.001) and high-risk plaque (odds ratio 3.4, 95%CI 1.3-9.1, p=0.02), but not segmental CAC score (odds ratio 1.0, 95%CI 1.0-1.0, p=0.47), were associated with culprit lesions of ACS. CONCLUSIONS: Total CAC burden was associated with ACS but segmental CAC was not associated with culprit lesions. Our findings suggest that total but not local CAC is a marker of ACS risk and support the hypothesis that extensive local CAC is a marker of plaque stability.
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