Hyung-Bok Park1, Ran Heo2, Bríain Ó Hartaigh3, Iksung Cho2, Heidi Gransar4, Ryo Nakazato5, Jonathon Leipsic6, G B John Mancini7, Bon-Kwon Koo8, Hiromasa Otake9, Matthew J Budoff10, Daniel S Berman4, Andrejs Erglis11, Hyuk-Jae Chang12, James K Min13. 1. Department of Radiology, New York-Presbyterian Hospital and the Weill Cornell Medical College, New York, New York; Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea; Cardiovascular Center, Myongji Hospital, Goyang, Korea. 2. Department of Radiology, New York-Presbyterian Hospital and the Weill Cornell Medical College, New York, New York; Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea. 3. Department of Radiology, New York-Presbyterian Hospital and the Weill Cornell Medical College, New York, New York. 4. Departments of Imaging and Medicine, Cedars-Sinai Heart Institute, Cedars-Sinai Medical Center, Los Angeles, California. 5. Cardiovascular Center, St. Luke's International Hospital, Tokyo, Japan. 6. Department of Radiology, St. Paul's Hospital, University of British Columbia, Vancouver, BC, Canada. 7. Department of Medicine, University of British Columbia, Vancouver, BC, Canada. 8. Department of Medicine, Seoul National University Hospital, Seoul, South Korea. 9. Department of Internal Medicine, Kobe University Graduate School of Medicine, Kobe, Japan. 10. Department of Medicine, Harbor UCLA Medical Center, Los Angeles, California. 11. Department of Medicine, Pauls Stradins Clinical University Hospital, Riga, Latvia. 12. Division of Cardiology, Severance Cardiovascular Hospital and Severance Biomedical Science Institute, Yonsei University College of Medicine, Seoul, South Korea. 13. Department of Radiology, New York-Presbyterian Hospital and the Weill Cornell Medical College, New York, New York. Electronic address: jkm2001@med.cornell.edu.
Abstract
OBJECTIVES: This study evaluated the association between atherosclerotic plaque characteristics (APCs) by coronary computed tomographic angiography (CTA), and lesion ischemia by fractional flow reserve (FFR). BACKGROUND: FFR is the gold standard for determining lesion ischemia. Although APCs by CTA-including aggregate plaque volume % (%APV), positive remodeling (PR), low attenuation plaque (LAP), and spotty calcification (SC)-are associated with future coronary syndromes, their relationship to lesion ischemia is unclear. METHODS: 252 patients (17 centers, 5 countries; mean age 63 years; 71% males) underwent coronary CTA, with FFR performed for 407 coronary lesions. Coronary CTA was interpreted for <50% and ≥50% stenosis, with the latter considered obstructive. APCs by coronary CTA were defined as: 1) PR, lesion diameter/reference diameter >1.10; 2) LAP, any voxel <30 Hounsfield units; and 3) SC, nodular calcified plaque <3 mm. Odds ratios (OR) and net reclassification improvement of APCs for lesion ischemia, defined by FFR ≤0.8, were analyzed. RESULTS: By FFR, ischemia was present in 151 lesions (37%). %APV was associated with a 50% increased risk of ischemia per 5% additional APV. PR, LAP, and SC were associated with ischemia, with a 3 to 5 times higher prevalence than in nonischemic lesions. In multivariable analyses, a stepwise increased risk of ischemia was observed for 1 (OR: 4.0, p < 0.001) and ≥2 (OR: 12.1, p < 0.001) APCs. These findings were APC dependent, with PR (OR: 5.3, p < 0.001) and LAP (OR: 2.1, p = 0.038) associated with ischemia, but not SC. When examined by stenosis severity, PR remained a predictor of ischemia for all lesions, whereas %APV and LAP were associated with ischemia for only ≥50%, but not for <50%, stenosis. CONCLUSIONS: %APV and APCs by coronary CTA improve identification of coronary lesions that cause ischemia. PR is associated with all ischemia-causing lesions, whereas %APV and LAP are only associated with ischemia-causing lesions ≥50%. (Determination of Fractional Flow Reserve by Anatomic Computed Tomographic Angiography; NCT01233518).
OBJECTIVES: This study evaluated the association between atherosclerotic plaque characteristics (APCs) by coronary computed tomographic angiography (CTA), and lesion ischemia by fractional flow reserve (FFR). BACKGROUND: FFR is the gold standard for determining lesion ischemia. Although APCs by CTA-including aggregate plaque volume % (%APV), positive remodeling (PR), low attenuation plaque (LAP), and spotty calcification (SC)-are associated with future coronary syndromes, their relationship to lesion ischemia is unclear. METHODS: 252 patients (17 centers, 5 countries; mean age 63 years; 71% males) underwent coronary CTA, with FFR performed for 407 coronary lesions. Coronary CTA was interpreted for <50% and ≥50% stenosis, with the latter considered obstructive. APCs by coronary CTA were defined as: 1) PR, lesion diameter/reference diameter >1.10; 2) LAP, any voxel <30 Hounsfield units; and 3) SC, nodular calcified plaque <3 mm. Odds ratios (OR) and net reclassification improvement of APCs for lesion ischemia, defined by FFR ≤0.8, were analyzed. RESULTS: By FFR, ischemia was present in 151 lesions (37%). %APV was associated with a 50% increased risk of ischemia per 5% additional APV. PR, LAP, and SC were associated with ischemia, with a 3 to 5 times higher prevalence than in nonischemic lesions. In multivariable analyses, a stepwise increased risk of ischemia was observed for 1 (OR: 4.0, p < 0.001) and ≥2 (OR: 12.1, p < 0.001) APCs. These findings were APC dependent, with PR (OR: 5.3, p < 0.001) and LAP (OR: 2.1, p = 0.038) associated with ischemia, but not SC. When examined by stenosis severity, PR remained a predictor of ischemia for all lesions, whereas %APV and LAP were associated with ischemia for only ≥50%, but not for <50%, stenosis. CONCLUSIONS: %APV and APCs by coronary CTA improve identification of coronary lesions that cause ischemia. PR is associated with all ischemia-causing lesions, whereas %APV and LAP are only associated with ischemia-causing lesions ≥50%. (Determination of Fractional Flow Reserve by Anatomic Computed Tomographic Angiography; NCT01233518).
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