Mhairi K Doris1, Yuka Otaki2, Yoav Arnson3, Balaji Tamarappoo4, Markus Goeller5, Heidi Gransar6, Frances Wang7, Sean Hayes8, John Friedman9, Louise Thomson10, Piotr Slomka11, Damini Dey12, Daniel Berman13. 1. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA; Centre for Cardiovascular Science, University of Edinburgh, Scotland, UK. Electronic address: Mhairi.Doris@ed.ac.uk. 2. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Yuka.Otaki@cshs.org. 3. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Yoav.Arnson@cshs.org. 4. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Balaji.Tamarappoo@cshs.org. 5. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: markus.goeller@cshs.org. 6. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Heidi.Gransar@cshs.org. 7. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Frances.Wang@cshs.org. 8. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Sean.Hayes@cshs.org. 9. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: John.Friedman@cshs.org. 10. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Louise.Thomson@cshs.org. 11. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Piotr.Slomka@cshs.org. 12. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Damini.Dey@cshs.org. 13. Department of Imaging and Medicine and Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA, USA. Electronic address: Daniel.Berman@cshs.org.
Abstract
AIMS: Non-invasive fractional flow reserve derived from coronary CT angiography (FFRCT) has been shown to be predictive of lesion-specific ischemia as assessed by invasive fractional flow reserve (FFR). However, in practice, clinicians are often faced with an abnormal distal FFRCT in the absence of a discrete obstructive lesion. Using quantitative plaque analysis, we sought to determine the relationship between an abnormal whole vessel FFRCT (V-FFRCT) and quantitative measures of whole vessel atherosclerosis in coronary arteries without obstructive stenosis. METHODS: FFRCT was calculated in 155 consecutive patients undergoing coronary CTA with ≥25% but less than 70% stenosis in at least one major epicardial vessel. Semi-automated software was used to quantify plaque volumes (total plaque [TP], calcified plaque [CP], non-calcified plaque [NCP], low-density non-calcified plaque [LD-NCP]), remodeling index [RI], maximal contrast density difference [CDD] and percent diameter stenosis [%DS]. Abnormal V-FFRCT was defined as a minimum value of ≤0.75 across the vessel (at the most distal region where FFRCT was computed). RESULTS: Vessels with abnormal V-FFRCT had higher per-vessel TP (554 vs 331 mm3), CP (59 vs 25 mm3), NCP (429 vs 295 mm3), LD-NCP (65 vs 35 mm3) volume and maximum CDD (21 vs 14%) than those with normal V-FFRCT (median, p < 0.05 for all). Using a multivariate analysis to adjust for CDD and %DS, all measures of plaque volume were predictive of abnormal V-FFRCT (OR 2.09, 1.36, 1.95, 1.95 for TP, CP, NCP and LD-NCP volume, respectively; p < 0.05 for all). CONCLUSION: Abnormal V-FFRCT in vessels without obstructive stenosis is associated with multiple markers of diffuse non-obstructive atherosclerosis, independent of stenosis severity. Whole vessel FFRCT may represent a novel measure of diffuse coronary plaque burden.
AIMS: Non-invasive fractional flow reserve derived from coronary CT angiography (FFRCT) has been shown to be predictive of lesion-specific ischemia as assessed by invasive fractional flow reserve (FFR). However, in practice, clinicians are often faced with an abnormal distal FFRCT in the absence of a discrete obstructive lesion. Using quantitative plaque analysis, we sought to determine the relationship between an abnormal whole vessel FFRCT (V-FFRCT) and quantitative measures of whole vessel atherosclerosis in coronary arteries without obstructive stenosis. METHODS: FFRCT was calculated in 155 consecutive patients undergoing coronary CTA with ≥25% but less than 70% stenosis in at least one major epicardial vessel. Semi-automated software was used to quantify plaque volumes (total plaque [TP], calcified plaque [CP], non-calcified plaque [NCP], low-density non-calcified plaque [LD-NCP]), remodeling index [RI], maximal contrast density difference [CDD] and percent diameter stenosis [%DS]. Abnormal V-FFRCT was defined as a minimum value of ≤0.75 across the vessel (at the most distal region where FFRCT was computed). RESULTS: Vessels with abnormal V-FFRCT had higher per-vessel TP (554 vs 331 mm3), CP (59 vs 25 mm3), NCP (429 vs 295 mm3), LD-NCP (65 vs 35 mm3) volume and maximum CDD (21 vs 14%) than those with normal V-FFRCT (median, p < 0.05 for all). Using a multivariate analysis to adjust for CDD and %DS, all measures of plaque volume were predictive of abnormal V-FFRCT (OR 2.09, 1.36, 1.95, 1.95 for TP, CP, NCP and LD-NCP volume, respectively; p < 0.05 for all). CONCLUSION: Abnormal V-FFRCT in vessels without obstructive stenosis is associated with multiple markers of diffuse non-obstructive atherosclerosis, independent of stenosis severity. Whole vessel FFRCT may represent a novel measure of diffuse coronary plaque burden.