Abstract 20274: The Ratio of Coronary Arterial Lumen Volume to Left Ventricle Mass on Coronary Computed Tomography Angiography Identifies Patients Prone to Vessel-Specific Ischemia Measured by Fractional Flow Reserve
Background: We hypothesize that in patients with suspected coronary artery disease (CAD), the ratio of coronary arterial lumen volume to myocardial mass (V/M) varies among subjects and that patients with low values of V/M are predisposed to ischemia. The purpose of this study was to quantify the relationship between V/M, plaque volume and FFR.
Methods and Results: V/M was computed in 254 patients with suspected CAD from the NXT trial (NCT01757678). All patients underwent clinically indicated coronary CTA, invasive angiography, and FFR studies. Nitroglycerin was administered in all patients prior to CT and angiography/FFR. The total arterial lumen volume was calculated as the sum of volumes of the patient-specific anatomical model derived from coronary CTA and, downstream of the image-based model, a morphometric model of the smaller arteries generated using branching laws. The total arterial lumen volume was divided by left ventricular mass. Calcified and noncalcified plaque volumes were quantified using semi-automated software. Vessel-specific ischemia was defined by invasive FFR ≤0.80. The mean value of V/M was 31.5 ± 8.9 mm3/g and the median value was 30.6 mm3/g. Low V/M ratio was defined as V/M<31 mm3/g and high V/M was defined as V/M≥31 mm3/g. Regardless of stenosis severity, patients with low V/M had lower measured FFR than those with high V/M (Low V/M: 0.79 ± 0.15, High V/M: 0.85 ± 0.12; p=0.0002) (Table 1). Patients with low V/M had more plaque than those with high V/M (Low V/M: 617 ± 402 mm3, High V/M: 396 ± 323; p<0.0001). When controlled for total plaque burden, V/M ratio remains a significant predictor of ischemia.
Conclusions: Patients with a small V/M ratio are at increased risk of ischemia independent of obstructive CAD likely due to an increased diffuse plaque burden. V/M is a novel metric derived from coronary CT angiography that may indicate balance or imbalance between the supply capacity of the coronary arterial tree and the demand for blood from the myocardium.
Author Disclosures: C.A. Taylor: Employment; Significant; Employee, HeartFlow, Inc. Ownership Interest; Significant; Shareholder, HeartFlow, Inc. S. Gaur: None. K.A. Øvrehus: None. D. Dey: Other; Modest; Royalties for software licensing. A. Ahmadi: None. S. Khem: Employment; Significant; Employee, HeartFlow, Inc. H.J. Kim: Employment; Significant; Employee, HeartFlow, Inc. A. Wilk: Employment; Significant; Employee, HeartFlow, Inc. C.K. Zarins: Employment; Significant; Employee, HeartFlow, Inc. Ownership Interest; Significant; Shareholder, HeartFlow, Inc. J. Jensen: None. S. Achenbach: Research Grant; Modest; Siemens Healthcare. D.S. Berman: Other; Modest; Royalties for software licensing. H. Bezerra: None. H.E. Bøtker: None. J. Leipsic: Consultant/Advisory Board; Modest; GE Healthcare, HeartFlow. J. Lesser: None. J. Narula: None. J. Lassen: None. B. De Bruyne: Research Grant; Modest; Abbott, St Jude Medical, Medtronic, Boston Scientific. Ownership Interest; Modest; Omega Pharma, Siemens, GE, Sanofi, HeartFlow, Bayer. Consultant/Advisory Board; Modest; St Jude Medical, Opsens, Boston Scientific. B. Norgaard: None.
- © 2016 by American Heart Association, Inc.