Stephanie L Sellers1, Tim A Fonte2, Rominder Grover3, John Mooney3, Jonathan Weir-McCall3, Karen Pl Lau1, Anesh Chavda3, Charis McNabney3, Amir Ahmadi3, Philipp Blanke3, Geoffrey W Payne4, Darra T Murphy3, Kevin Ong5, Charles A Taylor2, Jonathon A Leipsic6. 1. Department of Radiology, St Paul's Hospital and University of British Columbia, Vancouver, Canada; Centre for Heart Lung Innovation, St Paul's Hospital and University of British Columbia, Vancouver, Canada. 2. Heart Flow Inc, Redwood City, CA, USA. 3. Department of Radiology, St Paul's Hospital and University of British Columbia, Vancouver, Canada. 4. University of Northern British Columbia, Prince George, Canada. 5. Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, Canada. 6. Department of Radiology, St Paul's Hospital and University of British Columbia, Vancouver, Canada; Heart Flow Inc, Redwood City, CA, USA; Division of Cardiology, Department of Medicine, University of British Columbia, Vancouver, Canada. Electronic address: jleipsic@providencehealth.bc.ca.
Abstract
INTRODUCTION: Angina, myocardial ischemia, and coronary artery physiology in hypertrophic cardiomyopathy (HCM) are poorly understood. However, coronary computed tomography angiography (CCTA) with fractional flow reserve from CT (FFRCT) analysis offers a non-invasive method for evaluation of coronary artery volume to myocardial mass ratio (V/M) that may provide insight into such mechanisms. Thus, we sought to investigate changes in V/M in HCM. METHODS: A retrospective analysis was performed on 37 HCM patients and 37 controls matched for age, sex, and cardiovascular risk factors; CCTA-derived coronary artery lumen volume (V) and myocardial mass (M) were used to determine V/M. FFRCT values were calculated for the left anterior descending (LAD), left circumflex (LCx) and right coronary (RCA) arteries as well as the 3-vessel cumulative FFRCT values. RESULTS: HCM patients had significantly increased myocardial mass (176 ± 84 vs. 119 ± 27 g, p < 0.0001) and total coronary artery luminal volume (4112 ± 1139 vs. 3290 ± 924 mm3, p < 0.0001) that resulted from increases in segmented luminal volumes of both the left and right coronary artery systems. However, HCM patients had significantly decreased V/M (23.8 ± 5.9 vs. 26.5 ± 5.3 mm3/g; p = 0.026) which was further decreased when restricting V/M analysis to those HCM patients with septal hypertrophy (22.4 mm3/g, p = 0.01) that was mild-moderately predictive of HCM (AUC = 0.68). HCM patients also showed significantly lower nadir FFRCT values in the LCx (0.87 ± 0.06 vs. 0.91 ± 0.06, p = 0.02), and cumulative 3-vessel FFRCT values (2.58 ± 0.18 vs. 2.63 ± 0.14, p = 0.006). CONCLUSIONS: HCM patients demonstrate significantly greater coronary volume. Despite this, HCM patients suffer from decreased V/M. Further prospective studies evaluating the relationship between V/M, angina, and heart failure in HCM are needed.
INTRODUCTION:Angina, myocardial ischemia, and coronary artery physiology in hypertrophic cardiomyopathy (HCM) are poorly understood. However, coronary computed tomography angiography (CCTA) with fractional flow reserve from CT (FFRCT) analysis offers a non-invasive method for evaluation of coronary artery volume to myocardial mass ratio (V/M) that may provide insight into such mechanisms. Thus, we sought to investigate changes in V/M in HCM. METHODS: A retrospective analysis was performed on 37 HCM patients and 37 controls matched for age, sex, and cardiovascular risk factors; CCTA-derived coronary artery lumen volume (V) and myocardial mass (M) were used to determine V/M. FFRCT values were calculated for the left anterior descending (LAD), left circumflex (LCx) and right coronary (RCA) arteries as well as the 3-vessel cumulative FFRCT values. RESULTS: HCM patients had significantly increased myocardial mass (176 ± 84 vs. 119 ± 27 g, p < 0.0001) and total coronary artery luminal volume (4112 ± 1139 vs. 3290 ± 924 mm3, p < 0.0001) that resulted from increases in segmented luminal volumes of both the left and right coronary artery systems. However, HCM patients had significantly decreased V/M (23.8 ± 5.9 vs. 26.5 ± 5.3 mm3/g; p = 0.026) which was further decreased when restricting V/M analysis to those HCM patients with septal hypertrophy (22.4 mm3/g, p = 0.01) that was mild-moderately predictive of HCM (AUC = 0.68). HCM patients also showed significantly lower nadir FFRCT values in the LCx (0.87 ± 0.06 vs. 0.91 ± 0.06, p = 0.02), and cumulative 3-vessel FFRCT values (2.58 ± 0.18 vs. 2.63 ± 0.14, p = 0.006). CONCLUSIONS: HCM patients demonstrate significantly greater coronary volume. Despite this, HCM patients suffer from decreased V/M. Further prospective studies evaluating the relationship between V/M, angina, and heart failure in HCM are needed.
Authors: Daniëlle C J Keulards; Stephane Fournier; Marcel van 't Veer; Iginio Colaiori; Jo M Zelis; Mohamed El Farissi; Frederik M Zimmermann; Carlos Collet; Bernard De Bruyne; Nico H J Pijls Journal: Heart Date: 2020-05-29 Impact factor: 5.994