K Lance Gould1, Richard Kirkeeide, Nils P Johnson. 1. The Weatherhead P.E.T. Center for Preventing and Reversing Atherosclerosis and the Department of Medicine, Division of Cardiology, University of Texas Medical School at Houston, and Memorial Hermann Hospital, Houston, Tex., USA. k.lance.gould@uth.tmc.edu
Abstract
BACKGROUND: fluid dynamic analysis predicts a new concept in coronary physiology that we call "branch steal," whereby stenosis proximal and distal to arterial branching interact with the nonstenotic branch between stenosis that shunts or "steals" flow away from the distal stenotic artery during reactive hyperemia, tested experimentally. METHODS AND RESULTS: in 21 large hounds under surgical anesthesia, proximal and distal left circumflex and obtuse marginal coronary arteries were instrumented with electromagnetic flowmeters, proximal and distal machined Teflon screw-down stenosers with round concentric closing and distal silk-in-tubing sleeve occluders. Baseline reactive hyperemia was recorded after 15-second occlusions of both arteries at baseline and for progressive distal stenosis during each step of progressive proximal stenosis. At each combination of stenosis, a coronary arteriogram was obtained using left Judkins catheters and Philips cine calibrated with modulated transfer function to ± 0.1 mm accuracy for fluid dynamic analysis of arterial stenosis-branching anatomy. In 324 experiments of parent-child stenosis combinations of the left circumflex artery with an intervening obtuse marginal branch, coronary flow reserve (CFR) calculated by the fluid dynamic model accounting for stenosis-branch interactions and "branch steal" correlated with CFR directly measured by flowmeter (linear regression, CFRartgm=0.18+0.7×CFRflowmtr with Pearson r=0.73). Quantitative arteriography and positron emission tomography perfusion imaging confirmed the concept in clinical examples. CONCLUSIONS: functional severity of anatomically fixed stenosis is not constant, specific, or independent of other stenosis in branching coronary arteries but requires analysis as an integrated component of the entire branching coronary artery tree to guide revascularizations.
BACKGROUND: fluid dynamic analysis predicts a new concept in coronary physiology that we call "branch steal," whereby stenosis proximal and distal to arterial branching interact with the nonstenotic branch between stenosis that shunts or "steals" flow away from the distal stenotic artery during reactive hyperemia, tested experimentally. METHODS AND RESULTS: in 21 large hounds under surgical anesthesia, proximal and distal left circumflex and obtuse marginal coronary arteries were instrumented with electromagnetic flowmeters, proximal and distal machined Teflon screw-down stenosers with round concentric closing and distal silk-in-tubing sleeve occluders. Baseline reactive hyperemia was recorded after 15-second occlusions of both arteries at baseline and for progressive distal stenosis during each step of progressive proximal stenosis. At each combination of stenosis, a coronary arteriogram was obtained using left Judkins catheters and Philips cine calibrated with modulated transfer function to ± 0.1 mm accuracy for fluid dynamic analysis of arterial stenosis-branching anatomy. In 324 experiments of parent-child stenosis combinations of the left circumflex artery with an intervening obtuse marginal branch, coronary flow reserve (CFR) calculated by the fluid dynamic model accounting for stenosis-branch interactions and "branch steal" correlated with CFR directly measured by flowmeter (linear regression, CFRartgm=0.18+0.7×CFRflowmtr with Pearson r=0.73). Quantitative arteriography and positron emission tomography perfusion imaging confirmed the concept in clinical examples. CONCLUSIONS: functional severity of anatomically fixed stenosis is not constant, specific, or independent of other stenosis in branching coronary arteries but requires analysis as an integrated component of the entire branching coronary artery tree to guide revascularizations.
Authors: Catherine Pagiatakis; Jean-Claude Tardif; Philippe L L'Allier; Rosaire Mongrain Journal: Med Biol Eng Comput Date: 2017-05-13 Impact factor: 2.602
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Authors: Yousif Ahmad; Jeroen Vendrik; Ashkan Eftekhari; James P Howard; Christopher Cook; Christopher Rajkumar; Iqbal Malik; Ghada Mikhail; Neil Ruparelia; Nearchos Hadjiloizou; Sukhjinder Nijjer; Rasha Al-Lamee; Ricardo Petraco; Takayuki Warisawa; Gilbert W M Wijntjens; Karel T Koch; Tim van de Hoef; Guus de Waard; Mauro Echavarria-Pinto; Angela Frame; Nilesh Sutaria; Gajen Kanaganayagam; Ben Ariff; Jon Anderson; Andrew Chukwuemeka; Michael Fertleman; Sasha Koul; Juan F Iglesias; Darrel Francis; Jamil Mayet; Patrick Serruys; Justin Davies; Javier Escaned; Niels van Royen; Matthias Götberg; Christian Juhl Terkelsen; Evald Høj Christiansen; Jan J Piek; Jan Baan; Sayan Sen Journal: Circ Cardiovasc Interv Date: 2019-11-22 Impact factor: 6.546