title: Microvascular resistance is not influenced by epicardial coronary artery stenosis severity: experimental validation.
abstract: BACKGROUND
  The effect of epicardial artery stenosis on myocardial microvascular resistance remains controversial. Recruitable collateral flow, which may affect resistance, was not incorporated into previous measurements.
  
  
  RESULTS
  In an open-chest pig model, distal coronary pressure was measured with a pressure wire, and the apparent minimal microvascular resistance was calculated during peak hyperemia as pressure divided by flow, measured either with a flow probe around the coronary artery (R(micro app)) or with a novel thermodilution technique (apparent index of microcirculatory resistance [IMR(app)]). These apparent resistances were compared with the actual R(micro) and IMR after the coronary wedge pressure and collateral flow were incorporated into the calculation. Measurements were made at baseline (no stenosis) and after creation of moderate and severe epicardial artery stenoses. In 6 pigs, 189 measurements of R(micro) and IMR were made under the various epicardial artery conditions. Without consideration of collateral flow, R(micro app) (0.43+/-0.12 to 0.46+/-0.10 to 0.51+/-0.11 mm Hg/mL per minute) and IMR(app) (14+/-4 to 17+/-7 to 20+/-10 U) increased progressively and significantly with increasing epicardial artery stenosis (P<0.001 for both). With the incorporation of collateral flow, neither R(micro) nor IMR increased as a result of increasing epicardial artery stenosis.
  
  
  CONCLUSIONS
  After collateral flow is taken into account, the minimum achievable microvascular resistance is not affected by increasing epicardial artery stenosis.
authors.affiliation: Division of Cardiovascular Medicine, Stanford University Medical Center, Stanford, Calif, USA. wfearon@stanford.edu
authors.forename: William F
authors.initials: WF
authors.lastname: Fearon
authors.forename: Wilbert
authors.initials: W
authors.lastname: Aarnoudse
authors.forename: Nico H J
authors.initials: NH
authors.lastname: Pijls
authors.forename: Bernard
authors.initials: B
authors.lastname: De Bruyne
authors.forename: Leora B
authors.initials: LB
authors.lastname: Balsam
authors.forename: David T
authors.initials: DT
authors.lastname: Cooke
authors.forename: Robert C
authors.initials: RC
authors.lastname: Robbins
authors.forename: Peter J
authors.initials: PJ
authors.lastname: Fitzgerald
authors.forename: Alan C
authors.initials: AC
authors.lastname: Yeung
authors.forename: Paul G
authors.initials: PG
authors.lastname: Yock
mesh_terms: D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D003097:Collateral Circulation; D003326:Coronary Circulation / Q000187:drug effects; D023921:Coronary Stenosis / Q000503:physiopathology*; D008833:Microcirculation / Q000187:drug effects; D023421:Models, Animal; D010208:Papaverine / Q000494:pharmacology; D010496:Pericardium; D013552:Swine; D014655:Vascular Resistance; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D010208:Papaverine