title: Determinants of coronary steal in chronic total coronary occlusions donor artery, collateral, and microvascular resistance.
abstract: OBJECTIVE
  We aimed to assess the mechanisms of coronary steal by direct hemodynamic measurements of the collateral circulation in chronic total coronary occlusions (CTO).
  
  
  BACKGROUND
  Coronary steal may cause ischemia despite well-developed collaterals in coronary artery disease.
  
  
  METHODS
  Fifty-six patients were studied during recanalization of a CTO. Before recanalization, the fractional flow reserve in the donor artery (FFR(D)) at the takeoff of the collaterals and the coronary flow reserve were recorded. After crossing the occlusion, the distal coronary flow velocity was measured by a Doppler wire (APV(Occl)), and distal pressure by a pressure wire. Changes of these parameters were assessed during intravenous adenosine (140 microg/kg/min). Resistance indexes for the donor artery (R(D)), collaterals (R(C)), and microcirculation (R(P)) were calculated.
  
  
  RESULTS
  Adenosine caused a decrease of APV(Occl) (i.e., coronary steal, in 26 patients [group S], an increase in 19 patients [group R], and no change in 11 patients). The FFR(D) was lower in group S. R(D) and R(C) increased in group S, while R(D) did not change significantly and R(C) decreased in group R. Patients with steal had more severe regional dysfunction. Patients with steal but without an FFR(D) <0.8 tended to have an impaired microvascular function.
  
  
  CONCLUSIONS
  We could demonstrate that coronary steal in man is mainly due to a hemodynamically significant donor artery lesion, but can also occur due to an impaired vasodilatory reserve of the microcirculation in the absence of a donor artery lesion. Coronary steal may have an adverse influence on the preservation of myocardial function by collaterals.
authors.affiliation: Clinic for Internal Medicine I, Friedrich-Schiller-University Jena, Jena, Germany. gerald.werner@med.uni-jena.de
authors.forename: Gerald S
authors.initials: GS
authors.lastname: Werner
authors.forename: Michael
authors.initials: M
authors.lastname: Fritzenwanger
authors.forename: Dirk
authors.initials: D
authors.lastname: Prochnau
authors.forename: Gero
authors.initials: G
authors.lastname: Schwarz
authors.forename: Markus
authors.initials: M
authors.lastname: Ferrari
authors.forename: Wilbert
authors.initials: W
authors.lastname: Aarnoudse
authors.forename: Nico H J
authors.initials: NH
authors.lastname: Pijls
authors.forename: Hans R
authors.initials: HR
authors.lastname: Figulla
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D015906:Angioplasty, Balloon, Coronary; D001783:Blood Flow Velocity; D001794:Blood Pressure; D003097:Collateral Circulation; D003326:Coronary Circulation; D023921:Coronary Stenosis / Q000503:physiopathology* / Q000628:therapy; D003331:Coronary Vessels / Q000503:physiopathology; D015150:Echocardiography, Doppler; D005260:Female; D006801:Humans; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D014655:Vascular Resistance; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine