title: Influence of percutaneous coronary intervention on coronary microvascular resistance index.
abstract: BACKGROUND
  Coronary microvascular resistance during maximal hyperemia is generally assumed to be unaffected by percutaneous coronary interventions (PCIs). We assessed a velocity-based index of hyperemic microvascular resistance (h-MR(v)) by using prototypes of a novel, dual-sensor (Doppler velocity and pressure)-equipped guidewire before and after PCI to test this hypothesis.
  
  
  RESULTS
  Aortic pressure, flow velocity (h-v), and pressure (h-P(d)) distal to 24 coronary lesions were measured simultaneously during maximal hyperemia induced by intracoronary adenosine. Measurements were obtained in the reference vessel before PCI and in the target vessel before and after PCI, stenting, and ultrasound-guided, upsized stenting. h-P(d) increased from 57.9+/-17.0 to 85.5+/-15.6 mm Hg, and h-MR(v) (ie, h-P(d)/h-v) decreased from 2.74+/-1.40 to 1.58+/-0.61 mm Hg x cm(-1) . s after stenting (both P<0.001). The reduction in h-MR(v) accounted for 34% of the decrease in total coronary resistance achieved by PCI. h-MR(v) of the target vessel after PCI was lower than that of the corresponding reference vessel despite a higher h-P(d) in the reference vessel (P<0.01). Post-PCI baseline MR(v) was correlated with baseline P(d) before PCI (P<0.01).
  
  
  CONCLUSIONS
  PCI-induced restoration of P(d) resulted in a reduction of h-MR(v) in accordance with the pressure dependence of h-MR(v). The decrease in h-MR(v) to a level below that of the corresponding reference vessel in the immediate post-PCI period and a lowered baseline MR(v) suggest microvascular remodeling induced by long-term exposure to a low-pressure environment.
authors.affiliation: Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.
authors.forename: Bart-Jan
authors.initials: BJ
authors.lastname: Verhoeff
authors.forename: Maria
authors.initials: M
authors.lastname: Siebes
authors.forename: Martijn
authors.initials: M
authors.lastname: Meuwissen
authors.forename: Bektas
authors.initials: B
authors.lastname: Atasever
authors.forename: Michiel
authors.initials: M
authors.lastname: Voskuil
authors.forename: Robbert J
authors.initials: RJ
authors.lastname: de Winter
authors.forename: Karel T
authors.initials: KT
authors.lastname: Koch
authors.forename: Jan G P
authors.initials: JG
authors.lastname: Tijssen
authors.forename: Jos A E
authors.initials: JA
authors.lastname: Spaan
authors.forename: Jan J
authors.initials: JJ
authors.lastname: Piek
mesh_terms: D000241:Adenosine; D000368:Aged; D000787:Angina Pectoris / Q000503:physiopathology / Q000628:therapy; D015906:Angioplasty, Balloon, Coronary / Q000295:instrumentation; D001794:Blood Pressure; D017023:Coronary Angiography; D003326:Coronary Circulation; D003331:Coronary Vessels / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics; D006801:Humans; D006940:Hyperemia / Q000503:physiopathology; D008297:Male; D008833:Microcirculation; D008875:Middle Aged; D015607:Stents; D018084:Ultrasonography, Interventional; D014655:Vascular Resistance; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D000241:Adenosine