title: Paradoxical increase in microvascular resistance during tachycardia downstream from a severe stenosis in patients with coronary artery disease : reversal by angioplasty.
abstract: BACKGROUND
  The pathophysiology of microvascular response to a severe coronary stenosis has not been conclusively identified. The aim of this study was to characterize the human vasomotor response to pacing-induced ischemia of both the stenotic arterial segment and the distal microcirculation.
  
  
  RESULTS
  Sixteen patients with stable angina and single-vessel disease were studied. Blood flow velocity and transstenotic pressure gradient were monitored at baseline, after intracoronary adenosine (2 mg), and during ischemia induced by atrial pacing with and without adenosine. At the end of this protocol, the study was repeated after intracoronary phentolamine in 7 patients and after angioplasty in 9. Stenosis resistance was calculated as the ratio between mean pressure gradient and mean flow, and microvascular resistance as the ratio between mean distal pressure and mean flow; values were expressed as percent of baseline. Adenosine decreased (P<0.05) baseline microvascular resistance to 52+/-17%, but not stenosis resistance. Pacing increased both stenosis and microvascular resistances (244+/-96% and 164+/-60% of baseline, respectively, P<0.05). Addition of adenosine to pacing decreased both stenosis (143+/-96% of baseline, P<0.05 versus ischemia) and microvascular (51+/-17% of baseline, P<0.05 versus baseline and ischemia) resistances. Phentolamine did not affect coronary resistance at any step of the protocol. Angioplasty and stenting restored a progressive decline in microvascular resistance during pacing (51+/-19% of baseline, P<0.05 versus baseline).
  
  
  CONCLUSIONS
  In patients with coronary artery disease, tachycardia-induced ischemia was associated with elevated resistance of both the stenotic segment and the microvasculature. Revascularization prevents this paradoxical behavior.
authors.affiliation: CNR Institute of Clinical Physiology, Pisa, Italy. battesto@po.ifc.pi.cnr.it
authors.forename: G
authors.initials: G
authors.lastname: Sambuceti
authors.forename: M
authors.initials: M
authors.lastname: Marzilli
authors.forename: S
authors.initials: S
authors.lastname: Fedele
authors.forename: C
authors.initials: C
authors.lastname: Marini
authors.forename: A
authors.initials: A
authors.lastname: L'Abbate
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000368:Aged; D015906:Angioplasty, Balloon, Coronary; D003326:Coronary Circulation / Q000502:physiology*; D003327:Coronary Disease / Q000503:physiopathology* / Q000628:therapy; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D006801:Humans; D008875:Middle Aged; D010646:Phentolamine / Q000494:pharmacology; D013610:Tachycardia / Q000503:physiopathology*; D014655:Vascular Resistance
chemical_list: D000317:Adrenergic alpha-Antagonists; D000241:Adenosine; D010646:Phentolamine