title: Heterogeneity of vasomotor response to acetylcholine along the human coronary artery.
abstract: OBJECTIVE
  In view of the segmental occurrence of coronary atherosclerosis, we postulated that acetylcholine may cause heterogeneous vasomotion, depending on the extent of vessel analyzed, criteria for change in vessel caliber and dose of drug administered.
  
  
  BACKGROUND
  Previous studies have reported that acetylcholine causes constriction of atherosclerotic arteries. This dysfunction of endothelium-dependent dilation may be seen without angiographically detectable disease.
  
  
  METHODS
  We developed algorithms to quantitate the dimensions of a single coronary artery over virtually its entire length during a control state and during graded doses of intracoronary acetylcholine. On the basis of triplicate control angiograms, the limit of detection of a change from control diameter was 0.31 mm (> or = 2 SD).
  
  
  RESULTS
  Analysis of multiple segments (each 5.6 +/- 1.1 [mean +/- SD] mm) along a single coronary artery revealed a heterogeneous response to acetylcholine in 27 of 31 patients at the 10(-4) mol/liter dose and in 29 of 31 patients when responses at 10(-6), 10(-5) and 10(-4) mol/liter doses were combined; in this latter analysis, constriction and dilation in the same vessel occurred in 45% of the patients. With acetylcholine, most of 349 segments demonstrated no change, but the greatest frequency of vasoconstriction (24.6%) and vasodilation (6.9%) was seen at the 10(-4) mol/liter dose. Inducible vasomotion was observed as far distally as 7.3 cm from the site of acetylcholine infusion.
  
  
  CONCLUSIONS
  Response to intracoronary acetylcholine with mild coronary disease is heterogeneous; disparate dimensional responses may occur in different segments of the same vessel. Inclusion of all analyzable regions of a coronary artery and the use of a reproducibility limit for quantitative angiography are optimal for assessment of segmental coronary vasomotion.
authors.affiliation: University of California San Diego.
authors.forename: W F
authors.initials: WF
authors.lastname: Penny
authors.forename: H
authors.initials: H
authors.lastname: Rockman
authors.forename: J
authors.initials: J
authors.lastname: Long
authors.forename: V
authors.initials: V
authors.lastname: Bhargava
authors.forename: K
authors.initials: K
authors.lastname: Carrigan
authors.forename: A
authors.initials: A
authors.lastname: Ibriham
authors.forename: R
authors.initials: R
authors.lastname: Shabetai
authors.forename: J
authors.initials: J
authors.lastname: Ross
authors.forename: K L
authors.initials: KL
authors.lastname: Peterson
mesh_terms: D000109:Acetylcholine / Q000008:administration & dosage; D000465:Algorithms; D006328:Cardiac Catheterization; D017023:Coronary Angiography / Q000379:methods*; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000503:physiopathology*; D003331:Coronary Vessels / Q000187:drug effects* / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007091:Image Processing, Computer-Assisted; D007261:Infusions, Intra-Arterial; D008297:Male; D008875:Middle Aged; D012815:Signal Processing, Computer-Assisted; D014666:Vasomotor System / Q000187:drug effects* / Q000503:physiopathology
chemical_list: D000109:Acetylcholine