title: Influence of differential vascular remodeling on the coronary vasomotor response.
abstract: OBJECTIVE
  Arterial remodeling may increase or decrease the luminal encroachment of atherosclerotic plaques in the coronary circulation. However, the factors determining the nature and consequences of the remodeling process remain poorly characterized. The study aims were to assess whether the pattern of vascular remodeling influences the physical and vasomotor responses of the coronary arteries in vivo in man.
  
  
  METHODS
  Coronary vessel area, distensibility and stiffness were determined in positively, negatively and non-remodeled arterial segments using intravascular ultrasound and Doppler flow measurement. Epicardial vasomotor responses were determined following intracoronary boluses of acetylcholine (10(-6) and 10(-4) M), adenosine (24-30 microg) and nitroglycerin (200 microg).
  
  
  RESULTS
  Fifty-six coronary arterial segments were studied in 25 patients. In comparison to non- and positively remodeled segments, negatively remodeled segments had a higher stiffness index (67+/-16 vs. 33+/-5 and 38+/-8, respectively; P<0.02) and appeared to have lower compliance and distensibility (0.66+/-0.17 vs. 1.65+/-0.54 and 0.94+/-0.18/mmHg; P=NS). Non-remodeled segments had a greater change in vessel area with 10(-6) M acetylcholine (4.9+/-0.8%), compared to positively and negatively remodeled segments (0.6+/-1.8% and -4.9+/-1.8%, respectively, P<0.05). A significant degree of preservation of vasodilatation to 10(-6) M acetylcholine was evident in positively remodeled compared with negatively remodeled segments (P<0.05). Nitroglycerin caused greater vasodilatation in non-remodeled segments (7.2+/-3.8%) than either positively or negatively remodeled segments (4.7+/-0.9 and 3.7+/-0.6%, respectively, P<0.05).
  
  
  CONCLUSIONS
  Vascular remodeling is an important and major determinant of local epicardial vasomotor responses. Both structural and functional abnormalities are associated with negative remodeling that may contribute to the adverse effects of such lesions.
authors.affiliation: Department of Cardiology, Royal infirmary, 51 Little France Crescent, Little France, Edinburgh EH16 4SA, UK.
authors.forename: Andrew L
authors.initials: AL
authors.lastname: McLeod
authors.forename: David E
authors.initials: DE
authors.lastname: Newby
authors.forename: David B
authors.initials: DB
authors.lastname: Northridge
authors.forename: Keith A A
authors.initials: KA
authors.lastname: Fox
authors.forename: Neal G
authors.initials: NG
authors.lastname: Uren
mesh_terms: D000109:Acetylcholine; D000241:Adenosine; D000704:Analysis of Variance; D017023:Coronary Angiography; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D003331:Coronary Vessels / Q000000981:diagnostic imaging / Q000473:pathology*; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000473:pathology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin; D018608:Ultrasonography, Doppler; D018084:Ultrasonography, Interventional; D014665:Vasodilator Agents
chemical_list: D014665:Vasodilator Agents; D005996:Nitroglycerin; D000241:Adenosine; D000109:Acetylcholine