title: Coronary endothelial dysfunction is associated with a reduction in coronary artery compliance and an increase in wall shear stress.
abstract: OBJECTIVE
  Endothelial dysfunction is associated with arterial stiffness in large arteries. The purpose of this study was to investigate the association between coronary endothelial dysfunction, coronary artery compliance and wall shear stress in patients with early atherosclerosis.
  
  
  METHODS
  Coronary endothelial function was assessed according to responses to intracoronary acetylcholine in 120 patients without significant coronary stenosis. Acceleration of peak velocity (ACC), which is inversely related to coronary artery compliance, was derived from coronary flow velocity spectra, and wall shear rate (WSR) was calculated. Measurements were performed at baseline and after intracoronary nitroglycerin in order to eliminate the contribution of vascular smooth muscle tone to coronary artery compliance.
  
  
  RESULTS
  In all patients, heart rate significantly increased (72+/-1 to 77+/-1 bpm, p<0.01) and mean arterial pressure decreased (97+/-2 to 93+/-1 mm Hg, p<0.01) after nitroglycerin. Coronary blood flow (CBF) and resistance were not significantly changed, but the diastolic to systolic velocity ratio increased significantly (2.15+/-0.08 to 5.36+/-0.61, p<0.01). Patients with abnormal endothelial function (n=70) had a higher WSR at baseline (559+/-41 vs 440+/-26 s(-1), p<0.05) and after nitroglycerin (457+/-41 vs 339+/-29 s(-1), p<0.05), and a higher ACC after nitroglycerin (3.9+/-0.4 vs 2.8+/-0.4 m/s(2), p<0.05) than patients with normal function (n=50).
  
  
  CONCLUSIONS
  The current study demonstrates that intracoronary nitroglycerin does not contribute to an increase of CBF but alters the phasic coronary flow pattern. Furthermore, early coronary atherosclerosis characterised by endothelial dysfunction is associated with a decrease in coronary artery compliance and an increase in wall shear stress. Therefore, coronary wall properties are affected early in the atherosclerosis process.
authors.affiliation: Division of Cardiovascular Disease, Mayo Clinic, 200 First Street SW, Rochester, Minnesota 55905, USA. lerman.amir@mayo.edu
authors.forename: Takuro
authors.initials: T
authors.lastname: Takumi
authors.forename: Eric H
authors.initials: EH
authors.lastname: Yang
authors.forename: Verghese
authors.initials: V
authors.lastname: Mathew
authors.forename: Charanjit S
authors.initials: CS
authors.lastname: Rihal
authors.forename: Rajiv
authors.initials: R
authors.lastname: Gulati
authors.forename: Lilach O
authors.initials: LO
authors.lastname: Lerman
authors.forename: Amir
authors.initials: A
authors.lastname: Lerman
mesh_terms: D001783:Blood Flow Velocity / Q000187:drug effects; D003187:Compliance; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D005996:Nitroglycerin / Q000494:pharmacology; D013314:Stress, Mechanical; D014655:Vascular Resistance / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014665:Vasodilator Agents; D005996:Nitroglycerin
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