title: Control of shear stress in the epicardial coronary arteries of humans: impairment by atherosclerosis.
abstract: Altered arterial wall shear stress may adversely affect vascular endothelium and contribute to atherogenesis. This study examined the hypothesis that, in humans, dilation of normal coronary arteries with increased flow limits increases in shear stress and that loss of flow-mediated dilation in atherosclerosis results in failure to control shear stress. Coronary blood flow was increased by infusing adenosine (0.022 to 2.2 mg/min) through a 2.5F Doppler flow catheter positioned in the middle segment of the left anterior descending coronary artery in 8 patients with mild atherosclerosis but no flow-limiting stenosis and in 10 patients with entirely smooth coronary arteries. Quantitative angiography and coronary flow velocity were used to estimate shear stress in a proximal segment of the left anterior descending artery exposed to increased flow, but not to adenosine. The peak increase in blood flow was the same in smooth (371 +/- 65%) and irregular (377 +/- 50%) arteries. However, at peak flow, dilation was greater in smooth segments (16.3 +/- 2.7%) than in irregular segments (2.0 +/- 1.5%) (p less than 0.001). In each patient, smooth segments dilated with increasing shear stress (slope 7.4 +/- 0.9%), whereas irregular segments dilated less (slope 0.9 +/- 0.6%) and showed greater increases in shear stress (p less than 0.01). The peak increase in shear stress was less in smooth (189 +/- 23%) than in irregular (365 +/- 52%) segments (p less than 0.01). These results suggest a control mechanism in normal coronary arteries whereby increases in shear stress stimulate vasodilation and thus limit further increases in this force at the endothelial surface.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115.
authors.forename: J A
authors.initials: JA
authors.lastname: Vita
authors.forename: C B
authors.initials: CB
authors.lastname: Treasure
authors.forename: P
authors.initials: P
authors.lastname: Ganz
authors.forename: D A
authors.initials: DA
authors.lastname: Cox
authors.forename: R D
authors.initials: RD
authors.lastname: Fish
authors.forename: A P
authors.initials: AP
authors.lastname: Selwyn
mesh_terms: D000241:Adenosine / Q000494:pharmacology; D000293:Adolescent; D000328:Adult; D000368:Aged; D001783:Blood Flow Velocity / Q000187:drug effects; D017023:Coronary Angiography; D003324:Coronary Artery Disease / Q000503:physiopathology*; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000503:physiopathology*; D005260:Female; D006439:Hemodynamics / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D011673:Pulsatile Flow; D013314:Stress, Mechanical; D014463:Ultrasonography; D014664:Vasodilation / Q000502:physiology
chemical_list: D000241:Adenosine