K. Kugiyama et al., ASSOCIATION OF REMNANT LIPOPROTEIN LEVELS WITH IMPAIRMENT OF ENDOTHELIUM-DEPENDENT VASOMOTOR FUNCTION IN HUMAN CORONARY-ARTERIES, Circulation, 97(25), 1998, pp. 2519-2526
Citations number
24
Categorie Soggetti
Peripheal Vascular Diseas",Hematology,"Cardiac & Cardiovascular System
Background-It remains undetermined whether triglyceride-rich lipoprote
ins are an independent risk factor for atherosclerosis. Methods and Re
sults-The correlation of responses of coronary arterial diameter (quan
titative coronary angiography) and coronary blood flow (intracoronary
flow wire technique) to intracoronary infusion of acetylcholine (10 an
d 50 mu g/min) with coronary risk factors including remnant lipoprotei
n levels was statistically analyzed in 106 consecutive subjects with n
ormal coronary angiograms. Remnant Lipoproteins were isolated from fas
ting blood with an immunoaffinity mixed gel containing anti-apolipopro
tein (apo) A-1 and anti-apoB-100 monoclonal antibodies. In multivariat
e stepwise regression analysis, remnant lipoprotein levels had the mos
t significant correlation with. abnormal epicardial coronary vasomotor
responses to acetylcholine infusion, reflected by impaired dilation o
r constriction of the epicardial coronary arteries, and the levels als
o had an inverse and independent correlation with the coronary blood f
low increase in response to acetylcholine. In a subgroup of 53 consecu
tive subjects, constrictor responses of epicardial coronary diameters
to intracoronary infusion of N-G-monomethyl-L-arginine (50 mu mol/min
for 4 minutes) at baseline, reflecting the presence of coronary nitric
oxide bioactivity, had an inverse and independent correlation with re
mnant lipoprotein levels by use of multivariate analysis. Conclusions-
Remnant lipoprotein levels were independently associated with abnormal
endothelium-dependent vasomotor function in large and resistance coro
nary arteries in humans, indicating that remnant Lipoproteins may impa
ir endothelial vasomotor function in human coronary arteries. The decr
ease in coronary nitric oxide bioactivity may be responsible in part f
or the inhibitory effects of remnant lipoproteins.