(Circulation. 2000;101:491.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Cardiac and Thoracic Department, University of Pisa; and CNR Institute of Clinical Physiology and Scuola Superiore S. Anna (R.D.), Pisa, Italy.
Correspondence to Ugo Limbruno, MD, PhD, Cardiac and Thoracic Department, Cisanello Hospital, Via Paradisa 2, 56124, Pisa, Italy. E-mail ulimbru{at}tin.it
BackgroundCoronary artery disease (CAD) alters the vasomotor response to a variety of pharmacological agents. We tested the hypothesis that CAD also has an impact on the coronary vasomotor response to radiologic contrast media.
Methods and ResultsWe performed quantitative coronary
angiography in 42 patients without angiographic evidence of CAD and 38
patients with CAD in the left coronary artery. Angiographically
smooth coronary segments (n=235) were analyzed for
changes on luminal diameters and coronary venous oxygen
saturation in response to 3 media: the nonionic dimer iodixanol, the
nonionic monomer iopromide, and the ionic agent ioxaglate. In subjects
without CAD, we assessed the effects of intracoronary
administration of the nitric oxide synthase inhibitor
NG-monomethyl-L-arginine and of the
cyclooxygenase inhibitor
indomethacin on such changes. Iodixanol induced
coronary vasodilation in subjects without CAD (8.8±8.6%,
P<0.001). Patients with CAD exhibited no significant
diameter changes in segments
20 mm apart from a stenosis
(4.7±9.4%, P=NS) and significant constriction in
segments <20 mm from a stenosis (-3.8±4.6%,
P<0.05). Similar results were obtained with iopromide,
but no changes were found with ioxaglate. All contrast media induced
transient (<35 seconds) increases in coronary venous oxygen
saturation in all subjects. Indomethacin, but not
NG-monomethyl-L-arginine, blunted the
vasodilating effect of iodixanol and iopromide (by 80% and 76%,
respectively; P<0.001).
ConclusionsNonionic contrast media induce a vasodilatory response in normal vessels not by a mechanism involving increased flow or endothelial nitric oxide synthesis, but rather by depending on preserved vascular cyclooxygenase activity. CAD changes normal epicardial vasodilatory response into vasoconstriction.
Key Words: contrast media coronary disease vasoconstriction vasodilation endothelium-derived factors
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