The Impact of Coronary Artery Disease on the Coronary Vasomotor Response to Nonionic Contrast Media

Author:

Limbruno Ugo1,Petronio Anna Sonia1,Amoroso Giovanni1,Baglini Roberto1,Paterni Giovanni1,Merelli Antonella1,Mariotti Rita1,Raffaele De Caterina 1,Mariani Mario1

Affiliation:

1. From the Cardiac and Thoracic Department, University of Pisa; and CNR Institute of Clinical Physiology and Scuola Superiore S. Anna (R.D.), Pisa, Italy.

Abstract

Background —Coronary 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 Results —We 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 N G -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 N G -monomethyl- l -arginine, blunted the vasodilating effect of iodixanol and iopromide (by 80% and 76%, respectively; P <0.001). Conclusions —Nonionic 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.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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