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| Dr Warren Laskey is currently director of interventional cardiology at the Uniformed Services University of the Health Sciences in Bethesda, Maryland. Before that he was director of the cardiac catheterisation laboratory and associate director of the division of cardiology at the University of Maryland School of Medicine and, subsequently, director of the cardiac catheterisation laboratory at the National Naval Medical Center in Bethesda, Maryland. He is the author of over 100 publications on diverse areas of clinical cardiology with an emphasis on interventional cardiology, and served as co-principal investigator of the Contrast Media Utilization in High Risk PTCA (COURT) Trial. |
Radiographic contrast media and thrombosis:
the more we know, the more we need to know
Warren K Laskey
Division of Cardiology, Uniformed Services University of
the Health Sciences, Bethesda, MD, USA
Address for correspondence:
Dr WK Laskey, MD
Division of Cardiology, A-3060
Uniformed Services University of the Health Sciences
4301 Jones Bridge Road, Bethesda, MD 20814
Tel: +1-(301)-295-3623
Fax: +1-(410)-360-7306
Email: warrenlaskey@earthlink.net
Abstract
The diverse effects of radiographic contrast media (RCM) on virtually all organ systems extend to the haemostatic system. Before the advent of non-ionic RCM, little controversy surrounded these effects, i.e. inhibition of thrombin generation, disruptive effects on arterial endothelium and inhibition of platelet aggregation. Thus, ionic high osmolar contrast media (HOCM) were viewed as having ‘anti-coagulant’ and ‘anti-thrombotic’ properties. The fact that these inhibitory properties were chiefly in vitro phenomena, that significant dilution occurred in the circulation resulting in any local (inhibitory) effects being transient and that differentiation of effects caused by ionicity or osmolality were limited by the availability of RCM other than HOCM all contributed to the origin of the ‘clotting controversy’ when non-ionic RCM was introduced.
The following review takes its motivation from the clinical perspective. Thrombosis is viewed as the end result of the pathological interaction of vessel wall, blood flow and formed elements of the blood. The interaction of ionic and non-ionic RCM with each of these elements is discussed.While consensus exists with respect to the in vitro and in vivo anti-coagulant properties of RCM (inhibition of thrombin formation), less consensus focuses on the in vitro and in vivo effects of RCM on platelet function. Furthermore, extension of the in vitro data to the clinical setting is problematic given the lack of clinical data suggesting a pro-thrombotic effect of non-ionic RCM. As many of the potentially deleterious effects on endothelial and/or platelet function are the result of either RCM ionicity or osmolality, the results of studies with non-ionic, iso-osmolar RCM are discussed.
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