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Hematology 2005
© 2005 The American Society of Hematology

The Cardiovascular Pharmacology of COX-2 Inhibition

Susanne Fries and Tilo Grosser

Correspondence: Tilo Grosser, MD, Institute for Translational Medicine and Therapeutics, University of Pennsylvania School of Medicine, 809 Biomedical Research Building, 421 Curie Blvd., Philadelphia, PA 19104-6084; Phone (215) 573 7600, Fax (215) 573 9004, tilo{at}spirit.gcrc.upenn.edu

Abstract

Selective inhibitors of cyclooxygenase (COX)-2, the coxibs, were developed to inhibit inflammatory prostaglandins derived from COX-2, while sparing gastroprotective prostaglandins primarily formed by COX-1. However, COX-2-derived prostaglandins mediate not only pain and inflammation but also affect vascular function, the regulation of hemostasis/ thrombosis, and blood pressure control. All coxibs depress COX-2-dependent prostacyclin (PGI2) biosynthesis without effective suppression of platelet COX-1-derived thromboxane (Tx) A2, unlike aspirin or traditional nonsteroidal anti-inflammatory drugs, which inhibit both COX-1 and COX-2. The actions of PGI2 oppose mediators, which stimulate platelets, elevate blood pressure, and accelerate atherogenesis, including TxA2. Indeed, structurally distinct inhibitors of COX-2 have increased the likelihood of hypertension, myocardial infarction and stroke in controlled clinical trials. The detection of these events in patients is related to the duration of exposure and to their baseline risk of cardiovascular disease. Thus, coxibs should be withheld from patients with preexisting cardiovascular risk factors, and exposed patients at low cardiovascular baseline risk should be monitored for changes in their risk factor profile, such as increases in arterial blood pressure.


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Copyright © 2005 by the American Society of Hematology.