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How the Balancing Act Between Two Forms of the Cyclooxygenase Enzyme Protects the Heart

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www.ProHealth.com • May 6, 2002




(Philadelphia, PA) - Cyclooxygenase (COX) is a pharmacologically important enzyme that has a role in blood clotting and inflammation. The relationship between its two major forms and their products, however, has been largely undefined. In the April 19th issue of the journal Science, researchers at the University of Pennsylvania School of Medicine explain the balanced relationship between two products of the cyclooxygenases - prostacyclin (PGI2) and thromboxane (TxA2) - and their potential relevance to cardiovascular disease and the effects of selective inhibitors of COX-2, such as Merck's Vioxx (R) and Pharmacia / Upjohn's Celebrex (R).

COX-1, the form of cyclooxygenase found in platelets, makes TxA2, which causes blood vessels to constrict and platelets to become sticky - the first step in a heart attack or stroke. COX-2, by contrast, is expressed in blood vessels and is a major source of prostacyclin (PGI2), which dilates blood vessels and prevents the activation of platelets. Drugs that block COX-1 can thin blood, while drugs that block COX-2 can decrease pain associated with inflammation.

"Aspirin has been proven effective in lowering the risk of a second heart attack or stroke by blocking TxA2 formation by COX - 1, thereby thinning the blood," said Garret A. FitzGerald, MD, chair of the Penn Department of Pharmacology and director of the Penn Center for Experimental Therapeutics. "We had previously found evidence that selective COX-2 inhibitors, which are prescribed for the relief of pain and inflammation can allow TxA2 formation to go unchecked by suppressing the production of PGI2.

We wished to investigate the likely importance of this observation by clarifying the interplay of the two COX products in the cardiovascular system."

FitzGerald observed almost twenty years ago that formation of both thromboxane and prostacyclin is increased in patients with heart and blood vessel disease who benefit from aspirin. Given their opposing actions, he speculated that PGI2 production is stimulated as a response to platelet interactions with the vessel wall, to limit the harmful effects of thromboxane on the cardiovascular system - a speculation that the Science article upholds.

In mice bred to lack receptors for PGI2, FitzGerald and his colleagues showed that both the vascular response to injury and the corresponding activation of platelets were both markedly exaggerated. Similarly, mice that over-expressed receptors for TxA2 also produced these exaggerated effects. The effect was diminished when researchers either deleted the TxA2 receptor or blocked the receptor using an experimental drug. When the researchers deleted both the TxA2 receptor and the PGI2 receptor, it cancelled out the effect of inactivating the PGI2 receptor alone.

"We were struck by the increase in thromboxane formation
when prostacyclin was unable to work and wondered if it mediated the consequences of removing the PGI2 receptor," said Yan Cheng MD, PhD, first author on the paper. FitzGerald's group had shown previously that formation of both TxA2 and PGI2 are increased by percutaneous coronary angioplasty (PCA), a procedure mimicked in the animal studies. In humans, aspirin halves the chances of a heart attack complicating PCA.

The evidence that PGI2 restrains the harmful cardiovascular effects of TxA2 in vivo may have relevance to three important classes of cardiovascular drugs. Firstly, coincidental inhibition of both COX products may limit the effectiveness of aspirin. Indeed, an experimental formulation of aspirin that only targets platelets was developed by FitzGerald in collaboration with the Bayer corporation and has been shown to be effective in heart attack prevention.

However, whether it is superior to conventional forms of aspirin has never been assessed. Secondly, TxA2 receptor antagonists bypass suppression of PGI2 and may offer advantages over aspirin. The antagonist used in the Science study is under development by Servier. Finally, FitzGerald and colleagues reported several years ago that selective inhibitors of COX-2 inhibit PGI2, but not TxA2. The possibility that such drugs might constitute a cardiovascular risk has since attracted considerable attention.

"While such a clinical risk is far from established," said FitzGerald, "our results afford a credible mechanism by which a cardiovascular hazard might occur in that minority of individuals predisposed to thrombosis."

Source: University of Pennsylvania Medical Center



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