Vioxx Has No Effect on Arteries

New painkiller doesn't undercut aspirin in heart patients, study finds

TUESDAY, Nov. 18, 2003 (HealthDayNews) -- One of the new painkillers touted as being easier on the stomach than conventional medications doesn't appear to undercut aspirin's protective effect on the blood vessels of patients with artery disease.

But it doesn't appear to be helpful, either.

So says a study which found that one of the drugs, Vioxx, sold by Merck and Co., neither reduced nor increased the markers of inflammation and vessel health in patients taking aspirin and other drugs to control coronary artery disease. Vioxx is one of several medications called cox-2 inhibitors, named for their ability to block an inflammatory molecule called cyclooxygenase-2. Cox-2 shows up in narrowed arteries but not in healthy ones, leading researchers to speculate that cox-2 inhibitors might reduce inflammation associated with vessel disease.

The new work, reported in the Nov. 19 issue of the Journal of the American College of Cardiology, undermines a Swiss study released earlier this year. That study showed that another cox-2 inhibitor, celecoxib -- sold as Celebrex -- appeared to reduce inflammation and promote the healthy widening of blood vessels.

Nor does the latest study support, at least indirectly, fears of some researchers that cox-2 inhibitors may spur the formation of blood clots linked to abnormal vessel cells.

Dr. Subodh Verma, a heart specialist at the University of Toronto, calls the findings "reassuring." However, Verma, co-author of an editorial accompanying the journal article, says the neutral results apply only to patients also taking low doses of aspirin for their heart disease. "It's hard to know what the results would be without aspirin," Verma says. "This discussion and debate might be completely different."

Vioxx and Celebrex, sold by Pfizer Inc., have been heralded as major additions to arthritis care. Arthritis is a common condition -- one form, osteoarthritis, affects roughly 20 million Americans -- and many patients are older, and thus prime candidates for heart disease. Thus, there's ample overlap between the two conditions, and that means treatments often overlap, too.

The new study followed 60 men and women diagnosed with coronary heart disease. All were taking a daily, low dose of aspirin to prevent heart attacks, and half were also given 25 milligrams a day of Vioxx (or rofecoxib).

After eight weeks of treatment, the researchers, led by Dr. Lawrence Title of Queen Elizabeth II Health Sciences Centre in Halifax, Nova Scotia, compared several aspects of vessel health and inflammation between the two groups. These included the ability of vessels to dilate and levels of C-reactive protein, a potent signal of inflammation. But they found no meaningful differences between the two groups in these or other markers -- suggesting that piggybacking Vioxx onto aspirin therapy neither worsened nor improved vessel disease.

Dr. Frank Ruschitzka, a cardiologist at University Hospital in Zurich, Switzerland and leader of the Swiss study that contradicts the latest research, calls the new finding "interesting, as it indeed shows that rofecoxib doesn't decrease endothelial function, as hypothesized by some of the scientists worrying" that it might.

However, Ruschitzka says, what's true in Vioxx doesn't necessarily hold for Celebrex. Celebrex improves vessel cell function in patients with coronary artery disease and hypertension, he says. What's more, a head-to head comparison his group conducted found that Celebrex, but not Vioxx, improves vessel cell function and reduces oxidative stress and inflammation associated with high blood pressure in rats.

"This could fully explain the differences seen with rofecoxib and celecoxib," he says. A report on that study appears in the Nov. 11 issue of Circulation.

More information

For more on C-reactive protein, try MedlinePlus. For more on heart disease, check out the American College of Cardiology or the American Heart Association.

SOURCES: Subodh Verma, M.D., Ph.D., assistant professor, division of cardiac surgery, University of Toronto; Frank Ruschitzka, M.D., department of cardiology, University Hospital, Zurich; Nov. 19, 2003, Journal of the American College of Cardiology; Nov. 11, 2003, Circulation
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