Caregiver's Home Companion Free captioning phone for those with hearing loss.
 HOME PAGE  SEARCH Go

Posted: March 04, 2008

Popular Arthritis Drug Can Disrupt Heart Rhythm

Celebrex, a popular arthritis drug that blocks pain by inhibiting an enzyme known as COX-2, has been shown in laboratory studies to induce arrhythmia, or irregular beating of the heart.
 
Researchers at the University at Buffalo, conducting basic research on potassium channels, found that low concentrations of the drug, equivalent to a standard prescription, reduced the heart rate and induced pronounced arrhythmia in fruit flies and the heart cells of rats.
Arrhythmia refers to any change in the normal sequence of the heart’s electrical impulses – either too fast, called tachycardia, or too slow, called bradycardia. Either situation can cause the heart to pump less effectively, and in cases where arrhythmias last for some time, the condition can be life threatening or fatal. Arrhythmias are common; about 2.2 million Americans are living with just one type of arrhythmia, called atrial fibrillation, according to the American Heart Association.
In the Buffalo research, Celebrex was found to inhibit the normal passage of potassium ions into and out of heart cells through pores in the cell membrane known as delayed rectifier potassium channels.
 
"The adverse effects of drugs like Celebrex and Vioxx based on their selective inhibition of COX-2 currently are a topic of intense discussion in the medical community," said Satpal Singh, Ph.D., associate professor of pharmacology and toxicology in the UB School of Medicine and senior author on the study, which appears in the Journal of Biological Chemistry. Vioxx was withdrawn from the market in September 2004.
 
"We now have shown an important new effect of Celebrex through a totally different pathway, one that is unrelated to the drug's effect as a pain reducer," Singh said. "The adverse effect arising from this unexpected mechanism definitely needs to be studied more closely, because the potassium channels inhibited by the drug are present in heart, brain and many other tissues in the human body.
 
Aware that COX-2 inhibitors had been shown to produce cardiovascular side effects, the researchers first tested whether Celebrex would affect the heart in fruit flies, a good animal system for studies on heart in other species, including humans.
 
"When we found an effect on the fly heart, we began looking for the underlying mechanism," said Singh. "We searched the fly genome and were surprised to find that these flies don't have cyclooxygenases, the enzymes targeted by Celebrex.
 
"Because the main effect of the drug in our study was induction of arrhythmia, and arrhythmia is often the result of ion-channel dysfunction," continued Singh, "we examined the drug's effect on potassium channels and other ion channels in their models and were struck by the strong inhibition of the potassium channels."
 
The researchers now are examining the underlying molecular mechanisms responsible for the drug's action and its effect on other ion channels that play a prominent role in setting the rhythm of the heart.
 
"We are trying to determine whether the drug binds directly to the channels or to some other molecule, and if it acts by blocking the pore of the channel through which potassium ions travel or by some other mechanism," Singh said.
 
(Article courtesy of ConsumerAffairs.com)

Email or share this story Bookmark and Share

Search CaregiversHome
Find with keyword(s):

Enter a keyword or phrase to search CaregiversHome's archives for related news topics, the latest news stories, timely times, and reference articles.

© 2008 Pederson Publishing, Inc. All Rights Reserved.
Commercial use, redistribution or other forms of reuse of this information is strictly prohibited without the prior written permission of Pederson Publishing.

_____

View The Caregiver's Hotline in which this article first appeared

Back to Top

Privacy Statement Contact Us Site Map Products & Services Our Partners Advertise
© Copyright 2003-2020. Pederson Publishing, Inc. All rights reserved.