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Celebrex, other COX-2 Inhibitors May Cause Heart Arrhythmias

Jan 17, 2008 | Parker Waichman LLP Research on fruit flies and rats has found that COX-2 inhibitors, a class of painkillers that includes Celecoxib (brand name Celebrex) and the ill-fated Vioxx, can cause heart arrhythmias.    Since Vioxx was pulled from the market several years ago after being linked to heart attacks, research on COX-2 inhbitors has become more vigrourous.

In both fruit fly and rat models, researchers discovered that Celebrex can induce heart arrhythmia.  More interestingly, this effect is independent of the COX-2 enzyme.  Arrhythmias are disorders of the regular rhythmic beating of the heart and can occur in a healthy heart and be of minimal consequence.  They may also indicate a serious problem and lead to heart disease, stroke, or sudden cardiac death.  COX-2 inhibitors are newly developed drugs for inflammation that selectively block the COX-2 enzyme.  Blocking the COX-2 enzyme stops the production of the chemical messengers—or prostaglandins—that cause the pain and swelling of arthritis inflammation.  COX-2 selective inhibitors are a new class of nonsteroidal anti-inflammatory drugs, or NSAIDs that directly targets the COX-2 enzyme.  Because they selectively block the COX-2 enzyme—the enzyme responsible for inflammation and pain—and not the COX-1 enzyme, these drugs are uniquely different from traditional NSAIDs.

Satpal Singh and colleagues tested various Celecoxib doses on the heart rate of Drosophila, a genus of small flies often referred to as fruit flies or vinegar flies, because of their tendency to linger around over-ripe or rotting fruit, and a good model for human cardiac pharmacology.  To their surprise, administering 3 ƒÝm Celecoxib—which is not much higher than the plasma levels in humans taking the drug—reduced the heart rate and increased beating irregularities, while 30 ƒÝm was enough to stop the heart within one minute.  Researchers were surprised at the results because Drosophila do not have COX-2 enzymes.  Rather, Celecoxib could directly inhibit the potassium channels that help generate the electric current that drives heartbeat.  The researchers were able to achieve similar heart-stopping results in rat cardiac cells, whereas aspirin, another potent COX-2 inhibitor, had no effect, confirming that another mechanism is at work.  The drug also inhibited rat and human potassium channels expressed in a human cell line.

Singh and colleagues point out that since these arrhythmia effects bypass COX-2, it is unclear if other COX-2 inhibitors would yield similar results.  They also stress it is too early to speculate on human effects, although their results suggest Drosophila—one of the most valuable of organisms in biological research and has been used as a model research organism for almost a century—are a valuable tool to investigate other COX-2 drugs.

Late last summer, authors of an article published in a special cardiology issue of The Lancet wrote that use of celecoxib after stent implantation in patients with coronary artery disease is safe, reducing the need revascularisation of the target lesion; however, an accompanying comment warned that clinical trials indicated that long-term use of celecoxib can expose patients to an additional risk of heart attack.

A 2006 review of 138 randomized trials and almost 150,000 participants revealed selective COX-2 inhibitors were associated with a moderately increased risk of vascular events, mainly due to a twofold-increased risk of myocardial infarction.

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